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Título:

Prevalencia de dislipidemia en niños y adolescentes chinos: un metanálisis

Tipo de estudio: Metanálisis
Año: 2015
Resultados:En este metanálisis se incluyeron un total de 24 artículos, con un tamaño total de la muestra de 129 426. La prevalencia global combinada de dislipidemia total se estimó en un 25,3 % (IC del 95 %: 12,7 %-37,8 %). Las tasas de prevalencia de CT alto, LDL-C, TG, HDL-C bajo e hiperlipemia fueron 4,1 % (IC 95 %: 3,4 %-4,9 %), 5,3 % (IC 95 %: 3,9 %-6,7 %), 8,5 % ( IC del 95 %:6,3 %-10,7 %), 6,8 % (IC del 95 %: 3,7 %-9,9 %), 4,8 % (IC del 95 %:0,6 %-9,1 %), respectivamente. Las niñas (3,4%) tenían menor prevalencia de TG elevados que los niños (5,6%), pero tenían mayor prevalencia de otros tipos diferentes de dislipemia. Los niños de 7 a 18 años tenían una mayor prevalencia general de dislipidemia (31,6 %) en comparación con los niños de 2 a 6 años (9,0 %). No hubo diferencias estadísticamente significativas por subgrupos de edad, región y período en cuanto a las tasas de prevalencia de TG elevados, CT y HDL-C bajos (P > 0,05).
Conclusiones: La prevalencia de dislipidemia fue alta y con tendencia creciente entre niños y adolescentes en China. Deben enfatizarse y promoverse programas de prevención y detección temprana de lípidos séricos anormales.
https://pubmed.ncbi.nlm.nih.gov/25876870/

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Affiliations

¹ Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College; School of Public Health, Ningxia Medical University.

² Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College.

³ Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College. Email: jiemi@vip.163.com.

Affiliations

¹ Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College; School of Public Health, Ningxia Medical University.

² Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College.

³ Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College. Email: jiemi@vip.163.com.

Abstract

Objective: To quantify the prevalence of dyslipidemia among children and adolescents in China.

Methods: Chinese Biomedical Database (CBM), Wanfang Databases, China National Knowledge Infrastructrue (CNKI) and PubMed were comprehensively searched. Original reports were selected if data on prevalence estimates of dyslipdemia among children and adolescents in China, was provided under cross-sectional epidemiological studies. Quality of the literature was evaluated through the STROBE statement. The prevalence through Meta was estimated using the Strata 11.0 software. Subgroup analysis was undertaken on gender, age, regions and secular trends issues. Sensitivity analysis was performed to evaluate the impact of quality or standard of diagnosis.

Results: A total of 24 papers were included in this Meta-analysis, with the whole sample size as 129 426. The overall pooled-prevalence of total dsylipidemia was estimated at 25.3% (95% CI: 12.7%-37.8%). Prevalence rates of high TC, LDL-C, TG, low HDL-C and hyperlipemia were 4.1% (95% CI:3.4%-4.9%), 5.3% (95% CI:3.9%-6.7%), 8.5% (95% CI:6.3%-10.7%), 6.8% (95% CI: 3.7%-9.9%), 4.8% (95%CI:0.6%-9.1%), respectively. Girls (3.4%) had lower prevalence of high TG than boys (5.6%), but having higher prevalence of other different types dyslipidemia. Children aged 7-18 years had higher overall prevalence of dyslipidemia (31.6%) when compared to children aged 2-6 years (9.0%). There were no statistically significant differences for subgroups of age, region and period regarding the prevalence rates of high TG, TC and low HDL-C(P > 0.05).

Conclusion: Prevalence of dyslipidemia was high and with increasing trend among children and adolescents in China. Early screening and prevention programs on abnormal serum lipids should be emphasized and promoted.

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He H, Pan L, Du J, Liu F, Jin Y, Ma J, Wang L, Jia P, Hu Z, Shan G. He H, et al. Am J Hum Biol. 2019 Sep;31(5):e23286. doi: 10.1002/ajhb.23286. Epub 2019 Jun 28. Am J Hum Biol. 2019. PMID: 31254309

Maternal gestational diabetes and childhood hyperlipidemia.

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national center for biotechnology information

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[Prevalence of dyslipidemia in Chinese children and adolescents:a Meta-analysis] - PubMed

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1 Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College; School of Public Health, Ningxia Medical University. 2 Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College. 3 Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College.

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https://pubmed.ncbi.nlm.nih.gov/28978219/
La hiperlipidemia ligada a los casos de enfermedades cardiovasculares representan una de las principales causas de mortalidad en el mundo, especialmente en adultos habitantes de EE.UU (53%). Donde los pacientes con hipercolesterolemia familiar presentan el doble de riesgo de desarrollar ECV a edades más tempranas.

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Abstract

Cardiovascular disease (CVD) is the leading cause of death among adults in the United States, and people with hyperlipidemia are at roughly twice the risk of developing CVD as compared to those with normal total cholesterol levels.1 Patients with familial hypercholesterolemia (FH) have an even greater risk of developing CVD at an earlier age; therefore, early detection and treatment are imperative to reduce cardiovascular events and premature death. Statins are the mainstay treatment for hyperlipidemia; however, the limitations of statins include treatment resistance, intolerance due to adverse events, and a lack of adherence which contribute to poor outcomes. As such, many patients require adjunct therapies to properly control hyperlipidemia including niacin, bile acid sequestrants, fibric acids, and ezetimibe. FH can be even more challenging to treat, often requiring the use of lomitapide, mipomersen, proprotein convertase subtilisin/kexin type 9 inhibitors, or low-density lipoprotein cholesterol apheresis, in addition to high dose conjunction with statins or other agents.2 The approach to determining the appropriate treatment options has also undergone important changes. Guidelines for the management of patients with hyperlipidemia vary in their recommendations, with the American College of Cardiology/American Heart Association recommending that treatment decisions be based on the intensity of response associated with various statins, while multiple other guidelines (eg, National Lipid Association (NLA) and the American Association of Clinical Endocrinologists and American College of Endocrinology) still support attaining prespecified lipid values to reduce cardiovascular risk.3-5 This article will review the epidemiology of hyperlipidemia and FH, risk factors associated with the development of disease, as well as the efficacy and safety of statins and adjunct treatment options.

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Lipid Lowering Therapy and Circulating PCSK9 Concentration.

Nozue T. Nozue T. J Atheroscler Thromb. 2017 Sep 1;24(9):895-907. doi: 10.5551/jat.RV17012. Epub 2017 Aug 14. J Atheroscler Thromb. 2017. PMID: 28804094 Free PMC article. Review.

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national center for biotechnology information

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Epidemiology and management of hyperlipidemia - PubMed

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Cardiovascular disease (CVD) is the leading cause of death among adults in the United States, and people with hyperlipidemia are at roughly twice the risk of developing CVD as compared to those with normal total cholesterol levels.1 Patients with familial hypercholesterolemia (FH) have an even great ...

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https://pubmed.ncbi.nlm.nih.gov/15148063/

Título: Una dieta cetogénica baja en carbohidratos versus una dieta baja en grasas para tratar la obesidad y la hiperlipidemia: un ensayo aleatorizado y controlado
Tipo de estudio y año :ECA del 2004
Resultados : En comparación con los que recibieron la dieta baja en grasas, los que recibieron la dieta baja en carbohidratos tuvieron mayores reducciones en los niveles de triglicéridos séricos (cambio, -0,84 mmol/L frente a -0,31 mmol/L [-74,2 mg/dL frente a -27,9 mg /dL]; P = 0,004) y mayores aumentos en los niveles de colesterol de lipoproteínas de alta densidad (0,14 mmol/L vs -0,04 mmol/L [5,5 mg/dL vs -1,6 mg/dL]; P < 0,001). Los cambios en el nivel de colesterol de lipoproteínas de baja densidad no difirieron estadísticamente (0,04 mmol/L [1,6 mg/dL] con la dieta baja en carbohidratos y -0,19 mmol/L [-7,4 mg/dL] con la dieta baja en grasas; P = 0,2). Los efectos adversos menores fueron más frecuentes en el grupo de dieta baja en carbohidratos.
Conclusión : Yancy W concluyó que en comparación con una dieta baja en grasas, un programa de dieta baja en carbohidratos tuvo una mejor retención de participantes y una mayor pérdida de peso. Durante la pérdida de peso activa, los niveles de triglicéridos séricos disminuyeron más y el nivel de colesterol de lipoproteínas de alta densidad aumentó más con la dieta baja en carbohidratos que con la dieta baja en grasas.

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Estudio Nº01
Título:

Epidemiology and management of hyperlipidemia

Año y autor: Karr, Samantha; 2017
Tipo de estudio: Revisión sistemática

Resultados: En Estados Unidos, más de 100 millones de personas que corresponden a el 53 % de población adulta presentan LDL-c alto. Además, menos del 50% de los pacientes con LDL-c alto reciben tratamiento para reducir sus niveles, y entre los que reciben tratamiento, menos del 35% logran un control adecuado.
Conclusiones: Hay cambios en las recomendaciones de tratamiento para un mejor manejo de hiperlipidemias,  aunque las estatinas son el principal tratamiento de primera línea para la hiperlipidemia, muchos pacientes, especialmente aquellos con Hipercolesterolemia Familiar no logran objetivos óptimos de LDL-c, por lo que requieren tratamiento adicional. Además se han notificado mialgias y rabdomiolisis rara pero potencialmente mortal. Estos problemas en el tratamiento brindan la oportunidad de considerar el uso de inhibidores de PCSK9 para pacientes que no son adherentes a las estatinas, individuos que son intolerantes a las estatinas o aquellos que son resistentes a las estatinas.

Estudio Nº02
Título:

Prevalence of hyperlipidemia and its associated factors in university students in Colombia

Año y autor: Álvarez, A; 2020
Tipo de estudio: Estudio Transversal Descriptivo

Resultados: Se determinó la prevalencia de hiperlipidemia y sus factores asociados en los estudiantes de la Facultad de Salud de la Universidad Santiago de Cali en 2017. La prevalencia general de hiperlipidemia fue del 33,8%, con los siguientes valores de riesgo: triglicéridos (TG), 12,8%; hipercolesterolemia, 16,1%; colesterol de lipoproteínas de alta densidad (HDLc), 15,0%; y colesterol de lipoproteínas de baja densidad (LDLc), 42,2%.

Conclusiones: La prevalencia de hiperlipidemia en estudiantes universitarios fue del 33,8%, cuyo consumo de sexo (masculino) y bebidas alcohólicas son los principales factores que aumentan el riesgo de desarrollar hiperlipidemia.
Link: https://www.sciencedirect.com/science/article/pii/S240584402032260X

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Cardiovascular disease (CVD) is the leading cause of death among adults in the United States, and people with hyperlipidemia are at roughly twice the risk of developing CVD as compared to those with normal total cholesterol levels. ¹ Patients with familial hypercholesterolemia (FH) have an even greater risk of developing CVD at an earlier age; therefore, early detection and treatment are imperative to reduce cardiovascular events and premature death. Statins are the mainstay treatment for hyperlipidemia; however, the limitations of statins include treatment resistance, intolerance due to adverse events, and a lack of adherence which contribute to poor outcomes. As such, many patients require adjunct therapies to properly control hyperlipidemia including niacin, bile acid sequestrants, fibric acids, and ezetimibe. FH can be even more challenging to treat, often requiring the use of lomitapide, mipomersen, proprotein convertase subtilisin/kexin type 9 inhibitors, or low-density lipoprotein cholesterol apheresis, in addition to high dose conjunction with statins or other agents. ² The approach to determining the appropriate treatment options has also undergone important changes. Guidelines for the management of patients with hyperlipidemia vary in their recommendations, with the American College of Cardiology/American Heart Association recommending that treatment decisions be based on the intensity of response associated with various statins, while multiple other guidelines (eg, National Lipid Association (NLA) and the American Association of Clinical Endocrinologists and American College of Endocrinology) still support attaining prespecified lipid values to reduce cardiovascular risk. ³⁻⁵ This article will review the epidemiology of hyperlipidemia and FH, risk factors associated with the development of disease, as well as the efficacy and safety of statins and adjunct treatment options.

Am J Manag Care. 2017;23:-S0

Hyperlipidemia involves an imbalance of cholesterol levels, including low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) in the blood. LDL-C and HDL-C regulate the amount of cholesterol in the body and an imbalance can increase the risk of cardiovascular events, including myocardial infarction and stroke. Other forms of hyperlipidemia include hypertriglyceridemia as well as mixed hyperlipidemia, in which both cholesterol and triglyceride levels are elevated. Elevated LDL-C can lead to a buildup of plaques within the arteries and is associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD), including coronary artery disease or stroke. As HDL-C functions to remove cholesterol from the body, increased levels of HDL-C (≥60 mg/dL) can help decrease the risk of ASCVD. ⁶
Epidemiology
In the United States, more than 100 million, or roughly 53% of adults, have elevated LDL-C levels. ⁷ Yet, fewer than 50% of patients with high LDL-C receive treatment to reduce their levels, and among those receiving treatment, fewer than 35% achieve adequate control. 1,7 Further, approximately 31 million American adults have total cholesterol levels that exceed 240 mg/dL, placing them at about twice the risk of ASCVD compared to those with total cholesterol levels that are at goal. ¹
Risk Factors for Hyperlipidemia
There are 2 types of FH: homozygous (HoFH) and heterozygous FH (HeFH). In the United States, HeFH is more common, affecting approximately 1 in 500 people, and is associated with LDL-C levels of 200 to 450 mg/dL. 19,20 Patients with HeFH often develop coronary artery disease before the age of 60 years. ¹⁵ HoFH is rarer, affecting roughly 1 in 300,000 to 1,000,000 people, but is associated with much higher LDL-C levels compared with HeFH (450 to >1000 mg/dL). 11,19,21 If left untreated, patients with HoFH may die before the age of 20 years. ¹⁵
Management of Hyperlipidemia and FH Statins
Statins reduce total cholesterol and LDL-C via inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. Multiple studies have clearly shown that statins can lower LDL-C levels, thereby reducing the risk of developing CVD in patients with elevated LDL-C and reducing mortality and disease progression among patients with clinical ASCVD. 3,22-29 Statins are the mainstay of treatment for hyperlipidemia, including use in FH. 3,4

Seven statins are currently approved by the FDA for the treatment of hyperlipidemia in combination with a heart-healthy diet. ³⁰⁻³⁷ A meta-analysis of 26 randomized trials involving 170,000 patients treated with various statins showed that a decrease in LDL-C of 39 mg/dL was associated with a 24% risk reduction in major vascular events. ²⁹ The trials included patients being treated for either primary or secondary prevention of cardiovascular disease, and the duration of treatment was at least 2 years. In general, statins can reduce LDL-C by approximately 20% to 65% with greater reductions seen with atorvastatin, rosuvastatin, and pitavastatin; moderate decreases with lovastatin and simvastatin; and the lowest decreases with fluvastatin and pravastatin. 22,24-28,35 All but pitavastatin have indications for patients with FH.

While statins are generally well tolerated, they are associated with numerous adverse effects, including gastrointestinal events, musculoskeletal pain, respiratory infections, and headaches. 30-34,36,37 Statins can also be associated with elevated blood glucose and glycated hemoglobin (A1C) levels. ³⁸⁻⁴⁰ Increases in liver enzyme transaminases can occur infrequently, and statins are contraindicated in patients with active liver disease, as well as in patients with unexplained and chronic elevations in liver enzyme transaminases. Caution is advised regarding the concomitant use of most statins and anticoagulants; a reduction in the dose of the anticoagulant is recommended. 30-32,34,36,37
Limitations of Statins
While statin monotherapy can lower LDL-C levels in most patients, some patients are nonadherent, intolerant, or resistant, resulting in poor outcomes.
Nonadherence to Statin Treatment
Nonadherence to statin treatment is a common issue, and has been shown to lead to an increased risk of ASCVD and mortality. 10,48-50 Studies have found that 10% to 30% of patients never fill their first statin prescription, and adherence rates are roughly 25% to 50% among patients with acute coronary syndrome and those receiving statins for primary prevention of ASCVD. ⁵¹⁻⁵⁷ Further, within the first year, approximately 50% of patients discontinue statin therapy, and discontinuation rates at 2 years can be ≥75%. 10,58 Nonadherence and nonpersistence are associated with an increase in both ASCVD risk and mortality. ⁵⁰ Factors contributing to nonadherence include comorbidities, AEs, regimen complexity, age, sex, co-payment, and income. 10,57,59,60 Data from a meta-analysis of 22 cohort studies revealed that patients ≥70 years and <50 years of age were more likely to be nonadherent compared with those 50 to 69 years of age. ⁵⁷ In addition, nonadherence was greater among women and patients with lower incomes. Conversely, better adherence was noted among patients with a history of myocardial infarction or stroke, hypertension, or diabetes. Recommendations for addressing nonadherence include assessing the number of missed doses per month and discussing any barriers to adherence with the patient. ⁶¹ Medication therapy management, pharmacy disease management programs, and other pharmacist-driven efforts can help to improve clinical outcomes, improve adherence, and minimize cost. ⁶²
Statin Intolerance
Statin intolerance is often associated with poor adherence. Results of a meta-analysis comparing high-intensity and moderate-intensity statins revealed an increased risk of adverse events and adverse event-related treatment discontinuation with higher intensity statins ⁶³; however, another more recent meta-analysis noted less risk with rosuvastatin. ⁶⁴ Patients drinking grapefruit juice, especially large quantities, should be reminded of the potential for an interaction with statins, metabolized by CYP3A4. In addition, drugs that affect the CYP3A4 pathway can alter the metabolism of statins that are major substrates of CYP3A4, such as simvastatin, atorvastatin, and lovastatin. This can result in muscle-related adverse events. ⁶⁵⁻⁶⁸ Approximately 7% to 29% of patients receiving statins experience muscle-related adverse events, which can contribute to poor adherence and nonpersistence. 41,69-71 Rhabdomyolysis is a severe and potentially fatal form of muscle-related adverse event that occurs at a rate of 3.4 per 100,000 person-years. ⁷² A systematic review noted higher incidences of rhabdomyolysis among patients receiving simvastatin or atorvastatin as compared with pravastatin or fluvastatin, and among patients receiving fibrates in combination with statins. ⁶⁴ As pravastatin, fluvastatin, and rosuvastatin are only minor substrates of CYP3A4, these statins have a lower incidence of drug-drug interactions and also may be a better option for patients at an increased risk of developing rhabdomyolysis. 64,73 In cases where musculoskeletal events occur in patients receiving statins, it is important to first verify that statins are the cause of the events.
Statin Resistance Nonstatins
Several nonstatin therapies are available as adjunctive treatment for patients who do not respond adequately to statins or for those who are intolerant of statins. These include BASs, fibric acids, niacin, cholesterol absorption and synthesis inhibitors, as well as the recently approved class, PCSK9 inhibitors. ⁸⁸⁻⁹⁸
Bile Acid Sequestrants
BASs include cholestyramine, colestipol, and colesevelam. BASs reduce cholesterol by binding bile acids within the intestine, impeding bile acid reabsorption and enterohepatic cycling, increasing the conversion of cholesterol to bile acids, and increasing the number of hepatic LDLRs. This results in increased clearance of LDL-C and decreased LDL-C levels. 88-90,99 Colesevelam monotherapy is associated with a 15% to 20% reduction in LDL-C. 100,101 Studies have demonstrated that adding BASs to statins, fibrates, niacin, or ezetimibe can significantly reduce LDL-C levels compared with monotherapy. ¹⁰²⁻¹⁰⁹ The addition of colesevelam to statins and/or ezetimibe can further reduce LDL-C levels in adults and children (ages 10 -17 years) with FH compared with statin monotherapy. 110,111 In addition, a pooled analysis of 3 trials found that the combination of colesevelam and statins significantly decreased both LDL-C and A1C in patients with both hyperlipidemia and diabetes. ¹¹² The addition of colesevelam to therapy with atorvastatin and niacin led to a notable reduction in LDL-C (57%) compared with the combination of atorvastatin and niacin alone (47%). ¹¹³ While most BASs-associated AEs are tolerable, caution is recommended when prescribing BASs for patients with complete biliary obstruction due to an increased risk of new or worsening constipation. ⁸⁸⁻⁹⁰ Additionally, the labeling for some BASs can include a precaution regarding increased risk of bleeding. This risk exists when hypoprothrombinemia from vitamin K deficiency occurs due to reduction in absorption of fat-soluble vitamins related to chronic use of BASs. ⁸⁸⁻⁹⁰ In patients receiving any other medications in combination with BASs, administration should be spaced either 1 to 4 hours before, depending on the other medication, or 4 to 6 hours after BAS administration to reduce the chance of impaired absorption. ⁸⁹ Oral vitamin supplementation should be taken at least 4 hours before colesevelam. ⁹⁰
Fibric Acid Derivatives
Fibric acid derivatives are peroxisome proliferator-activated receptor α (PPARα) agonists that have been shown to reduce triglycerides by ≤50%, increasing HDL-C by ≤15%, LDL-C levels by 15% to 25%, and reducing major coronary events. ¹¹⁴⁻¹¹⁷ Similar to BASs, fibrates further reduce LDL-C levels when combined with statins compared with statins or fibrates alone. ¹¹⁸⁻¹²⁰ However, when used in combination with high-intensity statins, fibrates can increase the risk of myopathy and rhabdomyolysis. ¹²¹ The incidence of skeletal adverse events is higher when combining high-intensity statins with gemfibrozil compared to fenofibrate. ¹²² Guidelines recommend against using gemfibrozil in patients receiving statins, and fenofibrate should be restricted to patients receiving low-to-moderate dose statin therapy, as long as the benefits outweigh the risks. ³ In addition, fibrates are contraindicated in patients with hepatic or renal disease, unexplained persistent liver function abnormality, and in those with preexisting gallbladder disease. 91,92 Combination therapy of gemfibrozil plus repaglinide is also contraindicated. ⁹¹ Additionally, fenofibrate is contraindicated while breastfeeding. ⁹² Finally, caution is advised regarding the concomitant use of fibrates and anticoagulants, and increased monitoring of prothrombin time with international normalized ratio (INR) determination is recommended until these parameters have stabilized after 1 drug in this combination is added to the other. ⁹²

Niacin increases levels of HDL and reduces levels of very low-density lipoprotein (VLDL) which, in turn, reduces LDL-C levels. ¹²³ Studies involving the combination of niacin with statins have provided conflicting results. 100,124-127 In general, the addition of niacin to statins is associated with increased HDL-C, but is not associated with a significant reduction in LDL-C compared with statin monotherapy. In addition, results from multiple studies failed to show that the addition of niacin could reduce the risk of cardiovascular events, and indicated an increase in the risk of adverse events in patients receiving high-intensity statins compared with statin monotherapy. 128,129 The most common niacin-related adverse event is flushing. Laropiprant, a selective prostanoid receptor antagonist, can reduce the incidence and severity of niacin-related flushing when administered concomitantly. 130,131 However, results from the HPS2-THRIVE phase 3 study demonstrated that adding extended-release niacin and laropiprant to statin-based treatment was associated with an increase in diagnosis of type 2 diabetes as well as serious gastrointestinal and musculoskeletal events, infection, and bleeding. ¹²⁹ Niacin is contraindicated in patients with active liver disease, peptic ulcer disease, or arterial bleeding. ⁹³ Due to the increased risk of myopathy and rhabdomyolysis in patients receiving niacin in combination with either lovastatin or simvastatin, it is recommended that the dose of these statins not exceed 40 mg in patients receiving niacin. ⁹³ Caution should be used when prescribing niacin to patients with renal or hepatic impairment. In addition, the ACC notes that due to the lack of efficacy and potential for harm, niacin is not recommended for the treatment of hypercholesterolemia. ⁶¹
Lomitapide Mipomersen
Mipomersen is an antisense oligonucleotide that inhibits apo B100 synthesis and is indicated as adjunctive therapy to lipid-lowering medications and diet to reduce LDL-C, apo B, total cholesterol, and non-HDL-C in patients with HoFH. ⁹⁶ Approval of mipomersen was based on a randomized, double-blind, placebo-controlled phase 3 study of patients (N = 51) with HoFH who were 12 years of age or older and were currently receiving lipid-lowering agents at the maximum tolerated dose. ¹⁴⁹ There was a 24.7% mean reduction in LDL-C in patients receiving mipomersen (n = 34) compared with 3.3% in patients receiving placebo (n = 17; P = .0003). Statistically significant reductions in apo B, total cholesterol, and non-HDL-C were also noted. Additional trials have demonstrated the efficacy of mipomersen in reducing LDL-C in patients with HeFH, ¹⁵⁰ severe HeFH, ¹⁵¹ HeFH with coronary artery disease, ¹⁵² and HoFH. 148,153 Additional data indicate that mipomersen is efficacious in people with statin intolerance at high risk of ASCVD, ¹⁵⁴ and for those with severe hyperlipidemia at high risk of ASCVD. ¹⁵⁵ Common AEs associated with mipomersen include flu-like symptoms, injection-site reactions, headache, nausea, and alanine aminotransferase elevations. 148-151,153-155 Similar to lomitapide, mipomersen is contraindicated in patients with moderate or severe liver impairment, and is only available through a restricted REMS program. ⁹⁶ Fortunately, mipomersen was not noted to have any clinically relevant drug interactions in clinical trials.
PCSK9 Inhibitors Current Guidelines for the Management of Cholesterol
Numerous guidelines provide recommendations for the treatment of hyperlipidemia as well as FH. The 2013 ACC/AHA Guideline for the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults includes 4 main groups of patients for whom statin therapy could reduce the risk of ASCVD, along with recommendations for the intensity of statin therapy (Table 1 ³). ³

The ACC/AHA differs from the US Preventive Services Task Force (USPSTF) with regard to levels of statin intensity recommended. The USPSTF (Table 2 ¹⁶⁹) recommends the use of low-to-moderate intensity statins in patients with a 10-year risk of ASCVD ≥10%, but for adult patients with a 10-year ASCVD risk between 7.5% and 10%, a low-to-moderate intensity statin is an option to consider. ¹⁶⁹

In contrast to the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guidelines, which recommend a treat-to-target approach, the 2013 ACC/AHA guidelines endorse a tiered approach based on the average percentage by which a specific statin can reduce LDL-C. 3,117 Statin regimens that can reduce LDL-C ≥50% are considered high-intensity therapies, while those statins that reduce LDL-C by 30% to <50% are considered moderate intensity, and those statins that reduce LDL-C ≤30% are considered low intensity.

High-intensity statin therapy is recommended in patients with FH by the ACC/AHA as well as by the Canadian Cardiovascular Society (CCS) and the European Atherosclerosis Society (EAS). 47,61,170 Moderate-intensity therapy is recommended in patients who cannot tolerate high-intensity treatment. All guidelines for the treatment of FH recommend initiating treatment as soon as possible. In addition to statins, ezetimibe and PCSK9 inhibitors are recommended in patients who have an insufficient response to statins. 3,61 While the CCS and EAS recommend the incorporation of bile acid sequestrants in patients with FH in need of further LDL-C reductions, the ACC/AHA 2013 guideline only recommends the use of nonstatins that have been shown to improve cardiovascular outcomes in randomized clinical trials, such as ezetimibe. The ACC/AHA 2013 guideline does not recommend the addition of niacin to statins based on data from the HSP2-THRIVE and AIM-HIGH studies that demonstrated an improvement in surrogate markers (eg, lipid parameters), but failed to show an increased benefit in cardiovascular outcomes. 128,129 Similarly, the ACCORD study failed to show a benefit on ASCVD outcomes of adding fenofibrate to moderate-intensity statins, despite improvement in lipid parameters. ¹⁷¹ Thus, the ACC/AHA 2013 guideline does not recommend the addition of fenofibrate to statin therapy. In 2015, the AHA and ACC made additional recommendations for the sequencing of treatment for FH with the addition of adjunctive therapies if patients do not reach LDL-C levels after 3 months of treatment ( Figure ¹⁷²). 61,172 Finally, the EAS guidelines recommend that LDL apheresis in combination with statins be initiated in patients with HoFH as early as 5 years of age and no later than 8 years of age in pediatric patients. ¹² In addition, lomitapide and mipomersen can be considered as adjunctive treatments for these patients who do not achieve the recommended LDL cholesterol targets and remain at high cardiovascular risk.

The American Association of Clinical Endocrinologists and American College of Endocrinology (AACE/ACE) 2017 lipid guidelines created a new patient population category deemed as "extreme risk" that would include individuals who have 1) "progressive ASCVD, including unstable angina, that persists after achieving an LDL-C <70 mg/dL," 2) "established clinical cardiovascular disease in individuals with diabetes, stage III or IV chronic kidney disease (CKD), and/or HeFH," and/or 3) "a history of premature ASCVD (males <55 years, females aged <65 years)." ⁵ The treatment goals for individuals in this category are: LDL-C <55 mg/dL; non-HDL-C <80 mg/dL; and apo B <70 mg/dL. ⁵ Regarding PCSK9 inhibitors, the AACE/ACE guidelines suggest their use in 2 patient groups: 1) patients with FH as combination therapy with statins, 2) patients with clinical CVD who do not attain LDL-C/non-HDL-C goals with maximally tolerated statin treatment. In the latter patient population, PCSK9 inhibitor monotherapy should only be considered in patients who are statin intolerant. ⁵ PCSK9 inhibitors are also recommended in combination with statins in patients with FH to lower LDL-C levels. ⁵
Conclusion
Recent changes to treatment recommendations are providing greater guidance for the management of hyperlipidemia, which includes a treat-to-target approach as well as using therapies based on the expected response. Although statins are the mainstay front-line treatment for hyperlipidemia, many patients, especially those with FH, do not achieve optimal LDL-C goals, thus requiring additional treatment. Statin therapy can be complicated by AEs (eg, myalgias) and rare but life-threatening rhabdomyolysis. These issues in treatment provide an opportunity to consider the use of PCSK9 inhibitors for patients who are nonadherent to statins, individuals that are statin intolerant, or those who are statin resistant.

Author affiliation: Associate Professor, Midwestern University College of Pharmacy, Pharmacy Practice Department, Glendale, AZ.

Funding source: This activity is supported by an education grant from Amgen, Inc.

Author disclosure: Dr Karr has no relevant financial relationships with commercial interests to disclose.

Authorship information: Concept and design, drafting of the manuscript, critical revision of the manuscript for important intellectual content, and supervision.

Address correspondence to: skarrx@midwestern.edu.

1. Mozaffarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics-2016 update: a report from the American Heart Association. Circulation. 2016;133(4):e38-e360. doi: 10.1161/CIR.0000000000000350.

2. Raal FJ, Pilcher GJ, Panz VR, et al. Reduction in mortality in subjects with homozygous familial hypercholesterolemia associated with advances in lipid-lowering therapy. Circulation. 2011;124(20):2202-2207. doi: 10.1161/circulationaha.111.042523.

3. Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults. J Am Coll Cardiol. 2014;63(25):2889-2934. doi: 10.1016/j.jacc.2013.11.002.

4. Jacobson TA, Ito MK, Maki KC, et al. National Lipid Association recommendations for patient-centered management of dyslipidemia: part 1-full report. J Clin Lipidol. 2015;9(2):129-169. doi: 10.1016/j.jacl.2015.02.003.

5. Jellinger PS, Handelsman Y, Rosenblit PD, et al. American Association of Clinical Endocrinologists and American College of Endocrinology guidelines for management of dyslipidemia and prevention of cardiovascular disease. Endocr Pract. 2017;23(suppl 2):1-87. doi: 10.4158/EP171764.APPGL.

6. Cooney MT, Dudina A, De Bacquer D, et al. HDL cholesterol protects against cardiovascular disease in both genders, at all ages and at all levels of risk. Atherosclerosis. 2009;206(2):611-616. doi: 10.1016/j.atherosclerosis.2009.02.041.

7. Centers for Disease Control and Prevention (CDC). Vital signs: prevalence, treatment, and control of high levels of low-density lipoprotein cholesterol-United States, 1999-2002 and 2005-2008. MMWR Morb Mortal Wkly Rep. 2011;60(4):109-114.

8. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of childhood and adult obesity in the United States, 2011-2012. JAMA. 2014;311(8):806. doi: 10.1001/jama.2014.732.

9. ACC/AHA. ACC/AHA ASCVD Risk Calculator website. www.cvriskcalculator.com. Published 2016. Accessed May 23, 2017.

10. Krähenbühl S, Pavik-Mezzour I, von Eckardstein A. Unmet needs in LDL-C lowering: when statins won't do! Drugs. 2016;76(12):1175-1190. doi: 10.1007/s40265-016-0613-0.

11. Vogt A. The genetics of familial hypercholesterolemia and emerging therapies. Appl Clin Genet. 2015;8:27-36. doi: 10.2147/TACG.S44315.

12. Cuchel M, Bruckert E, Ginsberg HN, et al. Homozygous familial hypercholesterolaemia: new insights and guidance for clinicians to improve detection and clinical management. A position paper from the Consensus Panel on Familial Hypercholesterolaemia of the European Atherosclerosis Society. Eur Heart J. 2014;35(32):2146-2157. doi: 10.1093/eurheartj/ehu274.

13. Ito MK, Watts GF. Challenges in the diagnosis and treatment of homozygous familial hypercholesterolemia. Drugs. 2015;75(15):1715-1724. doi: 10.1007/s40265-015-0466-y.

14. Sjouke B, Kusters DM, Kindt I, et al. Homozygous autosomal dominant hypercholesterolaemia in the Netherlands: prevalence, genotype-phenotype relationship, and clinical outcome. Eur Heart J. 2015;36(9):560-565. doi: 10.1093/eurheartj/ehu058.

15. Nordestgaard BG, Chapman MJ, Humphries SE, et al. Familial hypercholesterolaemia is underdiagnosed and undertreated in the general population: guidance for clinicians to prevent coronary heart disease: consensus statement of the European Atherosclerosis Society. Eur Heart J. 2013;34(45):3478-3490. doi: 10.1093/eurheartj/eht273.

16. Khera AV, Won HH, Peloso GM, et al. Diagnostic yield and clinical utility of sequencing familial hypercholesterolemia genes in patients with severe hypercholesterolemia. J Am Coll Cardiol. 2016;67(22):2578-2589. doi: 10.1016/j.jacc.2016.03.520.

17. Perak AM, Ning H, de Ferranti SD, Gooding HC, Wilkins JT, Lloyd-Jones DM. Long-term risk of atherosclerotic cardiovascular disease in US adults with the familial hypercholesterolemia phenotype. Circulation. 2016;134(1):9-19. doi: 10.1161/circulationaha.116.022335.

18. de Ferranti SD, Rodday AM, Mendelson MM, Wong JB, Leslie LK, Sheldrick RC. Prevalence of familial hypercholesterolemia in the 1999 to 2012 United States National Health and Nutrition Examination Surveys (NHANES) clinical perspective. Circulation. 2016;133(11):1067-1072. doi: 10.1161/CIRCULATIONAHA.115.018791.

19. Vishwanath R, Hemphill LC. Familial hypercholesterolemia and estimation of US patients eligible for low-density lipoprotein apheresis after maximally tolerated lipid-lowering therapy. J Clin Lipidol. 2014;8(1):18-28. doi: 10.1016/j.jacl.2013.11.002.

20. Youngblom E, Pariani M, Knowles JW. Familial hypercholesterolemia. In: Pagon RA, Adam MP, Ardinger HH, et al, eds. GeneReviews. Seattle, WA: University of Washington, Seattle; 1993-2017..

21. Sjouke B, Hovingh GK, Kastelein JJP, Stefanutti C. Homozygous autosomal dominant hypercholesterolaemia. Curr Opin Lipidol. 2015;26(3):200-209. doi: 10.1097/MOL.0000000000000179.

22. Bertolini S, Bon GB, Campbell LM, et al. Efficacy and safety of atorvastatin compared to pravastatin in patients with hypercholesterolemia. Atherosclerosis. 1997;130(1-2):191-197.

23. Black D, Davidson M, Koren M, et al. Cost effectiveness of treatment to National Cholesterol Education Panel (NCEP) targets with HMG-CoA reductase inhibitors. Trial design. Pharmacoeconomics. 1997;12(2 Pt 2):278-285.

24. Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994;344(8934):1383-1389. doi: 10.1016/S0140-6736(94)90566-5.

25. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet. 2002;360(9326):7-22. doi: 10.1016/S0140-6736(02)09327-3.

26. Athyros VG, Papageorgiou AA, Mercouris BR, et al. Treatment with atorvastatin to the National Cholesterol Educational Program goal versus "usual" care in secondary coronary heart disease prevention. The GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study. Curr Med Res Opin. 2002;18(4):220-228.

27. Insull W, Black D, Dujovne C, et al. Efficacy and safety of once-daily vs twice-daily dosing with fluvastatin, a synthetic reductase inhibitor, in primary hypercholesterolemia. Arch Intern Med. 1994;154(21):2449-2455.

28. Davidson M, Ma P, Stein EA, et al. Comparison of effects on low-density lipoprotein cholesterol and high-density lipoprotein cholesterol with rosuvastatin versus atorvastatin in patients with type IIa or IIb hypercholesterolemia. Am J Cardiol. 2002;89(3):268-275. doi: 10.1016/S0002-9149(01)02226-3.

29. Cholesterol Treatment Trialists' (CTT) Collaboration, Baigent C, Blackwell L, et al. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010;376(9753):1670-1681. doi: 10.1016/S0140-6736(10)61350-5.

30. Lipitor [package insert]. New York, NY: Pfizer, Inc; 2015.

31. Lescol/Lescol XL [package insert]. East Hanover, NJ: Novartis Pharmaceuticals Corporation; 2012.

32. Mevacor [package insert]. Morgantown, WV: Mylan Pharmaceuticals, Inc; 2014.

33. Pravachol [package insert]. Princeton, NJ: Bristol-Myers Squibb Company; 2016.

34. Zocor [package insert]. Whitehouse Station, NJ: Merck & Co, Inc; 2015.

35. Davidson M, McKenney J, Stein E, et al. Comparison of one-year efficacy and safety of atorvastatin versus lovastatin in primary hypercholesterolemia. Atorvastatin Study Group I. Am J Cardiol. 1997;79(11):1475-1481.

36. Livalo [package insert]. Montgomery, AL: Kowa Pharmaceuticals America, Inc; 2016.

37. Crestor [package insert]. Wilmington, DE: AstraZeneca Pharmaceuticals, LP; 2016.

38. Shah RV, Goldfine AB. Statins and risk of new-onset diabetes mellitus. Circulation. 2012;126(18):e282-284. doi: 10.1161/circulationaha112.122135.

39. Skoumas J, Liontou C, Chrysohoou C, et al. Statin therapy and risk of diabetes in patients with heterozygous familial hypercholesterolemia or familial combined hyperlipidemia. Atherosclerosis. 2014;237(1):140-145. doi: 10.1016/j.atherosclerosis.2014.08.047.

40. Maki KC, Ridker PM, Brown WV, Grundy SM, Sattar N. The Diabetes Subpanel of the National Lipid Association Expert Panel. An assessment by the Statin Diabetes Safety Task Force: 2014 update. J Clin Lipidol. 2014;8(3):S17-S29. doi: 10.1016/j.jacl.2014.02.012.

41. Bruckert E, Hayem G, Dejager S, Yau C, Bégaud B. Mild to moderate muscular symptoms with high-dosage statin therapy in hyperlipidemic patients-the PRIMO study. Cardiovasc Drugs Ther. 2005;19(6):403-414. doi: 10.1007/s10557-005-5686-z.

42. Rosenbaum D, Dallongeville J, Sabouret P, Bruckert E. Discontinuation of statin therapy due to muscular side effects: a survey in real life. Nutr Metab Cardiovasc Dis. 2013;23(9):871-875. doi: 10.1016/j.numecd.2012.04.012.

43. Parker BA, Capizzi JA, Grimaldi AS, et al. Effect of statins on skeletal muscle function. Circulation. 2013;127(1):96-103. doi: 10.1161/CIRCULATIONAHA.112.136101.

44. Banach M, Rizzo M, Toth PP, et al. Statin intolerance-an attempt at a unified definition. Position paper from an International Lipid Expert Panel. Arch Med Sci. 2015;1(1):1-23. doi: 10.5114/aoms.2015.49807.

45. Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med. 2009;361(1):62-72. doi: 10.1056/NEJMra0801327.

46. Rosenson RS, Baker SK, Jacobson TA, Kopecky SL, Parker BA. The National Lipid Association's Muscle Safety Expert Panel. An assessment by the Statin Muscle Safety Task Force: 2014 update. J Clin Lipidol. 2014;8(3):S58-S71. doi: 10.1016/j.jacl.2014.03.004.

47. Mancini GBJ, Baker S, Bergeron J, et al. Diagnosis, prevention, and management of statin adverse effects and intolerance: Canadian Consensus Working Group update (2016). Can J Cardiol. 2016;32(7):S35-S65. doi: 10.1016/j.cjca.2016.01.003.

48. Rasmussen JN, Chong A, Alter DA. Relationship between adherence to evidence-based pharmacotherapy and long-term mortality after acute myocardial infarction. JAMA. 2007;297(2):177-186. doi: 10.1001/jama.297.2.177.

49. Bouchard MH, Dragomir A, Blais L, Bérard A, Pilon D, Perreault S. Impact of adherence to statins on coronary artery disease in primary prevention. Br J Clin Pharmacol. 2007;63(6):698-708. doi: 10.1111/j.1365-2125.2006.02828.x.

50. De Vera MA, Bhole V, Burns LC, Lacaille D. Impact of statin adherence on cardiovascular disease and mortality outcomes: a systematic review. Br J Clin Pharmacol. 2014;78(4):684-698.

51. Cheetham TC, Niu F, Green K, et al. Primary nonadherence to statin medications in a managed care organization. J Manag Care Pharm. 2013;19(5):367-373. doi: 10.18553/jmcp.2013.19.5.367.

52. Fischer MA, Stedman MR, Lii J, et al. Primary medication non-adherence: analysis of 195,930 electronic prescriptions. J Gen Intern Med. 2010;25(4):284-290. doi: 10.1007/s11606-010-1253-9.

53. Raebel MA, Ellis JL, Carroll NM, et al. Characteristics of patients with primary non-adherence to medications for hypertension, diabetes, and lipid disorders. J Gen Intern Med. 2012;27(1):57-64. doi: 10.1007/s11606-011-1829-z.

54. Liberman JN, Hutchins DS, Popiel RG, Patel MH, Jan SA, Berger JE. Determinants of primary nonadherence in asthma-controller and dyslipidemia pharmacotherapy. Am J Pharm Benefits. 2010;2(2):111-118.

55. Jackevicius CA, Mamdani M, Tu JV. Adherence with statin therapy in elderly patients with and without acute coronary syndromes. JAMA. 288(4):462-467.

56. Mann DM, Allegrante JP, Natarajan S, Halm EA, Charlson M. Predictors of adherence to statins for primary prevention. Cardiovasc Drugs Ther. 2007;21(4):311-316. doi: 10.1007/s10557-007-6040-4.

57. Mann DM, Woodward M, Muntner P, Falzon L, Kronish I. Predictors of nonadherence to statins: a systematic review and meta-analysis. Ann Pharmacother. 2010;44(9):1410-1421. doi: 10.1345/aph.1P150.

58. Chodick G, Shalev V, Gerber Y, et al. Long-term persistence with statin treatment in a not-for-profit health maintenance organization: a population-based retrospective cohort study in Israel. Clin Ther. 2008;30(11):2167-2179. doi: 10.1016/j.clinthera.2008.11.012.

59. Lemstra M, Blackburn D, Crawley A, Fung R. Proportion and risk indicators of nonadherence to statin therapy: a meta-analysis. Can J Cardiol. 2012;28(5):574-580. doi: 10.1016/j.cjca.2012.05.007.

60. Spinler SA, Cziraky MJ, Willey VJ, et al. Frequency of attainment of low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol goals in cardiovascular clinical practice (from the National Cardiovascular Data Registry PINNACLE Registry). Am J Cardiol. 2015;116(4):547-553. doi: 10.1016/j.amjcard.2015.05.011.

61. Lloyd-Jones DM, Morris PB, Ballantyne CM, et al. 2016 ACC expert consensus decision pathway on the role of non-statin therapies for LDL-cholesterol lowering in the management of atherosclerotic cardiovascular disease risk. J Am Coll Cardiol. 2016;68(1):92-125. doi: 10.1016/j.jacc.2016.03.519.

62. Ramalho de Oliveira D, Brummel AR, Miller DB. Medication therapy management: 10 years of experience in a large integrated health care system. J Manag Care Pharm. 2010;16(3):185-195. doi: 10.18553/jmcp.2010.16.3.185.

63. Silva M, Matthews ML, Jarvis C, et al. Meta-analysis of drug-induced adverse events associated with intensive-dose statin therapy. Clin Ther. 2007;29(2):253-260. doi: 10.1016/j.clinthera.2007.02.008.

64. Mendes P, Robles PG, Mathur S. Statin-induced rhabdomyolysis: a comprehensive review of case reports. Physiother Can. 2014;66(2):124-132. doi: 10.3138/ptc.2012-65.

65. Causevic-Ramosevac A, Semiz S. Drug interactions with statins. Acta Pharm. 2013;63(3):277-293. doi: 10.2478/acph-2013-0022.

66. Sirtori CR. The pharmacology of statins. Pharmacol Res. 2014;88:3-11. doi: 10.1016/j.phrs.2014.03.002.

67. Kellick KA, Bottorff M, Toth PP; The National Lipid Association's Safety Task Force. A clinician's guide to statin drug-drug interactions. J Clin Lipidol. 2014;8(3):S30-S46. doi: 10.1016/j.jacl.2014.02.010.

68. Hu M, Tomlinson B. Evaluation of the pharmacokinetics and drug interactions of the two recently developed statins, rosuvastatin and pitavastatin. Expert Opin Drug Metab Toxicol. 2014;10(1):51-65. doi: 10.1517/17425255.2014.851667.

69. Cohen JD, Brinton EA, Ito MK, Jacobson TA. Understanding Statin Use in America and Gaps in Patient Education (USAGE): an internet-based survey of 10,138 current and former statin users. J Clin Lipidol. 2012;6(3):208-215. doi: 10.1016/j.jacl.2012.03.003.

70. Zhang H, Plutzky J, Skentzos S, et al. Discontinuation of statins in routine care settings: a cohort study. Ann Intern Med. 2013;158(7):526-534. doi: 10.7326/0003-4819-158-7-201304020-00004.

71. El-Salem K, Ababneh B, Rudnicki S, et al. Prevalence and risk factors of muscle complications secondary to statins. Muscle Nerve. 2011;44(6):877-881. doi: 10.1002/mus.22205.

72. Law M, Rudnicka AR. Statin safety: a systematic review. Am J Cardiol. 2006;97(8A):52C-60C. doi: 10.1016/j.amjcard.2005.12.010.

73. Antons KA, Williams CD, Baker SK, Phillips PS. Clinical perspectives of statin-induced rhabdomyolysis. Am J Med. 2006;119(5):400-409. doi: 10.1016/j.amjmed.2006.02.007.

74. American College of Cardiology. ACC's Statin Intolerance Tool. American College of Cardiology website. http://tools.acc.org/statinintolerance/. Published December 2016. Accessed May 18, 2017.

75. Zaharan NL, Williams D, Bennett K. Statins and risk of treated incident diabetes in a primary care population. Br J Clin Pharmacol. 2013;75(4):1118-1124. doi: 10.1111/j.1365-2125.2012.04403.x.

76. Waters DD, Ho JE, Boekholdt SM, et al. Cardiovascular event reduction versus new-onset diabetes during atorvastatin therapy. J Am Coll Cardiol. 2013;61(2):148-152. doi: 10.1016/j.jacc.2012.09.042.

77. Preiss D, Seshasai SRK, Welsh P, et al. Risk of incident diabetes with intensive-dose compared with moderate-dose statin therapy: a meta-analysis. JAMA. 2011;305(24):2556. doi: 10.1001/jama.2011.860.

78. Carter AA, Gomes T, Camacho X, Juurlink DN, Shah BR, Mamdani MM. Risk of incident diabetes among patients treated with statins: population based study. BMJ. 2013;347:f4356. doi: 10.1136/bmj.f4356.

79. Wong ND, Chuang J, Zhao Y, Rosenblit PD. Residual dyslipidemia according to low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B among statin-treated US adults: National Health and Nutrition Examination Survey 2009-2010. J Clin Lipidol. 2015;9(4):525-532. doi: 10.1016/j.jacl.2015.05.003.

80. Della Badia LA, Elshourbagy NA, Mousa SA. Targeting PCSK9 as a promising new mechanism for lowering low-density lipoprotein cholesterol. Pharmacol Ther. 2016;164:183-194. doi: 10.1016/j.pharmthera.2016.04.011.

81. Braamskamp MJAM, Langslet G, McCrindle BW, et al. Efficacy and safety of rosuvastatin therapy in children and adolescents with familial hypercholesterolemia: results from the CHARON study. J Clin Lipidol. 2015;9(6):741-750. doi: 10.1016/j.jacl.2015.07.011.

82. Avis HJ, Hutten BA, Gagné C, et al. Efficacy and safety of rosuvastatin therapy for children with familial hypercholesterolemia. J Am Coll Cardiol. 2010;55(11):1121-1126. doi: 10.1016/j.jacc.2009.10.042.

83. Raal FJ, Pilcher GJ, Illingworth DR, et al. Expanded-dose simvastatin is effective in homozygous familial hypercholesterolaemia. Atherosclerosis. 1997;135(2):249-256.

84. Raal FJ, Pappu AS, Illingworth DR, et al. Inhibition of cholesterol synthesis by atorvastatin in homozygous familial hypercholesterolaemia. Atherosclerosis. 2000;150(2):421-428.

85. Marais AD, Raal FJ, Stein EA, et al. A dose-titration and comparative study of rosuvastatin and

atorvastatin in patients with homozygous familial hypercholesterolaemia. Atherosclerosis. 2008;

197(1):400-406. doi: 10.1016/j.atherosclerosis.2007.06.028.

86. Langslet G, Breazna A, Drogari E. A 3-year study of atorvastatin in children and adolescents with heterozygous familial hypercholesterolemia. J Clin Lipidol. 2016;10(5):1153-1162.e3. doi: 10.1016/j.jacl.2016.05.010.

87. Perez de Isla L, Alonso R, Watts GF, et al. Attainment of LDL-cholesterol treatment goals in patients with familial hypercholesterolemia: 5-year SAFEHEART registry follow-up. J Am Coll Cardiol. 2016;67(11):1278-1285. doi: 10.1016/j.jacc.2016.01.008.

88. Cholestyramine [package insert]. Maple Grove, MN: Upsher-Smith Laboratories, Inc; 2015.

89. Colestid [package insert]. New York, NY: Pfizer, Inc; 2014.

90. Welchol [package insert]. Parsippany, NJ: Daiichi Sankyo, Inc; 2014.

91. Lopid [package insert]. New York, NY: Pfizer, Inc; 2010.

92. Tricor [package insert]. Anngrove, Carrigtwohill Co. Cork, Ireland: Fournier Laboratories Ireland, Limited; 2013.

93. Niaspan [package insert]. North Chicago, IL: AbbVie, Inc; 2015.

94. Zetia [package insert]. Whitehouse Station, NJ: Merck & Co, Inc; 2013.

95. Juxtapid [package insert]. Cambridge, MA: Aegerion Pharmaceuticals, Inc; 2016.

96. Kynamro [package insert]. Cambridge, MA: Genzyme Corporation; 2016.

97. Praluent [package insert]. Bridgewater, NJ: Sanofi-Aventis US, LLC; 2015.

98. Repatha [package insert]. Thousand Oaks, CA: Amgen Inc; 2016.

99. Einarsson K, Ericsson S, Ewerth S, et al. Bile acid sequestrants: mechanisms of action on bile acid and cholesterol metabolism. Eur J Clin Pharmacol. 1991;40(suppl 1):S53-S58.

100. Bays HE, Dujovne CA, McGovern ME, et al. Comparison of once-daily, niacin extended-release/lovastatin with standard doses of atorvastatin and simvastatin (the ADvicor Versus Other Cholesterol-Modulating Agents Trial Evaluation [ADVOCATE]). Am J Cardiol. 2003;91(6):667-672.

101. Davidson MH, Dillon MA, Gordon B, et al. Colesevelam hydrochloride (Cholestagel): a new, potent bile acid sequestrant associated with a low incidence of gastrointestinal side effects. Arch Intern Med. 1999;159(16):1893-1900. doi: 10.1001/archinte.159.16.1893.

102. Knapp HH, Schrott H, Ma P, et al. Efficacy and safety of combination simvastatin and colesevelam in patients with primary hypercholesterolemia. Am J Med. 2001;110(5):352-360.

103. Bays HE, Davidson M, Jones MR, Abby SL. Effects of colesevelam hydrochloride on low-density lipoprotein cholesterol and high-sensitivity C-reactive protein when added to statins in patients with hypercholesterolemia. Am J Cardiol. 2006;97(8):1198-1205. doi: 10.1016/j.amjcard.2005.11.039.

104. Garber AJ, Abrahamson MJ, Barzilay JI, et al. AACE Comprehensive Diabetes Management Algorithm 2013. Endocr Pract. 2013;19(2):327-336.

105. Davidson MH, Toth P, Weiss S, et al. Low-dose combination therapy with colesevelam hydrochloride and lovastatin effectively decreases low-density lipoprotein cholesterol in patients with primary hypercholesterolemia. Clin Cardiol. 2001;24(6):467-474.

106. Hunninghake DB, Mellies MJ, Goldberg AC, et al. Efficacy and safety of pravastatin in patients with primary hypercholesterolemia. II. Once-daily versus twice-daily dosing. Atherosclerosis. 1990;85(2-3):219-227.

107. McKenney J, Jones M, Abby S. Safety and efficacy of colesevelam hydrochloride in combination with fenofibrate for the treatment of mixed hyperlipidemia. Curr Med Res Opin. 2005;21(9):1403-1412. doi: 10.1185/030079905X59157.

108. Davidson MH, Rooney M, Pollock E, Drucker J, Choy Y. Effect of colesevelam and niacin on low-density lipoprotein cholesterol and glycemic control in subjects with dyslipidemia and impaired fasting glucose. J Clin Lipidol. 2013;7(5):423-432. doi: 10.1016/j.jacl.2013.06.001.

109. Bays H, Rhyne J, Abby S, Lai Y-L, Jones M. Lipid-lowering effects of colesevelam HCl in combination with ezetimibe. Curr Med Res Opin. 2006;22(11):2191-2200. doi: 10.1185/030079906X148436.

110. Stein EA, Marais AD, Szamosi T, et al. Colesevelam hydrochloride: efficacy and safety in pediatric subjects with heterozygous familial hypercholesterolemia. J Pediatr. 2010;156(2):231-236.e3. doi: 10.1016/j.jpeds.2009.08.037.

111. Huijgen R, Abbink EJ, Bruckert E, et al. Colesevelam added to combination therapy with a statin and ezetimibe in patients with familial hypercholesterolemia: a 12-week, multicenter, randomized, double-blind, controlled trial. Clin Ther. 2010;32(4):615-625. doi: 10.1016/j.clinthera.2010.04.014.

112. Jialal I, Abby SL, Misir S, Nagendran S. Concomitant reduction in low-density lipoprotein cholesterol and glycated hemoglobin with colesevelam hydrochloride in patients with type 2 diabetes: a pooled analysis. Metab Syndr Relat Disord. 2009;7(3):255-258. doi: 10.1089/met.2009.0007.

113. Moore A, Phan BAP, Challender C, Williamson J, Marcovina S, Zhao XQ. Effects of adding extended-release niacin and colesevelam to statin therapy on lipid levels in subjects with atherosclerotic disease. J Clin Lipidol. 2007;1(6):620-625. doi: 10.1016/j.jacl.2007.09.001.

114. Brown W V, Dujovne CA, Farquhar JW, et al. Effects of fenofibrate on plasma lipids. Double-blind, multicenter study in patients with type IIA or IIB hyperlipidemia. Arteriosclerosis. 1996(6):670-678.

115. Knopp RH, Brown W V, Dujovne CA, et al. Effects of fenofibrate on plasma lipoproteins in hypercholesterolemia and combined hyperlipidemia. Am J Med. 1987;83(5B):50-59.

116. Insua A, Massari F, Rodríguez Moncalvo JJ, Rubén Zanchetta J, Insua AM. Fenofibrate or gemfibrozil for treatment of types IIa and IIb primary hyperlipoproteinemia: a randomized, double-blind, crossover study. Endocr Pract. 2002;8(2):96-101. doi: 10.4158/EP.8.2.96.

117. National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Third report of the National Cholesterol Education Program (NCEP) Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III) final report. Circulation. 2002;106(25):3143-3421.

118. Farnier M, Ducobu J, Bryniarski L. Long-term safety and efficacy of fenofibrate/pravastatin combination therapy in high risk patients with mixed hyperlipidemia not controlled by pravastatin monotherapy. Curr Med Res Opin. 2011;27(11):2165-2173. doi: 10.1185/03007995.2011.626398.

119. Roth EM, McKenney JM, Kelly MT, et al. Efficacy and safety of rosuvastatin and fenofibric acid combination therapy versus simvastatin monotherapy in patients with hypercholesterolemia and hypertriglyceridemia: a randomized, double-blind study. Am J Cardiovasc Drugs. 2010;10(3):175-186. doi: 10.2165/11533430-000000000-00000.

120. Athyros VG, Papageorgiou AA, Athyrou V V, Demitriadis DS, Pehlivanidis AN, Kontopoulos AG. Atorvastatin versus four statin-fibrate combinations in patients with familial combined hyperlipidaemia. J Cardiovasc Risk. 2002;9(1):33-39.

121. Enger C, Gately R, Ming EE, Niemcryk SJ, Williams L, McAfee AT. Pharmacoepidemiology safety study of fibrate and statin concomitant therapy. Am J Cardiol. 2010;106(11):1594-1601. doi: 10.1016/j.amjcard.2010.07.041.

122. Amend KL, Landon J, Thyagarajan V, Niemcryk S, McAfee A. Incidence of hospitalized rhabdomyolysis with statin and fibrate use in an insured US population. Ann Pharmacother. 2011;45(10):1230-1239. doi: 10.1345/aph.1Q110.

123. Probstfield JL, Hunninghake DB. Nicotinic acid as a lipoprotein-altering agent. Therapy directed by the primary physician. Arch Intern Med. 1994;154(14):1557-1559.

124. Insull W, Basile JN, Vo AN, Jiang P, Thakkar R, Padley RJ. Efficacy and safety of combination therapy with niacin extended-release and simvastatin versus atorvastatin in patients with dyslipidemia: The SUPREME Study. J Clin Lipidol. 2009;3(2):109-118. doi: 10.1016/j.jacl.2009.02.009.

125. Airan-Javia SL, Wolf RL, Wolfe ML, Tadesse M, Mohler E, Reilly MP. Atheroprotective lipoprotein effects of a niacin-simvastatin combination compared to low- and high-dose simvastatin monotherapy. Am Heart J. 2009;157(4):687.e1-687.e8. doi: 10.1016/j.ahj.2009.01.001.

126. Ballantyne CM, Davidson MH, McKenney JM, Keller LH, Bajorunas DR, Karas RH. Comparison of the efficacy and safety of a combination tablet of niacin extended-release and simvastatin with simvastatin 80 mg monotherapy: the SEACOAST II (high-dose) study. J Clin Lipidol. 2008;2(2):79-90. doi: 10.1016/j.jacl.2008.02.004.

127. Chen F, Maccubbin D, Yan L, et al. Lipid-altering efficacy and safety profile of co-administered extended release niacin/laropiprant and simvastatin versus atorvastatin in patients with mixed hyperlipidemia. Int J Cardiol. 2013;167(1):225-231. doi: 10.1016/j.ijcard.2011.12.103.

128. AIM-HIGH Investigators, Boden WE, Probstfield JL, et al. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med. 2011;365(24):2255-2267. doi: 10.1056/NEJMoa1107579.

129. HPS2-THRIVE Collaborative Group, Landray MJ, Haynes R, et al. Effects of extended-release niacin with laropiprant in high-risk patients. N Engl J Med. 2014;371(3):203-212. doi: 10.1056/NEJMoa1300955.

130. Paolini JF, Mitchel YB, Reyes R, et al. Effects of laropiprant on nicotinic acid-induced flushing in patients with dyslipidemia. Am J Cardiol. 2008;101(5):625-630. doi: 10.1016/j.amjcard.2007.10.023.

131. Maccubbin D, Bays HE, Olsson AG, et al. Lipid-modifying efficacy and tolerability of extended-release niacin/laropiprant in patients with primary hypercholesterolaemia or mixed dyslipidaemia. Int J Clin Pract. 2008;62(12):1959-1970. doi: 10.1111/j.1742-1241.2008.01938.x.

132. McKenney J, Ballantyne CM, Feldman TA, et al. LDL-C goal attainment with ezetimibe plus simvastatin coadministration vs atorvastatin or simvastatin monotherapy in patients at high risk of CHD. MedGenMed. 2005;7(3):3.

133. Ballantyne CM, Houri J, Notarbartolo A, et al. Effect of ezetimibe coadministered with atorvastatin in 628 patients with primary hypercholesterolemia: a prospective, randomized, double-blind trial. Circulation. 2003;107(19):2409-2415. doi: 10.1161/01.CIR.0000068312.21969.C8.

134. Ballantyne CM, Abate N, Yuan Z, King TR, Palmisano J. Dose-comparison study of the combination of ezetimibe and simvastatin (Vytorin) versus atorvastatin in patients with hypercholesterolemia: The Vytorin Versus Atorvastatin (VYVA) Study. Am Heart J. 2005;149(3):464-473. doi: 10.1016/j.ahj.2004.11.023.

135. Davidson MH, McGarry T, Bettis R, et al. Ezetimibe coadministered with simvastatin in patients with primary hypercholesterolemia. J Am Coll Cardiol. 2002;40(12):2125-2134.

136. Kerzner B, Corbelli J, Sharp S, et al. Efficacy and safety of ezetimibe coadministered with lovastatin in primary hypercholesterolemia. Am J Cardiol. 2003;91(4):418-424.

137. Goldberg AC, Sapre A, Liu J, Capece R, Mitchel YB; Ezetimibe Study Group. Efficacy and safety of ezetimibe coadministered with simvastatin in patients with primary hypercholesterolemia: a randomized, double-blind, placebo-controlled trial. Mayo Clin Proc. 2004;79(5):620-629. doi: 10.1016/S0025-6196(11)62283-0.

138. Masana L, Mata P, Gagné C, et al. Long-term safety and, tolerability profiles and lipid-modifying efficacy of ezetimibe coadministered with ongoing simvastatin treatment: a multicenter, randomized, double-blind, placebo-controlled, 48-week extension study. Clin Ther. 2005;27(2):174-184. doi: 10.1016/j.clinthera.2005.02.011.

139. Melani L, Mills R, Hassman D, et al. Efficacy and safety of ezetimibe coadministered with

pravastatin in patients with primary hypercholesterolemia: a prospective, randomized, double-blind trial. Eur Heart J. 2003;24(8):717-728.

140. Robinson JG, Ballantyne CM, Grundy SM, et al. Lipid-altering efficacy and safety of ezetimibe/

simvastatin versus atorvastatin in patients with hypercholesterolemia and the metabolic syndrome (from the VYMET study). Am J Cardiol. 2009;103(12):1694-1702. doi: 10.1016/j.amjcard.2009.05.003.

141. Bohula EA, Giugliano RP, Cannon CP, et al. Achievement of dual low-density lipoprotein cholesterol and high-sensitivity C-reactive protein targets more frequent with the addition of ezetimibe to

simvastatin and associated with better outcomes in IMPROVE-IT. Circulation. 2015;132(13):1224-1233. doi: 10.1161/CIRCULATIONAHA.115.018381.

142. Cannon CP, Blazing MA, Giugliano RP, et al. Ezetimibe added to statin therapy after acute coronary syndromes. N Engl J Med. 2015;372(25):2387-2397. doi: 10.1056/NEJMoa1410489.

143. Feldman T, Koren M, Insull W, et al. Treatment of high-risk patients with ezetimibe plus simvastatin co-administration versus simvastatin alone to attain National Cholesterol Education Program Adult Treatment Panel III low-density lipoprotein cholesterol goals. Am J Cardiol. 2004;93(12):1481-1486. doi: 10.1016/j.amjcard.2004.02.059.

144. Gagné C, Gaudet D, Bruckert E; Ezetimibe Study Group. Efficacy and safety of ezetimibe coadministered with atorvastatin or simvastatin in patients with homozygous familial hypercholesterolemia. Circulation. 2002;105(21):2469-2475.

145. Stein E, Stender S, Mata P, et al. Achieving lipoprotein goals in patients at high risk with severe hypercholesterolemia: efficacy and safety of ezetimibe co-administered with atorvastatin. Am Heart J. 2004;148(3):447-455. doi: 10.1016/j.ahj.2004.03.052.

146. van der Graaf A, Cuffie-Jackson C, Vissers MN, et al. Efficacy and safety of coadministration of ezetimibe and simvastatin in adolescents with heterozygous familial hypercholesterolemia. J Am Coll Cardiol. 2008;52(17):1421-1429. doi: 10.1016/j.jacc.2008.09.002.

147. Foody JM, Brown WV, Zieve F, et al. Safety and efficacy of ezetimibe/simvastatin combination versus atorvastatin alone in adults ≥65 years of age with hypercholesterolemia and with or at moderately high/high risk for coronary heart disease (the VYTELD study). Am J Cardiol. 2010;106(9):1255-1263. doi: 10.1016/j.amjcard.2010.06.051.

148. Cuchel M, Meagher EA, du Toit Theron H, et al. Efficacy and safety of a microsomal triglyceride transfer protein inhibitor in patients with homozygous familial hypercholesterolaemia: a single-arm, open-label, phase 3 study. Lancet. 2013;381(9860):40-46. doi: 10.1016/S0140-6736(12)61731-0.

149. Raal FJ, Santos RD, Blom DJ, et al. Mipomersen, an apolipoprotein B synthesis inhibitor, for lowering of LDL cholesterol concentrations in patients with homozygous familial hypercholesterolaemia: a randomised, double-blind, placebo-controlled trial. Lancet. 2010;375(9719):998-1006. doi: 10.1016/S0140-6736(10)60284-X.

150. Akdim F, Stroes ESG, Sijbrands EJG, et al. Efficacy and safety of mipomersen, an antisense inhibitor of apolipoprotein B, in hypercholesterolemic subjects receiving stable statin therapy. J Am Coll Cardiol. 2010;55(15):1611-1618. doi: 10.1016/j.jacc.2009.11.069.

151. McGowan MP, Tardif JC, Ceska R, et al. Randomized, placebo-controlled trial of mipomersen in patients with severe hypercholesterolemia receiving maximally tolerated lipid-lowering therapy. PLoS One. 2012;7(11):e49006. doi: 10.1371/journal.pone.0049006.

152. Stein EA, Dufour R, Gagne C, et al. Apolipoprotein B synthesis inhibition with mipomersen in heterozygous familial hypercholesterolemia: results of a randomized, double-blind, placebo-controlled trial to assess efficacy and safety as add-on therapy in patients with coronary artery disease. Circulation. 2012;126(19):2283-2292. doi: 10.1161/CIRCULATIONAHA.112.104125.

153. Santos RD, Duell PB, East C, et al. Long-term efficacy and safety of mipomersen in patients with familial hypercholesterolaemia: 2-year interim results of an open-label extension. Eur Heart J. 2015;36(9):566-575. doi: 10.1093/eurheartj/eht549.

154. Visser ME, Wagener G, Baker BF, et al. Mipomersen, an apolipoprotein B synthesis inhibitor, lowers low-density lipoprotein cholesterol in high-risk statin-intolerant patients: a randomized, double-blind, placebo-controlled trial. Eur Heart J. 2012;33(9):1142-1149. doi: 10.1093/eurheartj/ehs023.

155. Thomas GS, Cromwell WC, Ali S, Chin W, Flaim JD, Davidson M. Mipomersen, an apolipoprotein B synthesis inhibitor, reduces atherogenic lipoproteins in patients with severe hypercholesterolemia at high cardiovascular risk: a randomized, double-blind, placebo-controlled trial. J Am Coll Cardiol. 2013;62(23):2178-2184. doi: 10.1016/j.jacc.2013.07.081.

156. Ginsberg HN, Rader DJ, Raal FJ, et al. Efficacy and safety of alirocumab in patients with heterozygous familial hypercholesterolemia and LDL-C of 160 mg/dL or higher. Cardiovasc Drugs Ther. 2016;30(5):473-483. doi: 10.1007/s10557-016-6685-y.

157. Moriarty PM, Thompson PD, Cannon CP, et al. Efficacy and safety of alirocumab vs ezetimibe in statin-intolerant patients, with a statin rechallenge arm: The ODYSSEY ALTERNATIVE randomized trial. J Clin Lipidol. 2015;9(6):758-769. doi: 10.1016/j.jacl.2015.08.006.

158. Kastelein JJP, Ginsberg HN, Langslet G, et al. ODYSSEY FH I and FH II: 78 week results with alirocumab treatment in 735 patients with heterozygous familial hypercholesterolaemia. Eur Heart J. 2015;36(43):ehv370. doi: 10.1093/eurheartj/ehv370.

159. Robinson JG, Farnier M, Krempf M, et al. Efficacy and safety of alirocumab in reducing lipids and cardiovascular events. N Engl J Med. 2015;372(16):1489-1499. doi: 10.1056/NEJMoa1501031.

160. Cannon CP, Cariou B, Blom D, et al. Efficacy and safety of alirocumab in high cardiovascular risk patients with inadequately controlled hypercholesterolaemia on maximally tolerated doses of statins: the ODYSSEY COMBO II randomized controlled trial. Eur Heart J. 2015;36(19):1186-1194. doi: 10.1093/eurheartj/ehv028.

161. Kereiakes DJ, Robinson JG, Cannon CP, et al. Efficacy and safety of the proprotein convertase subtilisin/kexin type 9 inhibitor alirocumab among high cardiovascular risk patients on maximally tolerated statin therapy: The ODYSSEY COMBO I study. Am Heart J. 2015;169(6):906-915.e13. doi: 10.1016/j.ahj.2015.03.004.

162. Bays H, Gaudet D, Weiss R, et al. Alirocumab as add-on to atorvastatin versus other lipid treatment strategies: ODYSSEY OPTIONS I Randomized Trial. J Clin Endocrinol Metab. 2015;100(8):3140-3148. doi: 10.1210/jc.2015-1520.

163. Farnier M, Jones P, Severance R, et al. Efficacy and safety of adding alirocumab to rosuvastatin versus adding ezetimibe or doubling the rosuvastatin dose in high cardiovascular-risk patients: The ODYSSEY OPTIONS II randomized trial. Atherosclerosis. 2016;244:138-146. doi: 10.1016/j.atherosclerosis.2015.11.010.

164. Nissen SE, Stroes E, Dent-Acosta RE, et al. Efficacy and tolerability of evolocumab vs ezetimibe in patients with muscle-related statin intolerance: The GAUSS-3 Randomized Clinical Trial. JAMA. 2016;315(15):1580-1590. doi: 10.1001/jama.2016.3608.

165. Raal FJ, Honarpour N, Blom DJ, et al. Inhibition of PCSK9 with evolocumab in homozygous familial hypercholesterolaemia (TESLA Part B): a randomised, double-blind, placebo-controlled trial. Lancet. 2015;385(9965):341-350. doi: 10.1016/S0140-6736(14)61374-X.

166. Raal FJ, Stein EA, Dufour R, et al. PCSK9 inhibition with evolocumab (AMG 145) in heterozygous familial hypercholesterolaemia (RUTHERFORD-2): a randomised, double-blind, placebo-controlled trial. Lancet. 2015;385(9965):331-340. doi: 10.1016/S0140-6736(14)61399-4.

167. Stroes E, Colquhoun D, Sullivan D, et al. Anti-PCSK9 antibody effectively lowers cholesterol in patients with statin intolerance: the GAUSS-2 randomized, placebo-controlled phase 3 clinical trial of evolocumab. J Am Coll Cardiol. 2014;63(23):2541-2548. doi: 10.1016/j.jacc.2014.03.019.

168. Robinson JG, Nedergaard BS, Rogers WJ, et al. Effect of evolocumab or ezetimibe added to moderate- or high-intensity statin therapy on LDL-C lowering in patients with hypercholesterolemia: the LAPLACE-2 randomized clinical trial. JAMA. 2014;311(18):1870-1882. doi: 10.1001/jama.2014.4030.

169. Bibbins-Domingo K, Grossman DC, Curry SJ, et al. Statin use for the primary prevention of cardiovascular disease in adults: US Preventive Services Task Force recommendation statement. JAMA. 2016;316(19):1997. doi: 10.1001/jama.2016.15450.

170. Catapano AL, Graham I, De Backer G, et al. 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias. Eur Heart J. 2016;37(39):2999-3058. doi: 10.1093/eurheartj/ehw272.

171. ACCORD Study Group, Ginsberg HN, Elam MB, et al. Effects of combination lipid therapy in type 2 diabetes mellitus. N Engl J Med. 2010;362(17):1563-1574. doi: 10.1056/NEJMoa1001282.

172. Gidding SS, Champagne MA, de Ferranti SD, et al. The agenda for familial hypercholesterolemia: a scientific statement from the American Heart Association. Circulation. 2015;132(22):2167-2192. doi: 10.1161/CIR.0000000000000297.

# data[].attributes.attachment_link.authors[].name
Samantha Karr, PharmD, FCCP, BCPS, BCACP, BC-ADM

# data[].attributes.attachment_link.title
Epidemiology and Management of Hyperlipidemia

# data[].attributes.attachment_link.description
Cardiovascular disease (CVD) is the leading cause of death among adults in the United States, and people with hyperlipidemia are at roughly twice the risk of developing CVD as compared to those with normal total cholesterol levels.

# data[].attributes.body
Titulo: Prevalencia, tratamiento y control de la hipercolesterolemia en pacientes de alto riesgo cardiovascular: evidencias de una revisión sistemática de la literatura en España

Tipo de estudio:

revisión sistemática

Año: 2015
Resultados: La prevalencia de hipercolesterolemia varió del 50 al 84% en diabéticos, del 30 al 60% en pacientes con DM o riesgo SCORE elevado, del 64 al 74% con enfermedad coronaria, del 40 al 70% en pacientes con accidente cerebrovascular y del 60 al 80% en aquellos con enfermedad arterial periférica. A pesar de constatar que la mayoría se encontraba en tratamiento farmacológico, el control aceptable de los lípidos séricos fue muy variable, oscilando entre el 15% y el 65%. Entre aquellos con hipercolesterolemia familiar heterocigota, el 95-100 % recibió tratamiento, pero menos del 50 % logró sus objetivos terapéuticos.
Conclusiones: Se puede encontrar una prevalencia elevada de hipercolesterolemia en grupos objetivo de alto riesgo CV. Aunque la mayoría de los pacientes están recibiendo tratamiento farmacológico, las tasas de control lipídico continúan siendo bajas, tanto en prevención primaria como secundaria.
https://pubmed.ncbi.nlm.nih.gov/26499178/

# data[].attributes.attachment_link.title
Prevalence, Treatment, and Control of Hypercholesterolemia in High Cardiovascular Risk Patients: Evidences from a Systematic Literature Review in Spain - PubMed

# data[].attributes.attachment_link.description
1 Department of Internal Medicine, University Hospital Mutua Terrassa, Barcelona, Spain. adelasierra@mutuaterrassa.cat. 2 Lipid Unit, Internal Medicine Service, University Hospital of Bellvitge, Barcelona, Spain. 3 Internal Medicine Service, University Hospital Alcorcón Foundation, Madrid, Spain. 4 Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofıa University Hospital, University of Cordoba and CIBER Fisiopatologia Obesidad y Nutricion, Instituto de Salud Carlos III, Cordoba, Spain.

# data[].attributes.body
https://scielo.conicyt.cl/pdf/rchnut/v45n2/0716-1549-rchnut-45-02-0135.pdf
TITULO:  Asociación entre la participación en programas de asistencia alimentaria y patrones del perfil lipídico en Perú.
TIPO DE ESTUDIO: Transversal descriptivo.
AÑO: 2018
AUTOR: Paredes J. y Antonio Bernabé A.
RESULTADOS:  De un total de 4.209 sujetos enrolados en el estudio original, los datos de 4.028 fueron analizados para el presente estudio, 2.012 (50.1%) mujeres, y un promedio de edad de 42,1±15,3. Del total evaluado, 20.1% pertenecían a Lima Metropolitana, mientras que 18,9 % eran del resto de la Costa. Por otro lado, solo 123 (3,1 %, IC95%: 2,5-3,6) reportaron ser beneficiarios del programa Comedores Populares, mientras que 827 (20,5%; IC95%: 19,3-21,8) reportaron ser beneficiarios del Vaso de Leche. Solo 49 (1,2%) del total de participantes reportaron estar en ambos programas de asistencia alimentaria.
CONCLUSIONES:  Ser beneficiario del programa Comedor Popular estuvo asociado a más del doble de probabilidad de presentar LDL-c elevado. De otro lado, ser beneficiario del Vaso de Leche, sin embargo, tuvo resultados contradictorios: aumentó la probabilidad de presentar HDL-c bajo, pero redujo la probabilidad de presentar hipertrigliceridemia. Nuestros hallazgos sugieren la necesidad de intervenciones para mejorar la dieta provista en ciertos programas de asistencia alimentaria.

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Estudio: https://www.ajmc.com/view/epidemiology-and-management-of-hyperlipidemia-article
Título: Epidemiología y manejo de la hiperlipidemia

Año: 2017
Tipo de estudio: Artículo de revisión
Resultados: En dicho estudio nos especifica que en los EE.UU hay más de 100 millones (53%) de adultos que tienen niveles elevados de LDLc, de los cuales menos del 50% reciben tratamiento, sin embargo, solo el 35% logran un control adecuado. En estas personas con hiperlipidemia tienen el doble de riesgo de desarrollar enfermedades cardiovasculares en comparación con aquellos que tienen niveles normales de Col-T. Además, aproximadamente 31 millones de adultos estadounidenses tienen niveles de colesterol total que exceden los 240 mg/dL, lo que los coloca en aproximadamente el doble del riesgo de enfermedad cardiovascular aterosclerótica.

Los principales factores de riesgo encontrados fueron modificables, como la dieta alta en grasas saturadas o trans, inactividad física, tabaquismo y obesidad.
Conclusión: Los pacientes con hipercolesterolemia familiar (HF) tienen un riesgo aún mayor de desarrollar ECV a una edad más temprana; por lo tanto, la detección temprana y el tratamiento son imperativos para reducir los eventos cardiovasculares y la muerte prematura.

# data[].attributes.attachment_link.readable_text
Cardiovascular disease (CVD) is the leading cause of death among adults in the United States, and people with hyperlipidemia are at roughly twice the risk of developing CVD as compared to those with normal total cholesterol levels. ¹ Patients with familial hypercholesterolemia (FH) have an even greater risk of developing CVD at an earlier age; therefore, early detection and treatment are imperative to reduce cardiovascular events and premature death. Statins are the mainstay treatment for hyperlipidemia; however, the limitations of statins include treatment resistance, intolerance due to adverse events, and a lack of adherence which contribute to poor outcomes. As such, many patients require adjunct therapies to properly control hyperlipidemia including niacin, bile acid sequestrants, fibric acids, and ezetimibe. FH can be even more challenging to treat, often requiring the use of lomitapide, mipomersen, proprotein convertase subtilisin/kexin type 9 inhibitors, or low-density lipoprotein cholesterol apheresis, in addition to high dose conjunction with statins or other agents. ² The approach to determining the appropriate treatment options has also undergone important changes. Guidelines for the management of patients with hyperlipidemia vary in their recommendations, with the American College of Cardiology/American Heart Association recommending that treatment decisions be based on the intensity of response associated with various statins, while multiple other guidelines (eg, National Lipid Association (NLA) and the American Association of Clinical Endocrinologists and American College of Endocrinology) still support attaining prespecified lipid values to reduce cardiovascular risk. ³⁻⁵ This article will review the epidemiology of hyperlipidemia and FH, risk factors associated with the development of disease, as well as the efficacy and safety of statins and adjunct treatment options.

Am J Manag Care. 2017;23:-S0

Hyperlipidemia involves an imbalance of cholesterol levels, including low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) in the blood. LDL-C and HDL-C regulate the amount of cholesterol in the body and an imbalance can increase the risk of cardiovascular events, including myocardial infarction and stroke. Other forms of hyperlipidemia include hypertriglyceridemia as well as mixed hyperlipidemia, in which both cholesterol and triglyceride levels are elevated. Elevated LDL-C can lead to a buildup of plaques within the arteries and is associated with an increased risk of atherosclerotic cardiovascular disease (ASCVD), including coronary artery disease or stroke. As HDL-C functions to remove cholesterol from the body, increased levels of HDL-C (≥60 mg/dL) can help decrease the risk of ASCVD. ⁶
Epidemiology
In the United States, more than 100 million, or roughly 53% of adults, have elevated LDL-C levels. ⁷ Yet, fewer than 50% of patients with high LDL-C receive treatment to reduce their levels, and among those receiving treatment, fewer than 35% achieve adequate control. 1,7 Further, approximately 31 million American adults have total cholesterol levels that exceed 240 mg/dL, placing them at about twice the risk of ASCVD compared to those with total cholesterol levels that are at goal. ¹
Risk Factors for Hyperlipidemia
There are 2 types of FH: homozygous (HoFH) and heterozygous FH (HeFH). In the United States, HeFH is more common, affecting approximately 1 in 500 people, and is associated with LDL-C levels of 200 to 450 mg/dL. 19,20 Patients with HeFH often develop coronary artery disease before the age of 60 years. ¹⁵ HoFH is rarer, affecting roughly 1 in 300,000 to 1,000,000 people, but is associated with much higher LDL-C levels compared with HeFH (450 to >1000 mg/dL). 11,19,21 If left untreated, patients with HoFH may die before the age of 20 years. ¹⁵
Management of Hyperlipidemia and FH Statins
Statins reduce total cholesterol and LDL-C via inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. Multiple studies have clearly shown that statins can lower LDL-C levels, thereby reducing the risk of developing CVD in patients with elevated LDL-C and reducing mortality and disease progression among patients with clinical ASCVD. 3,22-29 Statins are the mainstay of treatment for hyperlipidemia, including use in FH. 3,4

Seven statins are currently approved by the FDA for the treatment of hyperlipidemia in combination with a heart-healthy diet. ³⁰⁻³⁷ A meta-analysis of 26 randomized trials involving 170,000 patients treated with various statins showed that a decrease in LDL-C of 39 mg/dL was associated with a 24% risk reduction in major vascular events. ²⁹ The trials included patients being treated for either primary or secondary prevention of cardiovascular disease, and the duration of treatment was at least 2 years. In general, statins can reduce LDL-C by approximately 20% to 65% with greater reductions seen with atorvastatin, rosuvastatin, and pitavastatin; moderate decreases with lovastatin and simvastatin; and the lowest decreases with fluvastatin and pravastatin. 22,24-28,35 All but pitavastatin have indications for patients with FH.

While statins are generally well tolerated, they are associated with numerous adverse effects, including gastrointestinal events, musculoskeletal pain, respiratory infections, and headaches. 30-34,36,37 Statins can also be associated with elevated blood glucose and glycated hemoglobin (A1C) levels. ³⁸⁻⁴⁰ Increases in liver enzyme transaminases can occur infrequently, and statins are contraindicated in patients with active liver disease, as well as in patients with unexplained and chronic elevations in liver enzyme transaminases. Caution is advised regarding the concomitant use of most statins and anticoagulants; a reduction in the dose of the anticoagulant is recommended. 30-32,34,36,37
Limitations of Statins
While statin monotherapy can lower LDL-C levels in most patients, some patients are nonadherent, intolerant, or resistant, resulting in poor outcomes.
Nonadherence to Statin Treatment
Nonadherence to statin treatment is a common issue, and has been shown to lead to an increased risk of ASCVD and mortality. 10,48-50 Studies have found that 10% to 30% of patients never fill their first statin prescription, and adherence rates are roughly 25% to 50% among patients with acute coronary syndrome and those receiving statins for primary prevention of ASCVD. ⁵¹⁻⁵⁷ Further, within the first year, approximately 50% of patients discontinue statin therapy, and discontinuation rates at 2 years can be ≥75%. 10,58 Nonadherence and nonpersistence are associated with an increase in both ASCVD risk and mortality. ⁵⁰ Factors contributing to nonadherence include comorbidities, AEs, regimen complexity, age, sex, co-payment, and income. 10,57,59,60 Data from a meta-analysis of 22 cohort studies revealed that patients ≥70 years and <50 years of age were more likely to be nonadherent compared with those 50 to 69 years of age. ⁵⁷ In addition, nonadherence was greater among women and patients with lower incomes. Conversely, better adherence was noted among patients with a history of myocardial infarction or stroke, hypertension, or diabetes. Recommendations for addressing nonadherence include assessing the number of missed doses per month and discussing any barriers to adherence with the patient. ⁶¹ Medication therapy management, pharmacy disease management programs, and other pharmacist-driven efforts can help to improve clinical outcomes, improve adherence, and minimize cost. ⁶²
Statin Intolerance
Statin intolerance is often associated with poor adherence. Results of a meta-analysis comparing high-intensity and moderate-intensity statins revealed an increased risk of adverse events and adverse event-related treatment discontinuation with higher intensity statins ⁶³; however, another more recent meta-analysis noted less risk with rosuvastatin. ⁶⁴ Patients drinking grapefruit juice, especially large quantities, should be reminded of the potential for an interaction with statins, metabolized by CYP3A4. In addition, drugs that affect the CYP3A4 pathway can alter the metabolism of statins that are major substrates of CYP3A4, such as simvastatin, atorvastatin, and lovastatin. This can result in muscle-related adverse events. ⁶⁵⁻⁶⁸ Approximately 7% to 29% of patients receiving statins experience muscle-related adverse events, which can contribute to poor adherence and nonpersistence. 41,69-71 Rhabdomyolysis is a severe and potentially fatal form of muscle-related adverse event that occurs at a rate of 3.4 per 100,000 person-years. ⁷² A systematic review noted higher incidences of rhabdomyolysis among patients receiving simvastatin or atorvastatin as compared with pravastatin or fluvastatin, and among patients receiving fibrates in combination with statins. ⁶⁴ As pravastatin, fluvastatin, and rosuvastatin are only minor substrates of CYP3A4, these statins have a lower incidence of drug-drug interactions and also may be a better option for patients at an increased risk of developing rhabdomyolysis. 64,73 In cases where musculoskeletal events occur in patients receiving statins, it is important to first verify that statins are the cause of the events.
Statin Resistance Nonstatins
Several nonstatin therapies are available as adjunctive treatment for patients who do not respond adequately to statins or for those who are intolerant of statins. These include BASs, fibric acids, niacin, cholesterol absorption and synthesis inhibitors, as well as the recently approved class, PCSK9 inhibitors. ⁸⁸⁻⁹⁸
Bile Acid Sequestrants
BASs include cholestyramine, colestipol, and colesevelam. BASs reduce cholesterol by binding bile acids within the intestine, impeding bile acid reabsorption and enterohepatic cycling, increasing the conversion of cholesterol to bile acids, and increasing the number of hepatic LDLRs. This results in increased clearance of LDL-C and decreased LDL-C levels. 88-90,99 Colesevelam monotherapy is associated with a 15% to 20% reduction in LDL-C. 100,101 Studies have demonstrated that adding BASs to statins, fibrates, niacin, or ezetimibe can significantly reduce LDL-C levels compared with monotherapy. ¹⁰²⁻¹⁰⁹ The addition of colesevelam to statins and/or ezetimibe can further reduce LDL-C levels in adults and children (ages 10 -17 years) with FH compared with statin monotherapy. 110,111 In addition, a pooled analysis of 3 trials found that the combination of colesevelam and statins significantly decreased both LDL-C and A1C in patients with both hyperlipidemia and diabetes. ¹¹² The addition of colesevelam to therapy with atorvastatin and niacin led to a notable reduction in LDL-C (57%) compared with the combination of atorvastatin and niacin alone (47%). ¹¹³ While most BASs-associated AEs are tolerable, caution is recommended when prescribing BASs for patients with complete biliary obstruction due to an increased risk of new or worsening constipation. ⁸⁸⁻⁹⁰ Additionally, the labeling for some BASs can include a precaution regarding increased risk of bleeding. This risk exists when hypoprothrombinemia from vitamin K deficiency occurs due to reduction in absorption of fat-soluble vitamins related to chronic use of BASs. ⁸⁸⁻⁹⁰ In patients receiving any other medications in combination with BASs, administration should be spaced either 1 to 4 hours before, depending on the other medication, or 4 to 6 hours after BAS administration to reduce the chance of impaired absorption. ⁸⁹ Oral vitamin supplementation should be taken at least 4 hours before colesevelam. ⁹⁰
Fibric Acid Derivatives
Fibric acid derivatives are peroxisome proliferator-activated receptor α (PPARα) agonists that have been shown to reduce triglycerides by ≤50%, increasing HDL-C by ≤15%, LDL-C levels by 15% to 25%, and reducing major coronary events. ¹¹⁴⁻¹¹⁷ Similar to BASs, fibrates further reduce LDL-C levels when combined with statins compared with statins or fibrates alone. ¹¹⁸⁻¹²⁰ However, when used in combination with high-intensity statins, fibrates can increase the risk of myopathy and rhabdomyolysis. ¹²¹ The incidence of skeletal adverse events is higher when combining high-intensity statins with gemfibrozil compared to fenofibrate. ¹²² Guidelines recommend against using gemfibrozil in patients receiving statins, and fenofibrate should be restricted to patients receiving low-to-moderate dose statin therapy, as long as the benefits outweigh the risks. ³ In addition, fibrates are contraindicated in patients with hepatic or renal disease, unexplained persistent liver function abnormality, and in those with preexisting gallbladder disease. 91,92 Combination therapy of gemfibrozil plus repaglinide is also contraindicated. ⁹¹ Additionally, fenofibrate is contraindicated while breastfeeding. ⁹² Finally, caution is advised regarding the concomitant use of fibrates and anticoagulants, and increased monitoring of prothrombin time with international normalized ratio (INR) determination is recommended until these parameters have stabilized after 1 drug in this combination is added to the other. ⁹²

Niacin increases levels of HDL and reduces levels of very low-density lipoprotein (VLDL) which, in turn, reduces LDL-C levels. ¹²³ Studies involving the combination of niacin with statins have provided conflicting results. 100,124-127 In general, the addition of niacin to statins is associated with increased HDL-C, but is not associated with a significant reduction in LDL-C compared with statin monotherapy. In addition, results from multiple studies failed to show that the addition of niacin could reduce the risk of cardiovascular events, and indicated an increase in the risk of adverse events in patients receiving high-intensity statins compared with statin monotherapy. 128,129 The most common niacin-related adverse event is flushing. Laropiprant, a selective prostanoid receptor antagonist, can reduce the incidence and severity of niacin-related flushing when administered concomitantly. 130,131 However, results from the HPS2-THRIVE phase 3 study demonstrated that adding extended-release niacin and laropiprant to statin-based treatment was associated with an increase in diagnosis of type 2 diabetes as well as serious gastrointestinal and musculoskeletal events, infection, and bleeding. ¹²⁹ Niacin is contraindicated in patients with active liver disease, peptic ulcer disease, or arterial bleeding. ⁹³ Due to the increased risk of myopathy and rhabdomyolysis in patients receiving niacin in combination with either lovastatin or simvastatin, it is recommended that the dose of these statins not exceed 40 mg in patients receiving niacin. ⁹³ Caution should be used when prescribing niacin to patients with renal or hepatic impairment. In addition, the ACC notes that due to the lack of efficacy and potential for harm, niacin is not recommended for the treatment of hypercholesterolemia. ⁶¹
Lomitapide Mipomersen
Mipomersen is an antisense oligonucleotide that inhibits apo B100 synthesis and is indicated as adjunctive therapy to lipid-lowering medications and diet to reduce LDL-C, apo B, total cholesterol, and non-HDL-C in patients with HoFH. ⁹⁶ Approval of mipomersen was based on a randomized, double-blind, placebo-controlled phase 3 study of patients (N = 51) with HoFH who were 12 years of age or older and were currently receiving lipid-lowering agents at the maximum tolerated dose. ¹⁴⁹ There was a 24.7% mean reduction in LDL-C in patients receiving mipomersen (n = 34) compared with 3.3% in patients receiving placebo (n = 17; P = .0003). Statistically significant reductions in apo B, total cholesterol, and non-HDL-C were also noted. Additional trials have demonstrated the efficacy of mipomersen in reducing LDL-C in patients with HeFH, ¹⁵⁰ severe HeFH, ¹⁵¹ HeFH with coronary artery disease, ¹⁵² and HoFH. 148,153 Additional data indicate that mipomersen is efficacious in people with statin intolerance at high risk of ASCVD, ¹⁵⁴ and for those with severe hyperlipidemia at high risk of ASCVD. ¹⁵⁵ Common AEs associated with mipomersen include flu-like symptoms, injection-site reactions, headache, nausea, and alanine aminotransferase elevations. 148-151,153-155 Similar to lomitapide, mipomersen is contraindicated in patients with moderate or severe liver impairment, and is only available through a restricted REMS program. ⁹⁶ Fortunately, mipomersen was not noted to have any clinically relevant drug interactions in clinical trials.
PCSK9 Inhibitors Current Guidelines for the Management of Cholesterol
Numerous guidelines provide recommendations for the treatment of hyperlipidemia as well as FH. The 2013 ACC/AHA Guideline for the Treatment of Blood Cholesterol to Reduce Atherosclerotic Cardiovascular Risk in Adults includes 4 main groups of patients for whom statin therapy could reduce the risk of ASCVD, along with recommendations for the intensity of statin therapy (Table 1 ³). ³

The ACC/AHA differs from the US Preventive Services Task Force (USPSTF) with regard to levels of statin intensity recommended. The USPSTF (Table 2 ¹⁶⁹) recommends the use of low-to-moderate intensity statins in patients with a 10-year risk of ASCVD ≥10%, but for adult patients with a 10-year ASCVD risk between 7.5% and 10%, a low-to-moderate intensity statin is an option to consider. ¹⁶⁹

In contrast to the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guidelines, which recommend a treat-to-target approach, the 2013 ACC/AHA guidelines endorse a tiered approach based on the average percentage by which a specific statin can reduce LDL-C. 3,117 Statin regimens that can reduce LDL-C ≥50% are considered high-intensity therapies, while those statins that reduce LDL-C by 30% to <50% are considered moderate intensity, and those statins that reduce LDL-C ≤30% are considered low intensity.

High-intensity statin therapy is recommended in patients with FH by the ACC/AHA as well as by the Canadian Cardiovascular Society (CCS) and the European Atherosclerosis Society (EAS). 47,61,170 Moderate-intensity therapy is recommended in patients who cannot tolerate high-intensity treatment. All guidelines for the treatment of FH recommend initiating treatment as soon as possible. In addition to statins, ezetimibe and PCSK9 inhibitors are recommended in patients who have an insufficient response to statins. 3,61 While the CCS and EAS recommend the incorporation of bile acid sequestrants in patients with FH in need of further LDL-C reductions, the ACC/AHA 2013 guideline only recommends the use of nonstatins that have been shown to improve cardiovascular outcomes in randomized clinical trials, such as ezetimibe. The ACC/AHA 2013 guideline does not recommend the addition of niacin to statins based on data from the HSP2-THRIVE and AIM-HIGH studies that demonstrated an improvement in surrogate markers (eg, lipid parameters), but failed to show an increased benefit in cardiovascular outcomes. 128,129 Similarly, the ACCORD study failed to show a benefit on ASCVD outcomes of adding fenofibrate to moderate-intensity statins, despite improvement in lipid parameters. ¹⁷¹ Thus, the ACC/AHA 2013 guideline does not recommend the addition of fenofibrate to statin therapy. In 2015, the AHA and ACC made additional recommendations for the sequencing of treatment for FH with the addition of adjunctive therapies if patients do not reach LDL-C levels after 3 months of treatment ( Figure ¹⁷²). 61,172 Finally, the EAS guidelines recommend that LDL apheresis in combination with statins be initiated in patients with HoFH as early as 5 years of age and no later than 8 years of age in pediatric patients. ¹² In addition, lomitapide and mipomersen can be considered as adjunctive treatments for these patients who do not achieve the recommended LDL cholesterol targets and remain at high cardiovascular risk.

The American Association of Clinical Endocrinologists and American College of Endocrinology (AACE/ACE) 2017 lipid guidelines created a new patient population category deemed as "extreme risk" that would include individuals who have 1) "progressive ASCVD, including unstable angina, that persists after achieving an LDL-C <70 mg/dL," 2) "established clinical cardiovascular disease in individuals with diabetes, stage III or IV chronic kidney disease (CKD), and/or HeFH," and/or 3) "a history of premature ASCVD (males <55 years, females aged <65 years)." ⁵ The treatment goals for individuals in this category are: LDL-C <55 mg/dL; non-HDL-C <80 mg/dL; and apo B <70 mg/dL. ⁵ Regarding PCSK9 inhibitors, the AACE/ACE guidelines suggest their use in 2 patient groups: 1) patients with FH as combination therapy with statins, 2) patients with clinical CVD who do not attain LDL-C/non-HDL-C goals with maximally tolerated statin treatment. In the latter patient population, PCSK9 inhibitor monotherapy should only be considered in patients who are statin intolerant. ⁵ PCSK9 inhibitors are also recommended in combination with statins in patients with FH to lower LDL-C levels. ⁵
Conclusion
Recent changes to treatment recommendations are providing greater guidance for the management of hyperlipidemia, which includes a treat-to-target approach as well as using therapies based on the expected response. Although statins are the mainstay front-line treatment for hyperlipidemia, many patients, especially those with FH, do not achieve optimal LDL-C goals, thus requiring additional treatment. Statin therapy can be complicated by AEs (eg, myalgias) and rare but life-threatening rhabdomyolysis. These issues in treatment provide an opportunity to consider the use of PCSK9 inhibitors for patients who are nonadherent to statins, individuals that are statin intolerant, or those who are statin resistant.

Author affiliation: Associate Professor, Midwestern University College of Pharmacy, Pharmacy Practice Department, Glendale, AZ.

Funding source: This activity is supported by an education grant from Amgen, Inc.

Author disclosure: Dr Karr has no relevant financial relationships with commercial interests to disclose.

Authorship information: Concept and design, drafting of the manuscript, critical revision of the manuscript for important intellectual content, and supervision.

Address correspondence to: skarrx@midwestern.edu.

1. Mozaffarian D, Benjamin EJ, Go AS, et al. Heart disease and stroke statistics-2016 update: a report from the American Heart Association. Circulation. 2016;133(4):e38-e360. doi: 10.1161/CIR.0000000000000350.

2. Raal FJ, Pilcher GJ, Panz VR, et al. Reduction in mortality in subjects with homozygous familial hypercholesterolemia associated with advances in lipid-lowering therapy. Circulation. 2011;124(20):2202-2207. doi: 10.1161/circulationaha.111.042523.

3. Stone NJ, Robinson JG, Lichtenstein AH, et al. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults. J Am Coll Cardiol. 2014;63(25):2889-2934. doi: 10.1016/j.jacc.2013.11.002.

4. Jacobson TA, Ito MK, Maki KC, et al. National Lipid Association recommendations for patient-centered management of dyslipidemia: part 1-full report. J Clin Lipidol. 2015;9(2):129-169. doi: 10.1016/j.jacl.2015.02.003.

5. Jellinger PS, Handelsman Y, Rosenblit PD, et al. American Association of Clinical Endocrinologists and American College of Endocrinology guidelines for management of dyslipidemia and prevention of cardiovascular disease. Endocr Pract. 2017;23(suppl 2):1-87. doi: 10.4158/EP171764.APPGL.

6. Cooney MT, Dudina A, De Bacquer D, et al. HDL cholesterol protects against cardiovascular disease in both genders, at all ages and at all levels of risk. Atherosclerosis. 2009;206(2):611-616. doi: 10.1016/j.atherosclerosis.2009.02.041.

7. Centers for Disease Control and Prevention (CDC). Vital signs: prevalence, treatment, and control of high levels of low-density lipoprotein cholesterol-United States, 1999-2002 and 2005-2008. MMWR Morb Mortal Wkly Rep. 2011;60(4):109-114.

8. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of childhood and adult obesity in the United States, 2011-2012. JAMA. 2014;311(8):806. doi: 10.1001/jama.2014.732.

9. ACC/AHA. ACC/AHA ASCVD Risk Calculator website. www.cvriskcalculator.com. Published 2016. Accessed May 23, 2017.

10. Krähenbühl S, Pavik-Mezzour I, von Eckardstein A. Unmet needs in LDL-C lowering: when statins won't do! Drugs. 2016;76(12):1175-1190. doi: 10.1007/s40265-016-0613-0.

11. Vogt A. The genetics of familial hypercholesterolemia and emerging therapies. Appl Clin Genet. 2015;8:27-36. doi: 10.2147/TACG.S44315.

12. Cuchel M, Bruckert E, Ginsberg HN, et al. Homozygous familial hypercholesterolaemia: new insights and guidance for clinicians to improve detection and clinical management. A position paper from the Consensus Panel on Familial Hypercholesterolaemia of the European Atherosclerosis Society. Eur Heart J. 2014;35(32):2146-2157. doi: 10.1093/eurheartj/ehu274.

13. Ito MK, Watts GF. Challenges in the diagnosis and treatment of homozygous familial hypercholesterolemia. Drugs. 2015;75(15):1715-1724. doi: 10.1007/s40265-015-0466-y.

14. Sjouke B, Kusters DM, Kindt I, et al. Homozygous autosomal dominant hypercholesterolaemia in the Netherlands: prevalence, genotype-phenotype relationship, and clinical outcome. Eur Heart J. 2015;36(9):560-565. doi: 10.1093/eurheartj/ehu058.

15. Nordestgaard BG, Chapman MJ, Humphries SE, et al. Familial hypercholesterolaemia is underdiagnosed and undertreated in the general population: guidance for clinicians to prevent coronary heart disease: consensus statement of the European Atherosclerosis Society. Eur Heart J. 2013;34(45):3478-3490. doi: 10.1093/eurheartj/eht273.

16. Khera AV, Won HH, Peloso GM, et al. Diagnostic yield and clinical utility of sequencing familial hypercholesterolemia genes in patients with severe hypercholesterolemia. J Am Coll Cardiol. 2016;67(22):2578-2589. doi: 10.1016/j.jacc.2016.03.520.

17. Perak AM, Ning H, de Ferranti SD, Gooding HC, Wilkins JT, Lloyd-Jones DM. Long-term risk of atherosclerotic cardiovascular disease in US adults with the familial hypercholesterolemia phenotype. Circulation. 2016;134(1):9-19. doi: 10.1161/circulationaha.116.022335.

18. de Ferranti SD, Rodday AM, Mendelson MM, Wong JB, Leslie LK, Sheldrick RC. Prevalence of familial hypercholesterolemia in the 1999 to 2012 United States National Health and Nutrition Examination Surveys (NHANES) clinical perspective. Circulation. 2016;133(11):1067-1072. doi: 10.1161/CIRCULATIONAHA.115.018791.

19. Vishwanath R, Hemphill LC. Familial hypercholesterolemia and estimation of US patients eligible for low-density lipoprotein apheresis after maximally tolerated lipid-lowering therapy. J Clin Lipidol. 2014;8(1):18-28. doi: 10.1016/j.jacl.2013.11.002.

20. Youngblom E, Pariani M, Knowles JW. Familial hypercholesterolemia. In: Pagon RA, Adam MP, Ardinger HH, et al, eds. GeneReviews. Seattle, WA: University of Washington, Seattle; 1993-2017..

21. Sjouke B, Hovingh GK, Kastelein JJP, Stefanutti C. Homozygous autosomal dominant hypercholesterolaemia. Curr Opin Lipidol. 2015;26(3):200-209. doi: 10.1097/MOL.0000000000000179.

22. Bertolini S, Bon GB, Campbell LM, et al. Efficacy and safety of atorvastatin compared to pravastatin in patients with hypercholesterolemia. Atherosclerosis. 1997;130(1-2):191-197.

23. Black D, Davidson M, Koren M, et al. Cost effectiveness of treatment to National Cholesterol Education Panel (NCEP) targets with HMG-CoA reductase inhibitors. Trial design. Pharmacoeconomics. 1997;12(2 Pt 2):278-285.

24. Scandinavian Simvastatin Survival Study Group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet. 1994;344(8934):1383-1389. doi: 10.1016/S0140-6736(94)90566-5.

25. Heart Protection Study Collaborative Group. MRC/BHF Heart Protection Study of cholesterol lowering with simvastatin in 20,536 high-risk individuals: a randomised placebo-controlled trial. Lancet. 2002;360(9326):7-22. doi: 10.1016/S0140-6736(02)09327-3.

26. Athyros VG, Papageorgiou AA, Mercouris BR, et al. Treatment with atorvastatin to the National Cholesterol Educational Program goal versus "usual" care in secondary coronary heart disease prevention. The GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study. Curr Med Res Opin. 2002;18(4):220-228.

27. Insull W, Black D, Dujovne C, et al. Efficacy and safety of once-daily vs twice-daily dosing with fluvastatin, a synthetic reductase inhibitor, in primary hypercholesterolemia. Arch Intern Med. 1994;154(21):2449-2455.

28. Davidson M, Ma P, Stein EA, et al. Comparison of effects on low-density lipoprotein cholesterol and high-density lipoprotein cholesterol with rosuvastatin versus atorvastatin in patients with type IIa or IIb hypercholesterolemia. Am J Cardiol. 2002;89(3):268-275. doi: 10.1016/S0002-9149(01)02226-3.

29. Cholesterol Treatment Trialists' (CTT) Collaboration, Baigent C, Blackwell L, et al. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010;376(9753):1670-1681. doi: 10.1016/S0140-6736(10)61350-5.

30. Lipitor [package insert]. New York, NY: Pfizer, Inc; 2015.

31. Lescol/Lescol XL [package insert]. East Hanover, NJ: Novartis Pharmaceuticals Corporation; 2012.

32. Mevacor [package insert]. Morgantown, WV: Mylan Pharmaceuticals, Inc; 2014.

33. Pravachol [package insert]. Princeton, NJ: Bristol-Myers Squibb Company; 2016.

34. Zocor [package insert]. Whitehouse Station, NJ: Merck & Co, Inc; 2015.

35. Davidson M, McKenney J, Stein E, et al. Comparison of one-year efficacy and safety of atorvastatin versus lovastatin in primary hypercholesterolemia. Atorvastatin Study Group I. Am J Cardiol. 1997;79(11):1475-1481.

36. Livalo [package insert]. Montgomery, AL: Kowa Pharmaceuticals America, Inc; 2016.

37. Crestor [package insert]. Wilmington, DE: AstraZeneca Pharmaceuticals, LP; 2016.

38. Shah RV, Goldfine AB. Statins and risk of new-onset diabetes mellitus. Circulation. 2012;126(18):e282-284. doi: 10.1161/circulationaha112.122135.

39. Skoumas J, Liontou C, Chrysohoou C, et al. Statin therapy and risk of diabetes in patients with heterozygous familial hypercholesterolemia or familial combined hyperlipidemia. Atherosclerosis. 2014;237(1):140-145. doi: 10.1016/j.atherosclerosis.2014.08.047.

40. Maki KC, Ridker PM, Brown WV, Grundy SM, Sattar N. The Diabetes Subpanel of the National Lipid Association Expert Panel. An assessment by the Statin Diabetes Safety Task Force: 2014 update. J Clin Lipidol. 2014;8(3):S17-S29. doi: 10.1016/j.jacl.2014.02.012.

41. Bruckert E, Hayem G, Dejager S, Yau C, Bégaud B. Mild to moderate muscular symptoms with high-dosage statin therapy in hyperlipidemic patients-the PRIMO study. Cardiovasc Drugs Ther. 2005;19(6):403-414. doi: 10.1007/s10557-005-5686-z.

42. Rosenbaum D, Dallongeville J, Sabouret P, Bruckert E. Discontinuation of statin therapy due to muscular side effects: a survey in real life. Nutr Metab Cardiovasc Dis. 2013;23(9):871-875. doi: 10.1016/j.numecd.2012.04.012.

43. Parker BA, Capizzi JA, Grimaldi AS, et al. Effect of statins on skeletal muscle function. Circulation. 2013;127(1):96-103. doi: 10.1161/CIRCULATIONAHA.112.136101.

44. Banach M, Rizzo M, Toth PP, et al. Statin intolerance-an attempt at a unified definition. Position paper from an International Lipid Expert Panel. Arch Med Sci. 2015;1(1):1-23. doi: 10.5114/aoms.2015.49807.

45. Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med. 2009;361(1):62-72. doi: 10.1056/NEJMra0801327.

46. Rosenson RS, Baker SK, Jacobson TA, Kopecky SL, Parker BA. The National Lipid Association's Muscle Safety Expert Panel. An assessment by the Statin Muscle Safety Task Force: 2014 update. J Clin Lipidol. 2014;8(3):S58-S71. doi: 10.1016/j.jacl.2014.03.004.

47. Mancini GBJ, Baker S, Bergeron J, et al. Diagnosis, prevention, and management of statin adverse effects and intolerance: Canadian Consensus Working Group update (2016). Can J Cardiol. 2016;32(7):S35-S65. doi: 10.1016/j.cjca.2016.01.003.

48. Rasmussen JN, Chong A, Alter DA. Relationship between adherence to evidence-based pharmacotherapy and long-term mortality after acute myocardial infarction. JAMA. 2007;297(2):177-186. doi: 10.1001/jama.297.2.177.

49. Bouchard MH, Dragomir A, Blais L, Bérard A, Pilon D, Perreault S. Impact of adherence to statins on coronary artery disease in primary prevention. Br J Clin Pharmacol. 2007;63(6):698-708. doi: 10.1111/j.1365-2125.2006.02828.x.

50. De Vera MA, Bhole V, Burns LC, Lacaille D. Impact of statin adherence on cardiovascular disease and mortality outcomes: a systematic review. Br J Clin Pharmacol. 2014;78(4):684-698.

51. Cheetham TC, Niu F, Green K, et al. Primary nonadherence to statin medications in a managed care organization. J Manag Care Pharm. 2013;19(5):367-373. doi: 10.18553/jmcp.2013.19.5.367.

52. Fischer MA, Stedman MR, Lii J, et al. Primary medication non-adherence: analysis of 195,930 electronic prescriptions. J Gen Intern Med. 2010;25(4):284-290. doi: 10.1007/s11606-010-1253-9.

53. Raebel MA, Ellis JL, Carroll NM, et al. Characteristics of patients with primary non-adherence to medications for hypertension, diabetes, and lipid disorders. J Gen Intern Med. 2012;27(1):57-64. doi: 10.1007/s11606-011-1829-z.

54. Liberman JN, Hutchins DS, Popiel RG, Patel MH, Jan SA, Berger JE. Determinants of primary nonadherence in asthma-controller and dyslipidemia pharmacotherapy. Am J Pharm Benefits. 2010;2(2):111-118.

55. Jackevicius CA, Mamdani M, Tu JV. Adherence with statin therapy in elderly patients with and without acute coronary syndromes. JAMA. 288(4):462-467.

56. Mann DM, Allegrante JP, Natarajan S, Halm EA, Charlson M. Predictors of adherence to statins for primary prevention. Cardiovasc Drugs Ther. 2007;21(4):311-316. doi: 10.1007/s10557-007-6040-4.

57. Mann DM, Woodward M, Muntner P, Falzon L, Kronish I. Predictors of nonadherence to statins: a systematic review and meta-analysis. Ann Pharmacother. 2010;44(9):1410-1421. doi: 10.1345/aph.1P150.

58. Chodick G, Shalev V, Gerber Y, et al. Long-term persistence with statin treatment in a not-for-profit health maintenance organization: a population-based retrospective cohort study in Israel. Clin Ther. 2008;30(11):2167-2179. doi: 10.1016/j.clinthera.2008.11.012.

59. Lemstra M, Blackburn D, Crawley A, Fung R. Proportion and risk indicators of nonadherence to statin therapy: a meta-analysis. Can J Cardiol. 2012;28(5):574-580. doi: 10.1016/j.cjca.2012.05.007.

60. Spinler SA, Cziraky MJ, Willey VJ, et al. Frequency of attainment of low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol goals in cardiovascular clinical practice (from the National Cardiovascular Data Registry PINNACLE Registry). Am J Cardiol. 2015;116(4):547-553. doi: 10.1016/j.amjcard.2015.05.011.

61. Lloyd-Jones DM, Morris PB, Ballantyne CM, et al. 2016 ACC expert consensus decision pathway on the role of non-statin therapies for LDL-cholesterol lowering in the management of atherosclerotic cardiovascular disease risk. J Am Coll Cardiol. 2016;68(1):92-125. doi: 10.1016/j.jacc.2016.03.519.

62. Ramalho de Oliveira D, Brummel AR, Miller DB. Medication therapy management: 10 years of experience in a large integrated health care system. J Manag Care Pharm. 2010;16(3):185-195. doi: 10.18553/jmcp.2010.16.3.185.

63. Silva M, Matthews ML, Jarvis C, et al. Meta-analysis of drug-induced adverse events associated with intensive-dose statin therapy. Clin Ther. 2007;29(2):253-260. doi: 10.1016/j.clinthera.2007.02.008.

64. Mendes P, Robles PG, Mathur S. Statin-induced rhabdomyolysis: a comprehensive review of case reports. Physiother Can. 2014;66(2):124-132. doi: 10.3138/ptc.2012-65.

65. Causevic-Ramosevac A, Semiz S. Drug interactions with statins. Acta Pharm. 2013;63(3):277-293. doi: 10.2478/acph-2013-0022.

66. Sirtori CR. The pharmacology of statins. Pharmacol Res. 2014;88:3-11. doi: 10.1016/j.phrs.2014.03.002.

67. Kellick KA, Bottorff M, Toth PP; The National Lipid Association's Safety Task Force. A clinician's guide to statin drug-drug interactions. J Clin Lipidol. 2014;8(3):S30-S46. doi: 10.1016/j.jacl.2014.02.010.

68. Hu M, Tomlinson B. Evaluation of the pharmacokinetics and drug interactions of the two recently developed statins, rosuvastatin and pitavastatin. Expert Opin Drug Metab Toxicol. 2014;10(1):51-65. doi: 10.1517/17425255.2014.851667.

69. Cohen JD, Brinton EA, Ito MK, Jacobson TA. Understanding Statin Use in America and Gaps in Patient Education (USAGE): an internet-based survey of 10,138 current and former statin users. J Clin Lipidol. 2012;6(3):208-215. doi: 10.1016/j.jacl.2012.03.003.

70. Zhang H, Plutzky J, Skentzos S, et al. Discontinuation of statins in routine care settings: a cohort study. Ann Intern Med. 2013;158(7):526-534. doi: 10.7326/0003-4819-158-7-201304020-00004.

71. El-Salem K, Ababneh B, Rudnicki S, et al. Prevalence and risk factors of muscle complications secondary to statins. Muscle Nerve. 2011;44(6):877-881. doi: 10.1002/mus.22205.

72. Law M, Rudnicka AR. Statin safety: a systematic review. Am J Cardiol. 2006;97(8A):52C-60C. doi: 10.1016/j.amjcard.2005.12.010.

73. Antons KA, Williams CD, Baker SK, Phillips PS. Clinical perspectives of statin-induced rhabdomyolysis. Am J Med. 2006;119(5):400-409. doi: 10.1016/j.amjmed.2006.02.007.

74. American College of Cardiology. ACC's Statin Intolerance Tool. American College of Cardiology website. http://tools.acc.org/statinintolerance/. Published December 2016. Accessed May 18, 2017.

75. Zaharan NL, Williams D, Bennett K. Statins and risk of treated incident diabetes in a primary care population. Br J Clin Pharmacol. 2013;75(4):1118-1124. doi: 10.1111/j.1365-2125.2012.04403.x.

76. Waters DD, Ho JE, Boekholdt SM, et al. Cardiovascular event reduction versus new-onset diabetes during atorvastatin therapy. J Am Coll Cardiol. 2013;61(2):148-152. doi: 10.1016/j.jacc.2012.09.042.

77. Preiss D, Seshasai SRK, Welsh P, et al. Risk of incident diabetes with intensive-dose compared with moderate-dose statin therapy: a meta-analysis. JAMA. 2011;305(24):2556. doi: 10.1001/jama.2011.860.

78. Carter AA, Gomes T, Camacho X, Juurlink DN, Shah BR, Mamdani MM. Risk of incident diabetes among patients treated with statins: population based study. BMJ. 2013;347:f4356. doi: 10.1136/bmj.f4356.

79. Wong ND, Chuang J, Zhao Y, Rosenblit PD. Residual dyslipidemia according to low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B among statin-treated US adults: National Health and Nutrition Examination Survey 2009-2010. J Clin Lipidol. 2015;9(4):525-532. doi: 10.1016/j.jacl.2015.05.003.

80. Della Badia LA, Elshourbagy NA, Mousa SA. Targeting PCSK9 as a promising new mechanism for lowering low-density lipoprotein cholesterol. Pharmacol Ther. 2016;164:183-194. doi: 10.1016/j.pharmthera.2016.04.011.

81. Braamskamp MJAM, Langslet G, McCrindle BW, et al. Efficacy and safety of rosuvastatin therapy in children and adolescents with familial hypercholesterolemia: results from the CHARON study. J Clin Lipidol. 2015;9(6):741-750. doi: 10.1016/j.jacl.2015.07.011.

82. Avis HJ, Hutten BA, Gagné C, et al. Efficacy and safety of rosuvastatin therapy for children with familial hypercholesterolemia. J Am Coll Cardiol. 2010;55(11):1121-1126. doi: 10.1016/j.jacc.2009.10.042.

83. Raal FJ, Pilcher GJ, Illingworth DR, et al. Expanded-dose simvastatin is effective in homozygous familial hypercholesterolaemia. Atherosclerosis. 1997;135(2):249-256.

84. Raal FJ, Pappu AS, Illingworth DR, et al. Inhibition of cholesterol synthesis by atorvastatin in homozygous familial hypercholesterolaemia. Atherosclerosis. 2000;150(2):421-428.

85. Marais AD, Raal FJ, Stein EA, et al. A dose-titration and comparative study of rosuvastatin and

atorvastatin in patients with homozygous familial hypercholesterolaemia. Atherosclerosis. 2008;

197(1):400-406. doi: 10.1016/j.atherosclerosis.2007.06.028.

86. Langslet G, Breazna A, Drogari E. A 3-year study of atorvastatin in children and adolescents with heterozygous familial hypercholesterolemia. J Clin Lipidol. 2016;10(5):1153-1162.e3. doi: 10.1016/j.jacl.2016.05.010.

87. Perez de Isla L, Alonso R, Watts GF, et al. Attainment of LDL-cholesterol treatment goals in patients with familial hypercholesterolemia: 5-year SAFEHEART registry follow-up. J Am Coll Cardiol. 2016;67(11):1278-1285. doi: 10.1016/j.jacc.2016.01.008.

88. Cholestyramine [package insert]. Maple Grove, MN: Upsher-Smith Laboratories, Inc; 2015.

89. Colestid [package insert]. New York, NY: Pfizer, Inc; 2014.

90. Welchol [package insert]. Parsippany, NJ: Daiichi Sankyo, Inc; 2014.

91. Lopid [package insert]. New York, NY: Pfizer, Inc; 2010.

92. Tricor [package insert]. Anngrove, Carrigtwohill Co. Cork, Ireland: Fournier Laboratories Ireland, Limited; 2013.

93. Niaspan [package insert]. North Chicago, IL: AbbVie, Inc; 2015.

94. Zetia [package insert]. Whitehouse Station, NJ: Merck & Co, Inc; 2013.

95. Juxtapid [package insert]. Cambridge, MA: Aegerion Pharmaceuticals, Inc; 2016.

96. Kynamro [package insert]. Cambridge, MA: Genzyme Corporation; 2016.

97. Praluent [package insert]. Bridgewater, NJ: Sanofi-Aventis US, LLC; 2015.

98. Repatha [package insert]. Thousand Oaks, CA: Amgen Inc; 2016.

99. Einarsson K, Ericsson S, Ewerth S, et al. Bile acid sequestrants: mechanisms of action on bile acid and cholesterol metabolism. Eur J Clin Pharmacol. 1991;40(suppl 1):S53-S58.

100. Bays HE, Dujovne CA, McGovern ME, et al. Comparison of once-daily, niacin extended-release/lovastatin with standard doses of atorvastatin and simvastatin (the ADvicor Versus Other Cholesterol-Modulating Agents Trial Evaluation [ADVOCATE]). Am J Cardiol. 2003;91(6):667-672.

101. Davidson MH, Dillon MA, Gordon B, et al. Colesevelam hydrochloride (Cholestagel): a new, potent bile acid sequestrant associated with a low incidence of gastrointestinal side effects. Arch Intern Med. 1999;159(16):1893-1900. doi: 10.1001/archinte.159.16.1893.

102. Knapp HH, Schrott H, Ma P, et al. Efficacy and safety of combination simvastatin and colesevelam in patients with primary hypercholesterolemia. Am J Med. 2001;110(5):352-360.

103. Bays HE, Davidson M, Jones MR, Abby SL. Effects of colesevelam hydrochloride on low-density lipoprotein cholesterol and high-sensitivity C-reactive protein when added to statins in patients with hypercholesterolemia. Am J Cardiol. 2006;97(8):1198-1205. doi: 10.1016/j.amjcard.2005.11.039.

104. Garber AJ, Abrahamson MJ, Barzilay JI, et al. AACE Comprehensive Diabetes Management Algorithm 2013. Endocr Pract. 2013;19(2):327-336.

105. Davidson MH, Toth P, Weiss S, et al. Low-dose combination therapy with colesevelam hydrochloride and lovastatin effectively decreases low-density lipoprotein cholesterol in patients with primary hypercholesterolemia. Clin Cardiol. 2001;24(6):467-474.

106. Hunninghake DB, Mellies MJ, Goldberg AC, et al. Efficacy and safety of pravastatin in patients with primary hypercholesterolemia. II. Once-daily versus twice-daily dosing. Atherosclerosis. 1990;85(2-3):219-227.

107. McKenney J, Jones M, Abby S. Safety and efficacy of colesevelam hydrochloride in combination with fenofibrate for the treatment of mixed hyperlipidemia. Curr Med Res Opin. 2005;21(9):1403-1412. doi: 10.1185/030079905X59157.

108. Davidson MH, Rooney M, Pollock E, Drucker J, Choy Y. Effect of colesevelam and niacin on low-density lipoprotein cholesterol and glycemic control in subjects with dyslipidemia and impaired fasting glucose. J Clin Lipidol. 2013;7(5):423-432. doi: 10.1016/j.jacl.2013.06.001.

109. Bays H, Rhyne J, Abby S, Lai Y-L, Jones M. Lipid-lowering effects of colesevelam HCl in combination with ezetimibe. Curr Med Res Opin. 2006;22(11):2191-2200. doi: 10.1185/030079906X148436.

110. Stein EA, Marais AD, Szamosi T, et al. Colesevelam hydrochloride: efficacy and safety in pediatric subjects with heterozygous familial hypercholesterolemia. J Pediatr. 2010;156(2):231-236.e3. doi: 10.1016/j.jpeds.2009.08.037.

111. Huijgen R, Abbink EJ, Bruckert E, et al. Colesevelam added to combination therapy with a statin and ezetimibe in patients with familial hypercholesterolemia: a 12-week, multicenter, randomized, double-blind, controlled trial. Clin Ther. 2010;32(4):615-625. doi: 10.1016/j.clinthera.2010.04.014.

112. Jialal I, Abby SL, Misir S, Nagendran S. Concomitant reduction in low-density lipoprotein cholesterol and glycated hemoglobin with colesevelam hydrochloride in patients with type 2 diabetes: a pooled analysis. Metab Syndr Relat Disord. 2009;7(3):255-258. doi: 10.1089/met.2009.0007.

113. Moore A, Phan BAP, Challender C, Williamson J, Marcovina S, Zhao XQ. Effects of adding extended-release niacin and colesevelam to statin therapy on lipid levels in subjects with atherosclerotic disease. J Clin Lipidol. 2007;1(6):620-625. doi: 10.1016/j.jacl.2007.09.001.

114. Brown W V, Dujovne CA, Farquhar JW, et al. Effects of fenofibrate on plasma lipids. Double-blind, multicenter study in patients with type IIA or IIB hyperlipidemia. Arteriosclerosis. 1996(6):670-678.

115. Knopp RH, Brown W V, Dujovne CA, et al. Effects of fenofibrate on plasma lipoproteins in hypercholesterolemia and combined hyperlipidemia. Am J Med. 1987;83(5B):50-59.

116. Insua A, Massari F, Rodríguez Moncalvo JJ, Rubén Zanchetta J, Insua AM. Fenofibrate or gemfibrozil for treatment of types IIa and IIb primary hyperlipoproteinemia: a randomized, double-blind, crossover study. Endocr Pract. 2002;8(2):96-101. doi: 10.4158/EP.8.2.96.

117. National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). Third report of the National Cholesterol Education Program (NCEP) Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III) final report. Circulation. 2002;106(25):3143-3421.

118. Farnier M, Ducobu J, Bryniarski L. Long-term safety and efficacy of fenofibrate/pravastatin combination therapy in high risk patients with mixed hyperlipidemia not controlled by pravastatin monotherapy. Curr Med Res Opin. 2011;27(11):2165-2173. doi: 10.1185/03007995.2011.626398.

119. Roth EM, McKenney JM, Kelly MT, et al. Efficacy and safety of rosuvastatin and fenofibric acid combination therapy versus simvastatin monotherapy in patients with hypercholesterolemia and hypertriglyceridemia: a randomized, double-blind study. Am J Cardiovasc Drugs. 2010;10(3):175-186. doi: 10.2165/11533430-000000000-00000.

120. Athyros VG, Papageorgiou AA, Athyrou V V, Demitriadis DS, Pehlivanidis AN, Kontopoulos AG. Atorvastatin versus four statin-fibrate combinations in patients with familial combined hyperlipidaemia. J Cardiovasc Risk. 2002;9(1):33-39.

121. Enger C, Gately R, Ming EE, Niemcryk SJ, Williams L, McAfee AT. Pharmacoepidemiology safety study of fibrate and statin concomitant therapy. Am J Cardiol. 2010;106(11):1594-1601. doi: 10.1016/j.amjcard.2010.07.041.

122. Amend KL, Landon J, Thyagarajan V, Niemcryk S, McAfee A. Incidence of hospitalized rhabdomyolysis with statin and fibrate use in an insured US population. Ann Pharmacother. 2011;45(10):1230-1239. doi: 10.1345/aph.1Q110.

123. Probstfield JL, Hunninghake DB. Nicotinic acid as a lipoprotein-altering agent. Therapy directed by the primary physician. Arch Intern Med. 1994;154(14):1557-1559.

124. Insull W, Basile JN, Vo AN, Jiang P, Thakkar R, Padley RJ. Efficacy and safety of combination therapy with niacin extended-release and simvastatin versus atorvastatin in patients with dyslipidemia: The SUPREME Study. J Clin Lipidol. 2009;3(2):109-118. doi: 10.1016/j.jacl.2009.02.009.

125. Airan-Javia SL, Wolf RL, Wolfe ML, Tadesse M, Mohler E, Reilly MP. Atheroprotective lipoprotein effects of a niacin-simvastatin combination compared to low- and high-dose simvastatin monotherapy. Am Heart J. 2009;157(4):687.e1-687.e8. doi: 10.1016/j.ahj.2009.01.001.

126. Ballantyne CM, Davidson MH, McKenney JM, Keller LH, Bajorunas DR, Karas RH. Comparison of the efficacy and safety of a combination tablet of niacin extended-release and simvastatin with simvastatin 80 mg monotherapy: the SEACOAST II (high-dose) study. J Clin Lipidol. 2008;2(2):79-90. doi: 10.1016/j.jacl.2008.02.004.

127. Chen F, Maccubbin D, Yan L, et al. Lipid-altering efficacy and safety profile of co-administered extended release niacin/laropiprant and simvastatin versus atorvastatin in patients with mixed hyperlipidemia. Int J Cardiol. 2013;167(1):225-231. doi: 10.1016/j.ijcard.2011.12.103.

128. AIM-HIGH Investigators, Boden WE, Probstfield JL, et al. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med. 2011;365(24):2255-2267. doi: 10.1056/NEJMoa1107579.

129. HPS2-THRIVE Collaborative Group, Landray MJ, Haynes R, et al. Effects of extended-release niacin with laropiprant in high-risk patients. N Engl J Med. 2014;371(3):203-212. doi: 10.1056/NEJMoa1300955.

130. Paolini JF, Mitchel YB, Reyes R, et al. Effects of laropiprant on nicotinic acid-induced flushing in patients with dyslipidemia. Am J Cardiol. 2008;101(5):625-630. doi: 10.1016/j.amjcard.2007.10.023.

131. Maccubbin D, Bays HE, Olsson AG, et al. Lipid-modifying efficacy and tolerability of extended-release niacin/laropiprant in patients with primary hypercholesterolaemia or mixed dyslipidaemia. Int J Clin Pract. 2008;62(12):1959-1970. doi: 10.1111/j.1742-1241.2008.01938.x.

132. McKenney J, Ballantyne CM, Feldman TA, et al. LDL-C goal attainment with ezetimibe plus simvastatin coadministration vs atorvastatin or simvastatin monotherapy in patients at high risk of CHD. MedGenMed. 2005;7(3):3.

133. Ballantyne CM, Houri J, Notarbartolo A, et al. Effect of ezetimibe coadministered with atorvastatin in 628 patients with primary hypercholesterolemia: a prospective, randomized, double-blind trial. Circulation. 2003;107(19):2409-2415. doi: 10.1161/01.CIR.0000068312.21969.C8.

134. Ballantyne CM, Abate N, Yuan Z, King TR, Palmisano J. Dose-comparison study of the combination of ezetimibe and simvastatin (Vytorin) versus atorvastatin in patients with hypercholesterolemia: The Vytorin Versus Atorvastatin (VYVA) Study. Am Heart J. 2005;149(3):464-473. doi: 10.1016/j.ahj.2004.11.023.

135. Davidson MH, McGarry T, Bettis R, et al. Ezetimibe coadministered with simvastatin in patients with primary hypercholesterolemia. J Am Coll Cardiol. 2002;40(12):2125-2134.

136. Kerzner B, Corbelli J, Sharp S, et al. Efficacy and safety of ezetimibe coadministered with lovastatin in primary hypercholesterolemia. Am J Cardiol. 2003;91(4):418-424.

137. Goldberg AC, Sapre A, Liu J, Capece R, Mitchel YB; Ezetimibe Study Group. Efficacy and safety of ezetimibe coadministered with simvastatin in patients with primary hypercholesterolemia: a randomized, double-blind, placebo-controlled trial. Mayo Clin Proc. 2004;79(5):620-629. doi: 10.1016/S0025-6196(11)62283-0.

138. Masana L, Mata P, Gagné C, et al. Long-term safety and, tolerability profiles and lipid-modifying efficacy of ezetimibe coadministered with ongoing simvastatin treatment: a multicenter, randomized, double-blind, placebo-controlled, 48-week extension study. Clin Ther. 2005;27(2):174-184. doi: 10.1016/j.clinthera.2005.02.011.

139. Melani L, Mills R, Hassman D, et al. Efficacy and safety of ezetimibe coadministered with

pravastatin in patients with primary hypercholesterolemia: a prospective, randomized, double-blind trial. Eur Heart J. 2003;24(8):717-728.

140. Robinson JG, Ballantyne CM, Grundy SM, et al. Lipid-altering efficacy and safety of ezetimibe/

simvastatin versus atorvastatin in patients with hypercholesterolemia and the metabolic syndrome (from the VYMET study). Am J Cardiol. 2009;103(12):1694-1702. doi: 10.1016/j.amjcard.2009.05.003.

141. Bohula EA, Giugliano RP, Cannon CP, et al. Achievement of dual low-density lipoprotein cholesterol and high-sensitivity C-reactive protein targets more frequent with the addition of ezetimibe to

simvastatin and associated with better outcomes in IMPROVE-IT. Circulation. 2015;132(13):1224-1233. doi: 10.1161/CIRCULATIONAHA.115.018381.

142. Cannon CP, Blazing MA, Giugliano RP, et al. Ezetimibe added to statin therapy after acute coronary syndromes. N Engl J Med. 2015;372(25):2387-2397. doi: 10.1056/NEJMoa1410489.

143. Feldman T, Koren M, Insull W, et al. Treatment of high-risk patients with ezetimibe plus simvastatin co-administration versus simvastatin alone to attain National Cholesterol Education Program Adult Treatment Panel III low-density lipoprotein cholesterol goals. Am J Cardiol. 2004;93(12):1481-1486. doi: 10.1016/j.amjcard.2004.02.059.

144. Gagné C, Gaudet D, Bruckert E; Ezetimibe Study Group. Efficacy and safety of ezetimibe coadministered with atorvastatin or simvastatin in patients with homozygous familial hypercholesterolemia. Circulation. 2002;105(21):2469-2475.

145. Stein E, Stender S, Mata P, et al. Achieving lipoprotein goals in patients at high risk with severe hypercholesterolemia: efficacy and safety of ezetimibe co-administered with atorvastatin. Am Heart J. 2004;148(3):447-455. doi: 10.1016/j.ahj.2004.03.052.

146. van der Graaf A, Cuffie-Jackson C, Vissers MN, et al. Efficacy and safety of coadministration of ezetimibe and simvastatin in adolescents with heterozygous familial hypercholesterolemia. J Am Coll Cardiol. 2008;52(17):1421-1429. doi: 10.1016/j.jacc.2008.09.002.

147. Foody JM, Brown WV, Zieve F, et al. Safety and efficacy of ezetimibe/simvastatin combination versus atorvastatin alone in adults ≥65 years of age with hypercholesterolemia and with or at moderately high/high risk for coronary heart disease (the VYTELD study). Am J Cardiol. 2010;106(9):1255-1263. doi: 10.1016/j.amjcard.2010.06.051.

148. Cuchel M, Meagher EA, du Toit Theron H, et al. Efficacy and safety of a microsomal triglyceride transfer protein inhibitor in patients with homozygous familial hypercholesterolaemia: a single-arm, open-label, phase 3 study. Lancet. 2013;381(9860):40-46. doi: 10.1016/S0140-6736(12)61731-0.

149. Raal FJ, Santos RD, Blom DJ, et al. Mipomersen, an apolipoprotein B synthesis inhibitor, for lowering of LDL cholesterol concentrations in patients with homozygous familial hypercholesterolaemia: a randomised, double-blind, placebo-controlled trial. Lancet. 2010;375(9719):998-1006. doi: 10.1016/S0140-6736(10)60284-X.

150. Akdim F, Stroes ESG, Sijbrands EJG, et al. Efficacy and safety of mipomersen, an antisense inhibitor of apolipoprotein B, in hypercholesterolemic subjects receiving stable statin therapy. J Am Coll Cardiol. 2010;55(15):1611-1618. doi: 10.1016/j.jacc.2009.11.069.

151. McGowan MP, Tardif JC, Ceska R, et al. Randomized, placebo-controlled trial of mipomersen in patients with severe hypercholesterolemia receiving maximally tolerated lipid-lowering therapy. PLoS One. 2012;7(11):e49006. doi: 10.1371/journal.pone.0049006.

152. Stein EA, Dufour R, Gagne C, et al. Apolipoprotein B synthesis inhibition with mipomersen in heterozygous familial hypercholesterolemia: results of a randomized, double-blind, placebo-controlled trial to assess efficacy and safety as add-on therapy in patients with coronary artery disease. Circulation. 2012;126(19):2283-2292. doi: 10.1161/CIRCULATIONAHA.112.104125.

153. Santos RD, Duell PB, East C, et al. Long-term efficacy and safety of mipomersen in patients with familial hypercholesterolaemia: 2-year interim results of an open-label extension. Eur Heart J. 2015;36(9):566-575. doi: 10.1093/eurheartj/eht549.

154. Visser ME, Wagener G, Baker BF, et al. Mipomersen, an apolipoprotein B synthesis inhibitor, lowers low-density lipoprotein cholesterol in high-risk statin-intolerant patients: a randomized, double-blind, placebo-controlled trial. Eur Heart J. 2012;33(9):1142-1149. doi: 10.1093/eurheartj/ehs023.

155. Thomas GS, Cromwell WC, Ali S, Chin W, Flaim JD, Davidson M. Mipomersen, an apolipoprotein B synthesis inhibitor, reduces atherogenic lipoproteins in patients with severe hypercholesterolemia at high cardiovascular risk: a randomized, double-blind, placebo-controlled trial. J Am Coll Cardiol. 2013;62(23):2178-2184. doi: 10.1016/j.jacc.2013.07.081.

156. Ginsberg HN, Rader DJ, Raal FJ, et al. Efficacy and safety of alirocumab in patients with heterozygous familial hypercholesterolemia and LDL-C of 160 mg/dL or higher. Cardiovasc Drugs Ther. 2016;30(5):473-483. doi: 10.1007/s10557-016-6685-y.

157. Moriarty PM, Thompson PD, Cannon CP, et al. Efficacy and safety of alirocumab vs ezetimibe in statin-intolerant patients, with a statin rechallenge arm: The ODYSSEY ALTERNATIVE randomized trial. J Clin Lipidol. 2015;9(6):758-769. doi: 10.1016/j.jacl.2015.08.006.

158. Kastelein JJP, Ginsberg HN, Langslet G, et al. ODYSSEY FH I and FH II: 78 week results with alirocumab treatment in 735 patients with heterozygous familial hypercholesterolaemia. Eur Heart J. 2015;36(43):ehv370. doi: 10.1093/eurheartj/ehv370.

159. Robinson JG, Farnier M, Krempf M, et al. Efficacy and safety of alirocumab in reducing lipids and cardiovascular events. N Engl J Med. 2015;372(16):1489-1499. doi: 10.1056/NEJMoa1501031.

160. Cannon CP, Cariou B, Blom D, et al. Efficacy and safety of alirocumab in high cardiovascular risk patients with inadequately controlled hypercholesterolaemia on maximally tolerated doses of statins: the ODYSSEY COMBO II randomized controlled trial. Eur Heart J. 2015;36(19):1186-1194. doi: 10.1093/eurheartj/ehv028.

161. Kereiakes DJ, Robinson JG, Cannon CP, et al. Efficacy and safety of the proprotein convertase subtilisin/kexin type 9 inhibitor alirocumab among high cardiovascular risk patients on maximally tolerated statin therapy: The ODYSSEY COMBO I study. Am Heart J. 2015;169(6):906-915.e13. doi: 10.1016/j.ahj.2015.03.004.

162. Bays H, Gaudet D, Weiss R, et al. Alirocumab as add-on to atorvastatin versus other lipid treatment strategies: ODYSSEY OPTIONS I Randomized Trial. J Clin Endocrinol Metab. 2015;100(8):3140-3148. doi: 10.1210/jc.2015-1520.

163. Farnier M, Jones P, Severance R, et al. Efficacy and safety of adding alirocumab to rosuvastatin versus adding ezetimibe or doubling the rosuvastatin dose in high cardiovascular-risk patients: The ODYSSEY OPTIONS II randomized trial. Atherosclerosis. 2016;244:138-146. doi: 10.1016/j.atherosclerosis.2015.11.010.

164. Nissen SE, Stroes E, Dent-Acosta RE, et al. Efficacy and tolerability of evolocumab vs ezetimibe in patients with muscle-related statin intolerance: The GAUSS-3 Randomized Clinical Trial. JAMA. 2016;315(15):1580-1590. doi: 10.1001/jama.2016.3608.

165. Raal FJ, Honarpour N, Blom DJ, et al. Inhibition of PCSK9 with evolocumab in homozygous familial hypercholesterolaemia (TESLA Part B): a randomised, double-blind, placebo-controlled trial. Lancet. 2015;385(9965):341-350. doi: 10.1016/S0140-6736(14)61374-X.

166. Raal FJ, Stein EA, Dufour R, et al. PCSK9 inhibition with evolocumab (AMG 145) in heterozygous familial hypercholesterolaemia (RUTHERFORD-2): a randomised, double-blind, placebo-controlled trial. Lancet. 2015;385(9965):331-340. doi: 10.1016/S0140-6736(14)61399-4.

167. Stroes E, Colquhoun D, Sullivan D, et al. Anti-PCSK9 antibody effectively lowers cholesterol in patients with statin intolerance: the GAUSS-2 randomized, placebo-controlled phase 3 clinical trial of evolocumab. J Am Coll Cardiol. 2014;63(23):2541-2548. doi: 10.1016/j.jacc.2014.03.019.

168. Robinson JG, Nedergaard BS, Rogers WJ, et al. Effect of evolocumab or ezetimibe added to moderate- or high-intensity statin therapy on LDL-C lowering in patients with hypercholesterolemia: the LAPLACE-2 randomized clinical trial. JAMA. 2014;311(18):1870-1882. doi: 10.1001/jama.2014.4030.

169. Bibbins-Domingo K, Grossman DC, Curry SJ, et al. Statin use for the primary prevention of cardiovascular disease in adults: US Preventive Services Task Force recommendation statement. JAMA. 2016;316(19):1997. doi: 10.1001/jama.2016.15450.

170. Catapano AL, Graham I, De Backer G, et al. 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias. Eur Heart J. 2016;37(39):2999-3058. doi: 10.1093/eurheartj/ehw272.

171. ACCORD Study Group, Ginsberg HN, Elam MB, et al. Effects of combination lipid therapy in type 2 diabetes mellitus. N Engl J Med. 2010;362(17):1563-1574. doi: 10.1056/NEJMoa1001282.

172. Gidding SS, Champagne MA, de Ferranti SD, et al. The agenda for familial hypercholesterolemia: a scientific statement from the American Heart Association. Circulation. 2015;132(22):2167-2192. doi: 10.1161/CIR.0000000000000297.

# data[].attributes.attachment_link.authors[].name
Samantha Karr, PharmD, FCCP, BCPS, BCACP, BC-ADM

# data[].attributes.attachment_link.title
Epidemiology and Management of Hyperlipidemia

# data[].attributes.attachment_link.description
Cardiovascular disease (CVD) is the leading cause of death among adults in the United States, and people with hyperlipidemia are at roughly twice the risk of developing CVD as compared to those with normal total cholesterol levels.

# data[].attributes.body
TÍTULO: Prevalencia de obesidad e hipercolesterolemia en trabajadores de una institución estatal de Lima - Perú
AÑO: 2002
TIPO DE ESTUDIO: Estudio transversal analítico
RESULTADOS: las prevalencias de obesidad y sobrepeso fueron 17,9% y 46,8%, respectivamente. Se encontró 123 (34,7%) sujetos con hipercolesterolemia. Las proporciones de sujetos con valores anormales de colesterol fueron: para HDL-C 0,0%, LDL-C 29,7%, triglicéridos 19,5%, CT/HDL-C 24,9% y LDL-C/HDL-C 16,7%. El sexo masculino, la edad mayor de 50 años y la condición de sedentario estuvieron asociadas con obesidad (p<0,05). El sexo masculino y la edad mayor de 40 años estuvieron asociadas con valores anormales de lípidos séricos. Los valores de colesterol total, LDL-C, triglicéridos, CT/HDL-C y LDL-C/HDL-C fueron significativamente mayores en los sujetos obesos (p<0,05). El nivel de HDL-C fue mayor en el grupo con peso adecuado (p<0,05).
CONCLUSIÓN: La obesidad e hipercolesterolemia son patologías relevantes en esta población laboral. Se recomienda establecer programas de prevención de factores de riesgo cardiovascular y modificación de estilos de vida en esta población.
http://www.scielo.org.pe/scielo.php?script=sci_arttext&pid=S1726-46342002000200007

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Prevalencia de obesidad e hipercolesterolemia en trabajadores de una institución estatal de Lima - Perú
Ángel Rosas A¹; Giancarlo Lama G²; Fernando Llanos-Zavalaga³; Jorge Dunstan Y².

1 Proyecto VIGIA (MINSA/USAID). Lima – Perú.
2 Departamento de Chequeos Médicos, Centro Médico Medicina Externa S.A. (MEDEX). Lima – Perú.
3 Instituto Nacional de Salud. Lima – Perú.

Objetivo: Determinar la prevalencia de obesidad e hipercolesterolemia en los trabajadores de una institución estatal de Lima - Perú. Materiales y métodos: en este estudio transversal analítico, evaluamos 359 trabajadores, que acudieron a su examen médico anual respectivo entre octubre y diciembre de 2001. A cada sujeto se le determinó peso y talla y se le tomó una muestra de 5 mL de sangre en ayunas. Se definió sobrepeso como índice de masa corporal (IMC)>25 y <30, obesidad como IMC>30 e hipercolesterolemia como colesterol total sérico >200 mg/dL. Resultados: las prevalencias de obesidad y sobrepeso fueron 17,9% y 46,8%, respectivamente. Se encontró 123 (34,7%) sujetos con hipercolesterolemia. Las proporciones de sujetos con valores anormales de colesterol fueron: para HDL-C 0,0%, LDL-C 29,7%, triglicéridos 19,5%, CT/HDL-C 24,9% y LDL-C/HDL-C 16,7%. El sexo masculino, la edad mayor de 50 años y la condición de sedentario estuvieron asociadas con obesidad (p<0,05). El sexo masculino y la edad mayor de 40 años estuvieron asociadas con valores anormales de lípidos séricos. Los valores de colesterol total, LDL-C, triglicéridos, CT/HDL-C y LDL-C/HDL-C fueron significativamente mayores en los sujetos obesos (p<0,05). El nivel de HDL-C fue mayor en el grupo con peso adecuado (p<0,05). Conclusiones: la obesidad e hipercolesterolemia son patologías relevantes en esta población laboral. Se recomienda establecer programas de prevención de factores de riesgo cardiovascular y modificación de estilos de vida en esta población.

Palabras clave: Prevalencia; Obesidad; Hiperlipidemia; Trabajadores; Población urbana (fuente: BIREME).

Objective: To determine the prevalence of obesity and hypercholesterolemia in workers of a government institution in Lima - Perú. Materials and methods: An analytical cross sectional study was performed, evaluating 359 workers who went to their annual medical check-up between October and December 2001. Weight and height were measured in each subject, and a 5 mL fasting blood sample was taken. Being overweight was defined as a body mass index (BMI) >25 and <30, Obesity as a BMI>30, and hypercholesterolemia as total cholesterol (TC) >200 mg/dL. Results: The prevalence of obesity and being overweight was 17,9% and 46,8%, respectively. Hypercholesterolemia was found in 123 (34,7%) subjects. The rates for abnormal cholesterol values were as follows: HDL-C, 0,0%; LDL-C, 29,7%; triglycerides, 19.5%; TC/HDL-C, 24,9%, and LDL-C/HDL-C, 16,7%. Masculine sex, age greater than 50 years and sedentarism were associated with abnormal values for serum lipids. TC, LDL-C, and triglyceride values, as well as TC/HDL- C and LDL-C/HDL-C rates were significantly higher in obese subjects. However, HDL-C values were higher in the group of subjects with an adequate weight. Conclusion: Obesity and hypercholesterolemia were relevant conditions in this working population. We recommend to establish programs for the cardiovascular risk factors prevention and changes in life style in this population.

Key words: Prevalencia; Obesity; Hyperlipidemia; Workers; Urban population (source: BIREME).

En la última década se han producido importantes cambios en los perfiles de mortalidad y morbilidad de nuestro país ¹. La tasa de mortalidad por enfermedades crónicas no transmisibles en el Perú está superando a la tasa de mortalidad por enfermedades transmisibles, constituyéndose como causas principales de muerte y morbilidad en población adulta y adulta mayor enfermedades tales como: la enfermedad coronaria, el accidente cerebrovascular (ACV), la hipertensión arterial (HTA), las neoplasias malignas y la diabetes mellitus (DM) 2,3 .

Diversos estudios han demostrado que la DM, la intolerancia a la glucosa, la HTA, el tabaquismo, la obesidad y la hipercolesterolemia son factores de riesgo para enfermedad coronaria y ACV en población adulta ⁴⁻¹¹. La acción conjunta o individualizada de estos factores de riesgo ha llevado a que la morbimortalidad, debida a patología cardiovascular haya alcanzado niveles de pandemia.

La obesidad y el sobrepeso son condiciones de salud que han presentado un aumento progresivo en las últimas tres décadas, tanto en países desarrollados como en los países en desarrollo 12,13, aplicándose a dicho fenómeno la denominación de "epidemia". La obesidad se convirtió en el primer caso de enfermedad crónica no transmisible (ECNT), a la cual la Organización Mundial de la Salud (OMS) y la Organización Panamericana de la Salud (OPS) ¹⁴ prestan gran atención a su evolución por su alta prevalencia, por las enfermedades crónicas asociadas a ésta, además de los altos costos que implica su tratamiento. Posteriormente, se agregó la vigilancia por la OMS y OPS de otras ECNT, tales como DM tipo 2, ciertas dislipidemias, HTA y aterosclerosis.

El informe de la OPS sobre la calidad de los datos de salud ocupacional en América Latina y el Caribe ¹⁵, señaló que existe ausencia de datos confiables y sistematizados sobre la situación de salud de los trabajadores; constituyéndose un problema de gran magnitud por la significativa pérdida económica y social que constituyen los accidentes, y las enfermedades crónicas y de origen ocupacional. La falta de información adecuada y completa impide que las autoridades de salud y los empresarios tomen decisiones, y que los trabajadores y la opinión pública se movilicen para mejorar las condiciones de trabajo o soliciten programas promocionales y preventivos que reduzcan los riesgos de desarrollar enfermedades.

Una parte considerable de la población adulta en nuestro país es población laboral, siendo en esta población donde resultan interesantes e importantes las intervenciones preventivas. Por tanto, el ámbito de la medicina laboral representa un lugar privilegiado para la realización de ensayos de prevención primaria de enfermedades cardiovasculares. Otros espacios para prevención primaria serían la población infantil y adolescente.

Nuestra investigación tuvo por objetivo determinar las prevalencias de obesidad e hipercolesterolemia en una población laboral de una institución estatal de Lima. El conocimiento de la prevalencia de estos factores de riesgo para enfermedades cardiovasculares servirá de base para la implementación de estrategias eficaces de prevención orientadas a cambios en el estilo de vida y control de estos factores de riesgo en dicha población.

En el presente estudio de tipo transversal analítico, se incluyeron todos los trabajadores de la sede central de una institución estatal de Lima – Perú, que asistieron a su examen médico respectivo, durante los meses de octubre a diciembre de 2001. En esta sede central, los trabajadores realizan actividades administrativas del sector público, de lunes a viernes con horarios de trabajo de 8 a.m. a 5 p.m. Este trabajo no demanda mucha actividad física, realizándose la mayor parte de las actividades en posición sentada. Fueron excluidos aquellos trabajadores que no deseaban participar en el estudio y aquellos que recibían algún tratamiento farmacológico, tanto para obesidad como para dislipidemia.

El peso fue medido en kilogramos, sin zapatos y con la ropa que portaban (ligera), a través de balanzas de pie previamente calibradas con una precisión de ±0,5 Kg. La talla fue medida en metros, estando el trabajador descalzo y en posición supina utilizando un tallímetro también calibrado con una precisión de ±0,3 cm. Ambas mediciones fueron realizadas por personal capacitado y estandarizado para evitar el sesgo de observación y registradas en una ficha de recolección de datos previamente validada que incluía además datos sobre edad, sexo, sedentarismo y resultados de la prueba de colesterol sérico total y fraccionado.

Se calculó el índice de masa corporal (IMC) en cada trabajador, índice antropométrico que relaciona el peso en kilogramos sobre la talla al cuadrado en metros (P/T2). Las definiciones de obesidad y sobrepeso fueron hechas siguiendo los criterios de Bray ¹⁶ y de la OMS ¹⁷ : sobrepeso (IMC de 25,0 a 29,9), obesidad leve (IMC de 30,0 a 34,9), obesidad moderada (IMC de 35,0 a 39,9) y obesidad severa (IMC>40,0). Se consideró además como bajo peso un IMC<19. Se definió sedentarismo como "la no práctica de ejercicio alguno por un tiempo mayor o igual a 30 minutos al día por lo menos una vez por semana". En esta definición se incluyó las caminatas que podrían realizar los trabajadores en sus desplazamientos hacia su centro de trabajo y viceversa.

Luego de la medición antropométrica se procedió a la toma de una muestra de 5 mL de sangre venosa del brazo izquierdo de cada participante en un tubo al vacío, en condiciones adecuadas de asepsia y antisepsia. La muestra fue transportada al laboratorio, siendo procesada el mismo día. Se utilizó una solución de vainillina al 9,02 mmol/L en ácido fosfórico, que reaccionó con una solución de ácido sulfúrico. La muestra fue leída en un espectrofotómetro a 530 nm (Kit de Wiener Lab, Argentina). Se consideraron como valores anormales 18: colesterol total >200 mg/dL, HDL-C<35 mg/dL, LDL-C>130 mg/dL y triglicéridos>200 mg/dL. Además, se consideró anormales los índices CT/HDL-C>5,0 y LDL-C/HDL-C>3,5. Las consideraciones éticas estuvieron circunscritas al anonimato y confidencialidad de las respuestas.

Los datos fueron ingresados en una base previamente diseñada, usando para su procesamiento y análisis el paquete estadístico SPSS 9,0 para Windows. Los resultados fueron expresados en frecuencias relativas y absolutas. En el análisis estadístico de las variables cuantitativas se utilizó pruebas paramétricas y no paramétricas según correspondía, previo test de normalidad (Kolmogorov-Smirnov). Para el análisis de variables cualitativas se utilizó la prueba de Chi-cuadrado. Aquellas variables que resultaron significativas (p<0,05) fueron ingresadas a un análisis multivariado de regresión logística a fin de identificar las variables que se encontraban independientemente asociadas a obesidad y a las anormalidades lipídicas específicas, e identificar las variables de confusión.

Se incluyeron 359 (90,6%) trabajadores de un total de 396 con que cuenta la institución estatal con sede en Lima: 177 (49,3%) varones y 182 (50,7%) mujeres. La edad promedio de los trabajadores fue 42,5±7,8 años, siendo 34,6% menores de 40 años, 47,8% entre 40 y 50 años y 17,6% mayores de 50 años. Más del 50% de los trabajadores fueron sedentarios.

El promedio encontrado de IMC fue 26,2±4,0 kg/m2 y la evaluación del estado nutricional según este indicador señaló: 123 (34,5%) trabajadores con peso adecuado, 167 (46,8%) con sobrepeso y 64 (17,9%) con obesidad. Además, 2 trabajadores (0,8%) tuvieron bajo peso ( Tabla Nº 1).

Tabla Nº 1. Características generales de la población estudiada

Los valores promedios para lípidos séricos y los porcentajes de valores lipídicos anormales en la población laboral estudiada se muestran en la Tabla Nº 2. Se encontró valores anormales para colesterol total en 123 (34,7%) sujetos (10,5% con un CT mayor de 240 mg/dL), LDL-C en 105 (29,7%), triglicéridos en 69 (19,5%), relación CT/ HDL-C en 88 (24,9%) y relación LDL-C/HDL-C en 59 (16,7%).

Tabla Nº 2. Lípidos séricos en la población estudiada.

Los trabajadores del sexo masculino presentaron mayores porcentajes de sobrepeso y obesidad que aquellos del sexo femenino (p<0,001) ( Tabla Nº 3). Se observó un incremento de los porcentajes de obesidad y sobrepeso con la edad, siendo el grupo mayor de 50 años el de mayor porcentaje de trabajadores con sobrepeso y obesidad (p=0,004). Se encontró asociación significativa entre el sedentarismo y el porcentaje de trabajadores con obesidad (p=0,016).

Tabla Nº 3. Índice de masa corporal según sexo, edad y sedentarismo.

En la Tabla Nº 4, se observa el porcentaje de valores anormales de lípidos séricos según sexo y edad. Los trabajadores varones presentaron más anormalidades que las mujeres en los siguientes lípidos séricos y relaciones lipídicas: colesterol total (p=0,006), triglicéridos (p<0,001), relación CT/HDL-C (p<0,001) y relación LDL-C/HDL-C (p<0,001). El grupo etáreo de 40 a 50 años presentó los más altos porcentajes de anormalidades en el colesterol total (p<0,001), LDL-C (p=0,001), relación CT/HDL-C (p=0,004) y relación LDL- C/HDL-C (p<0,012). Los trabajadores mayores de 50 años presentaron los porcentajes más altos de triglicéridos anormales (p<0,001). No se encontró asociación entre la anormalidad de alguno de los lípidos o relación lipídica y la condición de sedentarismo.

Tabla Nº 4. Porcentaje (%) de valores anormales de lípidos séricos según sexo y edad

Se observó una tendencia creciente de las medias de los valores séricos del colesterol total (p<0,001), triglicéridos (p<0,001), relación CT/HDL-C (p<0,001) y relación LDL-C/ HDL-C (p=0,007), conforme aumentaba el IMC; siendo estos valores lipídicos mayores en el grupo de trabajadores catalogados como obesos ( Tabla Nº 5). En cambio, el HDL-C mostró una tendencia inversa al aumento del IMC, con valores más altos dentro del grupo con peso adecuado (p<0,001).

Tabla Nº 5. Valores de lípidos séricos según IMC.

En la Tabla Nº 6, se muestran los resultados del análisis de regresión logística. El sexo masculino en el trabajador estuvo independientemente asociado a la obesidad y los valores anormales de colesterol total, triglicéridos, relación CT/HDL-C y relación LDL-C/HDL-C. La edad de 40 a 50 años estuvo independientemente asociada al LDL-C y a triglicéridos anormales. La edad mayor de 50 años también estuvo asociada a valores de triglicéridos anormales.

Tabla Nº 6. Resultados del análisis de regresión logística

En el presente estudio, usando las definiciones propuestas por la OMS según IMC ¹⁷, encontramos prevalencias de sobrepeso y obesidad en los trabajadores de la sede central de una institución estatal de Lima de 46,8% y 17,9%, respectivamente. Dichas prevalencias son similares a las encontradas por Zubiate ¹⁹, quien encontró 51,5% de sobrepeso y 17,6% de obesidad en una muestra de aproximadamente 4800 trabajadores de distintos centros laborales en Lima, señalando que dichas prevalencias son más elevadas en la Costa y Lima que en la Sierra y Selva. Seclén, por su parte, en un estudio usando muestreo aleatorio de viviendas unifamiliares por métodos multietápicos y por conglomerados, encontró altas prevalencias de obesidad en una población urbana de Piura (36,71%), con cifras algo menores, pero igualmente importantes, en Lima (22,8%), Tarapoto (18,3%) y Huaraz (17,0%). Lamentablemente estos resultados en la población son sobredimensionados, ya que en este estudio se definió obesidad como IMC>2720. Los estudios realizados en población general, en América Latina durante la última década, indican que la prevalencia de obesidad (IMC>30) en población adulta fluctúa entre 4,8% y 48,1% 21,22 mientras que en Europa, esta prevalencia fluctúa entre 7,4% y 16,1% 23-25 .

Las prevalencias de sobrepeso y obesidad fueron significativamente mayores en los varones (59,1% y 21,6%, respectivamente) respecto a las mujeres (35,4% y 14,6%, respectivamente). La literatura señala resultados variables para la asociación obesidad y género. En México, la prevalencia de obesidad, es a predominio femenino, al igual que en Brasil, Chile, Costa Rica, y Trinidad y Tobago 21,22,26. Por otro lado, estudios realizados en Canadá y Estados Unidos ²⁷ muestran mayor prevalencia de obesidad (IMC>30) en hombres. El estudio realizado por Camacho ²⁸ en Perú, en pacientes hipertensos, también muestra un leve predominio masculino (51,1%). Contrariamente, los estudios de Pajuelo ²⁹ y Zubiate (población laboral) ¹⁹ , y últimamente el de Seclén ²⁰, encontraron que la prevalencia de obesidad fue a predominio de mujeres en Lima, Costa y Sierra, mientras que en la Selva fue a predominio masculino.

Además de la diferencia según sexo, el análisis bivariado también mostró elevadas prevalencias de sobrepeso y obesidad en los grupos de mayor edad, y en aquellos trabajadores que no practicaban algún tipo de actividad física. El análisis multivariado sólo con estas variables, confirmó al sexo masculino y al sedentarismo, como predictores de obesidad en los trabajadores, siendo la edad una variable confusora. Se debe resaltar la importancia de una intervención preventiva de enfermedades cardiovasculares en esta subpoblación, sobre todo al considerar que el sexo masculino, el sedentarismo y la obesidad han sido considerados como factores de riesgo para el desarrollo de enfermedades cardiovasculares, sobre todo del tipo coronario ³⁰.

La prevalencia de hipercolesterolemia (colesterol sérico > 200 mg/dL) de nuestra población laboral fue 34,7%. Pocos estudios, en nuestro país, han reportado la prevalencia de esta patología en población general y menos aún en población laboral. Seclén estudió este factor de riesgo para enfermedades cardiovasculares en ciudades de Lima, Costa, Sierra y Selva ²⁰; encontrando específicamente para una población limeña una prevalencia de 22,7% de hipercolesterolemia, aunque definiendo ésta como un colesterol total sérico (CT) con valor superior a 240 mg/dL. Los trabajadores con un CT mayor de 240 mg/dL en nuestro estudio sólo alcanzaron 10,5%.

La prevalencia de anormalidades de los otros valores de lípidos séricos fue: HDL (0,0%), LDL-C (29,7%) y triglicéridos (19,5%). La ausencia de anormalidad en el HDL-C, factor protector de enfermedad coronaria ³¹, debe tener en cuenta la variabilidad de esta medición y la variabilidad individual: un tercio de las mediciones de HDL-C varían en más del 10% del valor referencial, y la variación individual es mayor al 20%; por lo que una única muestra es inadecuada para categorizar al sujeto, recomendándose como mínimo dos muestras ³². En relación al LDL-C, debemos mencionar que la literatura señala que sus niveles séricos se hallan relacionados a procesos aterogénicos, correlacionando positivamente con el porcentaje de la superficie de los vasos comprometidos ³³. En nuestro estudio existe una proporción considerable de la población con este factor de riesgo para enfermedad coronaria 34,35 .

Usando las relaciones entre los valores lipídicos CT/HDL-C y LDL-C/HDL-C, propuestas como factores predictores de riesgo cardiovascular en varios estudios ³⁶⁻³⁸ , tenemos que 24,9% (CT/HDL-C>5,0) y 16,7% (LDL-C/HDL-C>3,5) trabajadores se encontrarían en riesgo de algún problema coronario.

El análisis bivariado encontró que los trabajadores varones también mostraron una mayor prevalencia de valores anormales en todos los lípidos séricos respecto a las mujeres (p<0,05), con excepción del LDL-C que no alcanzó la significancia estadística. El grupo etáreo de 40 a 50 años también mostró una mayor prevalencia de valores anormales, con excepción de los triglicéridos en donde la mayor prevalencia fue en los mayores de 50 años. No se encontró diferencias en los valores lipídicos entre los trabajadores con y sin sedentarismo. El análisis multivariado (Tabla Nº 6) señaló al sexo masculino como único factor predictor de hipercolesterolemia, siendo la edad sólo una variable confusora en este grupo laboral.

También encontramos que los valores lipídicos séricos (a excepción del HDL-C) se incrementaban conforme aumentaba el IMC de los trabajadores, observándose los más altos promedios en aquellos trabajadores con obesidad y sobrepeso. El HDL-C, en cambio, tuvo un comportamiento inverso encontrándose los más bajos promedios también en los trabajadores con obesidad y sobrepeso. Respecto a estos hallazgos debemos señalar que tanto el sobrepeso como la obesidad han sido relacionados con un incremento de riesgo de un gran número de patologías, entre ellas la dislipidemia ³⁹. La presencia de obesidad exacerba anormalidades metabólicas como la reducción de HDL y aumento de LDL y triglicéridos9.

Nuestra investigación resalta a la obesidad e hipercolesterolemia, como patologías prevalentes en esta población laboral. El conocimiento de la prevalencia de estos factores de riesgo para enfermedades cardiovasculares debe servir de base para la implementación de estrategias y programas eficaces de prevención y control (al interior de las instituciones o centros de trabajo) orientados a cambios en el estilo de vida y control de éstos y otros factores de riesgo cardiovascular en dicha población laboral.

1. Ministerio de Salud. Análisis de la situación de salud del Perú - 2001. 1a. ed. Lima: OGE/MINSA; 2002. [ Links ]

2. Annual Statistic Sanitary Mondiale 1992. Causes of death by sex and age - Peru 1989. Washington: World Bank; 1992. [ Links ]

3. Informe sobre el desarrollo mundial 1993. Invertir en salud, indicadores del desarrollo mundial. Oxford: Oxford University Press; 1993. [ Links ]

4. Kannel WB, Cordon T. Cardiovascular risk factors in the aged: the Framingham Study. In: Haynes SG, Feinicib M. Second conference on the epidemiology of aging. Bethesda: National Institutes of Health; 1980. [ Links ]

5. Kannel WB. Risk factors in hypertension. J Cardiovasc Pharmacol 1989;13 (Supll 1): S4. [ Links ]

6. Kannel WB. Factores de riesgo de coronariopatía: actualización del estudio de Framingham. Hospital Practice 1991; 6(1): 54-62. [ Links ]

7. Garfinkel L. Overweight and cancer. Health Implications of Obesity. National Institutes of Health Consensus Development Conference. Ann Intern Med 1985; 103: 989-94. [ Links ]

8. World Health Organization. Physical status: The use and interpretation of anthropometry: Report of a WHO Expert Committee. Geneva: WHO; 1995. Technical Report Series N°854. [ Links ]

9. Maggio CA, Pi-Sunyer X. The prevention and treatment of obesity. Diabetes Care 1997; 20: 1744-71. [ Links ]

10. Must A, Spadano J, Coakley E, Field E, Colditz G, Diezt W. The disease burden associated with overweight and besity. JAMA 1999; 282: 1523-9. [ Links ]

11. Rose G, Hamilton PS, Keen H. Reid DD, McCartney P, Jarrett RJ. Myocardial ischemia, risk factors and death from coronary heart disease. Lancet 1977; 1: 105. [ Links ]

12. National Center for Health Statistics. National Health Examination Survey I (1960-62). Hyattsville: NCHS/CDC; 1963. [ Links ]

13. Campos H, Mata L, Siles X, Vives M, Ordovas J.M, Schaefer EJ. Prevalence of cardiovascular risk factors in rural and urban Costa Rica. Circulation 1992; 85: 648-58. [ Links ]

14. Wilding J. Obesity treatment. BMJ 1997; 315: 997-1000. [ Links ]

15. Organización Panamericana de la Salud. Calidad de los datos de salud ocupacional en América Latina y el Caribe. Rev Panam Salud Pública 1999; 5(1): 66-7. [ Links ]

16. Bray GA. Clasificación y valoración de las obesidades. Clin Med North Am 1989; 73: 1-15. [ Links ]

17. Metropolitan Life Insurance Company. New weight standard for men and women. Stat Bull Metropol Life Insur Co1983; 64: 2. [ Links ]

18. Expert Panel. Summary of the Second Report of the National Cholesterol Education Program (NCEP). Expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel II). JAMA 1993; 259: 3015-23. [ Links ]

19. Zubiate, M. Diabetes mellitus: etnia, geografía y hábitos de vida. Estudios en la altura. En: I Reunión Científica Conjunta GLED/ EDEG; 5-8 Abril 1999; Buenos Aires, Argentina; 1999. [ Links ]

20. Seclén S, Leey J, Villena A, Herrera B, Menacho C, et al. Prevalencia de obesidad, diabetes mellitus, hipertensión arterial e hipercolesterolemia como factores de riesgo coronario y cerebro vascular en población adulta de la costa, sierra y selva del Perú. Acta Médica Peruana 1999; 17: 8-13. [ Links ]

21. Monteiro CA, Mandini L, Medenus de Souza AL, Popkin BM. The Nutrition Transition in Brazil. Euro J Clin Nutr 1995; 49: 105- 13. [ Links ]

22. Átala E. Análisis de la situación nutricional de la población de Santiago. Rev Med Chile 1993; 121: 819-26. [ Links ]

23. Popkin BM, Drewnowki A. Dietary fats and the nutrition transition: news trends in the global diet. Nutr Rev 1997; 55: 31-43. [ Links ]

24. Ashell J. Mobility in men and women. Int J Obes 1994;18(Suppl 1): S1. [ Links ]

25. Pagano R, La Vecchia D. Overweight and obesity in Italy 1990-1991. Int J Obes 1995; 8: 665. [ Links ]

26. Ministerio de Salud. Encuesta Nacional de Nutrición y Antropometría -1996. San José-Costa Rica: MINSA; 1996. [ Links ]

27. National Center for Health Statistics. Second National Health and Nutrition Examination Survey (1976-1980). Hyattsville:NCHS /CDC; 1981. [ Links ]

28. Camacho L, Uribe L, Narro M. Prevalencia de obesidad en pacientes hipertensos. Boletín de la Sociedad Peruana de Medicina Interna 2000; 13: 101-4. [ Links ]

29. Pajuelo J. La obesidad en el Perú. Lima: Ed. Nueva perspectiva; 1997. [ Links ]

30. Hennekens Ch. Increasing burden of cardiovascular disease: Current knowledge and future directions for research on risk factors. Circulation 1998; 97: 1095. [ Links ]

31. Gordon T, Castelli WP, Hjortland MC. High density lipoprotein as a protective factor against coronary heart disease: The Framingham Study. Am J Med 1977; 62: 707-14. [ Links ]

32. Barter PJ, Rye KA. High-density lipoproteins and coronary hearth disease. J Cardiovasc Risk 1994; 1: 217-21. [ Links ]

33. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the third report of the National Cholesterol Education Program (NCEP) Expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III). JAMA 2001; 285: 2486-97. [ Links ]

34. Jones MB, Gofman JW, Lindgren FT, Lyon TP, Graham DB. Lipoproteins in atherosclerosis and related condition. Am J Med 1951; 11: 358-80. [ Links ]

35. Barr DP, Russ EM, Eder HA. Protein lipid relationship in human plasma in atherosclerosis and related condition. Am J Med 1951; 11: 480-93. [ Links ]

36. Brolons C, Ribera A, Perkih RM. Worldwide distribution of blood lipids and lipoproteins in child and adolescents: a review study. Atherosclerosis 1998; 139: 1-9. [ Links ]

37. Castelli WP, Garrison RJ, Wilson PW, Abbott RD, Kalousdian S, Kannel WB. Incidence of coronary heart disease and lipoprotein cholesterol level: The Framingham Study. JAMA 1986; 256: 2835-8. [ Links ]

38. Grover S, Palmer C, Caupal L. Serum lipid screening to iden tify high-risk individuals for coronary death. Arch Intern Med 2000; 154: 679-84. [ Links ]

39. Kuczmarski RJ, Flegal KM, Campbell SM. Increasing of overweight among US adults: The National Health and Nutrition Examination Surveys, 1960 to 1991. JAMA 1994; 72: 205. [ Links ]

Correspondencia: Ángel Martín Rosas Aguirre. Dirección: Av. Williams 130. Calera de la Merced, Surquillo. Lima – Perú. Teléfono: (0511) 7347904.
E-mail: arosas@ins.gob.pe

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Prevalencia de obesidad e hipercolesterolemia en trabajadores de una institución estatal de Lima - Perú

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Citado por SciELO Similares en SciELO Prevalencia de obesidad e hipercolesterolemia en trabajadores de una institución estatal de Lima - Perú Ángel Rosas A1; Giancarlo Lama G2; Fernando Llanos-Zavalaga3; Jorge Dunstan Y2. 1 Proyecto VIGIA (MINSA/USAID). Lima - Perú. 2 Departamento de Chequeos Médicos, Centro Médico Medicina Externa S.A. (MEDEX).

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TITULO DE ESTUDIO:  Asociación entre la participación en programas de asistencia alimentaria y patrones del perfil lipídico en Perú.
Autor:  Jacqueline Paredes-Aramburú, Antonio Bernabé-Ortiz.
Año de publicación: 2018

Epidemiología:
La dislipidemia es considerada un factor de riesgo para la salud cardiovascular. A nivel global, la Organización Mundial de la Salud reportó que la prevalencia de hipercolesterolemia es de 39% en personas mayores de 25 años de edad. Por ejemplo, la región europea presenta un 54% de hipercolesterolemia en ambos sexos, mientras que las regiones del sureste de Asia y África reportan cifras de 29% y 22%, respectivamente . Asimismo, los resultados de una encuesta aplicada en 8 países mostraron que el 9% de individuos en Tailandia y 53% en Estados Unidos de América son personas con diagnóstico de hipercolesterolemia . Sin tratamiento, las dislipidemias son un pilar para desarrollar enfermedades crónicas no transmisibles. En el caso del Perú, la prevalencia de hipercolesterolemia se presenta casi en la quinta parte (19,6%) de la población peruana mayor de 20 años; mientras que altos niveles de triglicéridos y LDL afectan aproximadamente al 15% y 13% respectivamente.
https://scielo.conicyt.cl/pdf/rchnut/v45n2/0716-1549-rchnut-45-02-0135.pdf

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TITULO: Hipercolesterolemia en el adulto mayor
TIPO DE ESTUDIO: Articulo de Revisión
AÑO: 2020
RESULTADOS: La Organización Mundial de la Salud (OMS) estimó que la hipercolesterolemia está asociada a la enfermedad coronaria, representado por más de 4 millones de muertes por año. La decisión clínica para el control de los factores de riesgo de enfermedad cardiovascular en ancianos contempla no solo la edad, sino también la esperanza de vida y la capacidad funcional.
Más del 80 % de los individuos que mueren por enfermedad arterial coronaria son mayores de 65 años, situación relacionada con el envejecimiento poblacional. El hábito de fumar, la hipertensión arterial, la dislipidemia y la diabetes mellitus son los principales factores de riesgo por grupos etarios. Sin embargo, el riesgo incrementa a medida que avanza la edad
CONCLUSIONES: La hipercolesterolemia constituye un factor de riesgo modificable, por tanto, se recomienda establecer estrategias de prevención que modifiquen de manera positiva el estilo de vida del adulto mayor. Además, la utilización de estatinas debe ser en dosis de baja a moderada intensidad, considerando las interacciones farmacológicas y efectos adversos, presencia de comorbilidades y expectativa de vida.

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PREVALENCIA DE SOBREPESO, OBESIDAD Y DISLIPIDEMIA EN TRABAJADORES DE SALUD DEL NIVEL PRIMARIO
Tipo de estudio:  Estudio observacional y transversal.
Año: 2017
Objetivo:  El objetivo de este estudio es determinar la prevalencia de sobrepeso, obesidad y dislipidemia en trabajadores de la salud
Resultados:
La prevalencia global de dislipidemia fue de 87,7% (143/163) (IC 95%: 82,4; 93,1), la hipercolesterolemia fue de 30,1 % (IC 95%: 22,5; 37,4), la hipertrigliceridemia de 40,5% (IC 95%: 32,6; 48,3), el HDL bajo de 69,3 % (IC 95%: 61,9; 76,7) y el LDL elevado 55,2% (IC 95%: 42,3; 63,1), sin significancia estadística.
Conclusiones:
Se concluyó que la prevalencia de dislipidemia global fue alta y más de la mitad de los trabajadores de la salud presentaron sobrepeso u obesidad, así como la tercera parte tuvieron obesidad abdominal.

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https://docs.bvsalud.org/biblioref/2019/06/999307/estudio-descriptivo-prevalencia-de-dislipidemia-en-adultos-de-4_zCrAn1d.pdf
Estudio Descriptivo: Prevalencia de Dislipidemia en Adultos de 40 - 64 Años, Cuenca - Ecuador, Enero a Julio 2014
Objetivo:  Determinar la prevalencia de dislipidemia en adultos del área urbana del cantón Cuenca.
Tipo de estudio:  Estudio descriptivo transversal
Año: 2014
Resultados: El promedio de edad fue 51 años, de los cuales el 71.9% fueron mujeres. La prevalencia de hipercolesterolemia fue 38.5%; en relación al sexo existió predominio en las mujeres con 34.4%, en los hombres el 28.7%. La prevalencia de hipertrigliceridemia fue de 58.5%.
Conclusiones:  Los resultados de este estudio permiten tener una visión real y actualizada de la prevalencia de este padecimiento a nivel local, lo que posibilitará plantear acciones de promoción de estilos de vida saludables priorizando la importancia del ejercicio y una alimentación saludable, así como actividades de prevención a fin de evitarla aparición de complicaciones.

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Título:

Prevalencia de colesterol alto autoinformada en la población brasileña: análisis de la Encuesta Nacional de Salud de 2013.

Tipo de estudio: Estudio descriptivo.
Año: 2017

Objetivos: Evaluar la prevalencia del diagnóstico médico autonotificado de colesterol alto en la población adulta brasileña mediante el uso de los datos de la Encuesta Nacional de Salud de 2013.

Resultados: La prevalencia del diagnóstico médico de colesterol alto fue del 12,5% (9,7% en hombres y 15,1% en mujeres), y las mujeres tenían un 60% más de probabilidad de un diagnóstico de colesterol alto que los hombres. La frecuencia del diagnóstico médico de colesterol alto aumentó hasta los 59 años, siendo mayor en individuos de raza blanca o de ascendencia asiática, en aquellos con mayor nivel educativo y en residentes de las regiones Sur y Sureste.

Conclusiones:  Se concluye en una muestra representativa de la población de Brasil que este estudio mostró que el 10% de los hombres y el 15% de las mujeres tenían diagnóstico médico de colesterol alto.

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Paulo A. Lotufo, 1, ² Raul D. Santos, 1, 2, ³ Andrei C. Sposito, ⁴ Marcelo Bertolami, ⁵ Jose Rocha-Faria Neto, ⁶ M. Cristina Izar, ⁷ Celia Szwarcwald, ⁸ Rogério R. Prado, ⁹ Sheila R. Stoppa, ⁹ Deborah C. Malta, 9, ¹⁰ and Isabela M. Bensenor 1, ²

Abstract

Background

Data on the prevalence of dyslipidemia in Brazil are scarce, with surveys available only for some towns.

Objective

To evaluate the prevalence of the self-reported medical diagnosis of high cholesterol in the Brazilian adult population by use of the 2013 National Health Survey data.

Methods

Descriptive study assessing the 2013 National Health Survey data, a household-based epidemiological survey with a nationally representative sample and self-reported information. The sample consisted of 60,202 individuals who reported a medical diagnosis of dyslipidemia. The point prevalence and 95% confidence interval (95%CI) for the medical diagnosis of high cholesterol/triglyceride by gender, age, race/ethnicity, geographic region and educational level were calculated. Adjusted odds ratio was calculated.

Results

Of the 60,202 participants, 14.3% (95%CI=13.7-14.8) never had their cholesterol or triglyceride levels tested, but a higher frequency of women, white individuals, elderly and those with higher educational level had their cholesterol levels tested within the last year. The prevalence of the medical diagnosis of high cholesterol was 12.5% (9.7% in men and 15.1% in women), and women had 60% higher probability of a diagnosis of high cholesterol than men. The frequency of the medical diagnosis of high cholesterol increased up to the age of 59 years, being higher in white individuals or those of Asian heritage, in those with higher educational level and in residents of the Southern and Southeastern regions.

Conclusion

The importance of dyslipidemia awareness in the present Brazilian epidemiological context must be emphasized to guide actions to control and prevent coronary heart disease, the leading cause of death in Brazil and worldwide.

Keywords: Cholesterol, Dyslipidemias, Epidemiology, Coronary Artery Disease, Prevalence, Health Survey

Introduction

Coronary artery disease or ischemic heart disease is one of the major causes of morbidity and mortality worldwide.1 At the beginning of the 1960s, long-term observation studies, mainly the Framingham Heart Study, reported that high cholesterol levels doubled the risk for myocardial infarction.2 Detailing the cholesterol fractions has allowed identifying low-density lipoprotein cholesterol (LDL-C) as the determinant of the atherogenic process, with a strong and constant association with cardiovascular events.3

A meta-analysis with over 170,000 individuals randomized to receive placebo or statins or low versus high doses of those drugs has shown that, for every 40-mg/dL reduction in LDL-C, there was a relative drop of 10%, 20%, 27%, 21% and 25% in all-cause mortality, mortality due to cardiovascular disease, myocardial infarction, ischemic stroke and myocardial revascularization, respectively. There was no beneficial difference regarding the previous presence of cardiovascular disease; however, the absolute benefit was proportional to the previous risk of cardiovascular events, being twice higher in secondary prevention.4

Despite the importance of the relation "cholesterol - coronary disease" and the evidence that justifies the control of cholesterol levels at the population level, population surveys conducted in several countries have revealed relatively low rates of diagnosis, knowledge, treatment and control of high cholesterol levels.5

The 2013 Brazilian National Health Survey (PNS) is a unique opportunity to estimate the population prevalence of self-reported dyslipidemia in adults (18 years or older), a representative sample of Brazil, its large geographic regions and federated units, urban and rural areas and self-reported educational level and race/ethnicity.

Methods

Sample

Descriptive study using 2013 PNS data. The PNS is an epidemiological survey based on households, a representative sample of Brazil, its large regions and federated units, capitals and metropolitan regions. Further information on the PNS can be found in other publications.6-7

The minimum sample size was 1,800 households per federated unit, with an initial total sample of 81,767 households planned. In addition, the sample was defined based on the level of accuracy desired for estimation of indicators of interest (proportions of individuals at certain categories). After data collection, registries of the interviews of 64,348 households were obtained, with 60,202 individuals interviewed. The other 4,146 residents selected were excluded because: (i) they refused to answer the specific questionnaire or (ii) had their information rejected in the automatic coherence screening performed by the Brazilian Institute of Geography and Statistics (IBGE). The rate of non-reply was 14.0%.

The PNS sample was designed in three stages. The primary units of sampling (PUS) were the census tracts or sets of sectors. The households were the secondary units, and the adult residents (≥ 18 years) were the tertiary units. Weight factors were calculated for each sample unit, considering the selection probability. The weight for the selected resident was calculated considering the household weight, non-reply adjustments by sex and calibration for the population totals by sex and age groups estimated with the weight of all residents. The PNS is part of the Integrated System of Household Surveys of IBGE, therefore, the PUS considered in this study are a subsample of the set of PUS existing in the master sample of IBGE. The households were selected based on the most recent version, available at the time, of the National Register of Addresses for Statistical Purposes. Details on the sampling process and weighing can be obtained in the previous publication on PNS results.8

Identification of dyslipidemia

At this stage of the survey, the information on the presence or absence of dyslipidemia was obtained via a self-report of the participants based on the results provided by their physicians about the diagnosis of "high cholesterol or triglyceride levels". The first question was "when did you have the last blood test to measure cholesterol and triglyceride levels". The alternatives ranged from"less than 6 month ago" to"more than 3 years ago" and "never". Only those reporting at least one cholesterol measurement were asked"has any physician ever diagnosed you with high cholesterol?" If the answer was positive, the following questions were asked"how old were you when first diagnosed with high cholesterol?" and "has any physician or health care provider given you a recommendation on high cholesterol?".

Statistical analysis and ethical procedures

Using the sample base, the point prevalence estimate and 95% confidence interval (95%CI) were calculated for 'the diagnosis of high cholesterol by a physician', 'undergoing a cholesterol test once' and 'measuring cholesterol or triglyceride levels'. The frequencies were stratified by sex, age group (18 to 29 years, 30 to 59, 60 to 64, 65 to 74, and 75 years and older), educational level (none and incomplete elementary school; complete elementary school and incomplete middle school; complete middle school and incomplete high school; and complete high school) and race/ethnicity (white, black and mixed). The prevalence rates were presented for the country, its large geographic regions, federated units and urban and rural areas. The raw frequency for each specific category was presented, as was the odds ratio adjusted for the other variables, except for itself. Data were analyzed with the Stata® software, 11.0 version (Stata Corp., College Station, United States), using the set of commands for data analysis of a complex sample (survey). Statistically significant differences at the 5% level were considered in the absence of 95%CI overlapping.

The PNS was approved by the National Committee on Ethics in Research (CONEP) of the National Board of Health (CNS), of the Brazilian Ministry of Health (protocol n° 328.159, of June 26, 2013). Participation in this study was voluntary and data confidentiality was guaranteed. The adults selected to answer the interview and who agreed to participate in this study signed the written informed consent.

Results

The PNS estimates discussed in this study are based on the answers of 60,202 individuals aged 18 years and more. The proportion of participants who never had their cholesterol and/or triglyceride levels measured was relatively low, 14.3% (95%CI = 13.7-14.8). Table 1 shows that more than half of the responders had their cholesterol and/or triglyceride levels measured within the past year, with a significantly higher number of women, elderly, white individuals and individuals with complete high educational level, and a lower number of residents of the Northern and Northeastern regions.

Table 1

Variables

%

95% CI

Raw OR

95% CI

p

Adjusted OR

95% CI

p

Lower

Upper

Lower

Upper

Lower

Upper

Table 2 shows that among those who reported undergoing at least one cholesterol measurement, the prevalence of a medical diagnosis of high cholesterol in the Brazilian population was 12.5% (9.7% for men and 15.1% for women). The women's probability of having a diagnosis of high cholesterol was 60% higher than that of men. The frequency of high cholesterol according to the age group for both sexes increased up to the age of 59 years; from 60 to 74 years, the values were constant, and from the age of 75 years on, the values decreased. The educational level as a socioeconomic indicator showed similar frequencies at the extremes of the category, "no education" and "complete high school". Participants self-reporting black race/ethnicity had significantly lower frequencies of medical diagnosis of high cholesterol. The lowest self-reported rates of high cholesterol were observed in the Northern and West-Central regions.

Table 2

Variables

%

95% CI

Raw OR

95% CI

p

Adjusted OR

95% CI

p

Lower

Upper

Lower

Upper

Lower

Upper

Figure 1 shows that half of the participants had their first medical diagnosis of high cholesterol in their fifth or sixth decade. One fifth of the interviewees reported having their first medical diagnosis of high cholesterol after the age of 60 years. Figure 2 shows the recommendations provided to individuals in the face of their medical diagnosis of high cholesterol, the most common being "to eat healthy", "to maintain an adequate weight" and "to practice physical activity". Drug prescription was recommended in two-thirds of the cases.

Discussion

This study shows, for the first time, the prevalence of dyslipidemia in a representative sample of the Brazilian population, in which one in every eight individuals self-reported having high cholesterol levels. The frequency of the self-reported diagnosis was higher among women, white and Asian-heritage individuals, those with higher educational level and residents of the Southern, Southeastern and West-Central regions.

According to the 2014 VIGITEL-BRASIL (Brazilian surveillance system on risk and protective factors of chronic diseases via telephone survey), performed in the 27 Brazilian capitals, the prevalence of a previous medical diagnosis of dyslipidemia was 20.0% (women, 22.2%, and men, 17.6%). In both sexes, the diagnosis of high cholesterol was associated with age increase and higher educational level. Such data are in accordance with the results of this analysis based on the PNS data.9

Prevalence studies of the medical diagnosis of high cholesterol have shown low sensitivity for the definitive diagnosis (55%) as shown in the Third National Health and Nutrition Examination Survey carried out in the United States (1988-1994) with a representative population of that country.10 In a survey involving 12 European countries, self-report associated with only 30% of the cases diagnosed with the specific test.11 Despite the low sensitivity, when participants of the Women´s Health Study reported their cholesterol level measured, there was strong association between those self-reported values and the higher incidence of cardiovascular disease in 10 years.12

The Brazilian Longitudinal Study of Adult Health (ELSA-Brasil) has compared the self-report of high cholesterol medical diagnosis with the diagnosis based on an LDL-cholesterol measurement greater than 130 mg/dL or the use of lipid-lowering drugs. The following were obtained: sensitivity of 51.5% (95%CI = 50.4%-52.5%); specificity of 86.0% (65.1-86.8); and positive and negative likelihood ratios of 3.7 (3.4-3.9) and 0.56 (0.55-0.58), respectively.

With this prevalence of self-reported high cholesterol of 12.5%, the real prevalence of dyslipidemia in the Brazilian population can be estimated as 46.6%.13

The 2013 PNS has the limitations of a population-based survey conducted in a country of continental dimensions. However, considering the Brazilian reality, the study design and operation reached an adequate level of quality. Data generalization was relatively safe for the national and regional projections. Surveys, such as the PNS, use self-reported information on medical diagnosis, which is a limited method of assessment. Evaluation by a physician, nurse or via a previously tested standard questionnaire has better accuracy as already proved in a systematic review of population surveys using self-report.14 However, considering Brazil's continental dimensions, that is the fastest and most inexpensive way to assess the prevalence of some conditions, such as high cholesterol.

The importance of the PNS data on the medical diagnosis of high cholesterol is justified by the data obtained from a review study of population surveys assessing the historical trend of cholesterol levels since 1980 in three million participants in Latin America, which has concluded that there were few studies on the diagnosis of dyslipidemia in those populations.5

The importance of dyslipidemia awareness in the current Brazilian epidemiological context should be emphasized to guide actions of control and prevention of coronary heart disease, the leading cause of death in Brazil and worldwide, and that determines higher mortality in disadvantaged social strata.15

Conclusion

In a representative population sample of Brazil, this study showed that 10% of the men and 15% of the women had a medical diagnosis of high cholesterol.

Footnotes

Author contributions
Conception and design of the research: Lotufo PA, Szwarcwald C, Stoppa SR, Malta DC. Acquisition of data: Szwarcwald C, Stoppa SR, Malta DC. Analysis and interpretation of the data: Lotufo PA, Santos RD, Prado RR, Bensenor IM. Statistical analysis: Lotufo PA, Prado RR, Stoppa SR, Malta DC. Obtaining financing: Szwarcwald C. Writing of the manuscript: Lotufo PA, Santos RD, Sposito AC, Bertolami M, Faria-Neto JR, Izar MC, Bensenor IM. Critical revision of the manuscript for intellectual content: Lotufo PA, Santos RD, Sposito AC, Bertolami M, Faria-Neto JR, Izar MC, Szwarcwald C, Prado RR, Stoppa SR, Malta DC, Bensenor IM.

Potential Conflict of Interest
No potential conflict of interest relevant to this article was reported.
Sources of Funding
This study was funded by Ministry of Health.
Study Association
This study is not associated with any thesis or dissertation work.

References

7. Instituto Brasileiro de Geografia e Estatística . Percepção do estado de saúde, estilos de vida e doenças crônicas. Rio de Janeiro: 2014. [ Google Scholar]

8. Souza Jr PR, Freitas MP, Antonaci GA, Szwarcwald CL. Desenho da amostra da Pesquisa Nacional de Saúde 2013 [Sampling Design for the National Health Survey, 2013] Epidemiol Serv Saúde. 2015;24(2):207-216. [ Google Scholar]

9. Ministério da Saúde. Secretaria de Vigilância em Saúde. Departamento de Vigilância de Doenças e Agravos não Transmissíveis e Promoção da Saúde . Vigitel Brasil 2014 : vigilância de fatores de risco e proteção para doenças crônicas por inquérito telefônico. Brasília: 2015. [ Google Scholar]

Articles from Arquivos Brasileiros de Cardiologia are provided here courtesy of Sociedade Brasileira de Cardiologia

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Self-Reported High-Cholesterol Prevalence in the Brazilian Population: Analysis of the 2013 National Health Survey

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Data on the prevalence of dyslipidemia in Brazil are scarce, with surveys available only for some towns.To evaluate the prevalence of the self-reported medical diagnosis of high cholesterol in the Brazilian adult population by use of the 2013 National Health ...

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Título: Etiología diversa de la hiperlipidemia entre niños hospitalizados en la región occidental de Arabia Saudita
Tipo de estudio: Estudio de Cohortes retrospectivo, transversal
Año: 2016
Resultados: De los 253 niños revisados, los que han demostrado tener un metabolismo lipídico anormal con síndrome nefrótico fueron el 35,6 %, diabetes mellitus 17,8 %, hiperlipidemia primaria/idiopática 19,4 %, hipotiroidismo 7,1 %, obesidad 4,3 %, síndrome metabólico 2,8 %, síndrome metabólico 2,8 %, enfermedad hepática 2% e insuficiencia renal crónica 1,2%
Conclusiones: La mayor prevalencia de hiperlipidemia estuvo en el síndrome nefrótico, seguido de la hiperlipidemia primaria/idiopática y la diabetes mellitus.

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Abstract

Objectives:

To determine the various etiologies of primary and secondary hyperlipidemia among children visiting the pediatric endocrine clinic.

Methods:

This is a retrospective, cross-sectional, cohort study conducted at King Abdulaziz University Hospital (KAUH), Jeddah, Kingdom of Saudi Arabia from January 2010 to 2015 that included 253 children aged from birth to 12 years old. Data were obtained by reviewing medical reports of patients who presented with hyperlipidemia to the clinic, and their laboratory investigation results using KAUH electronic "Phoenix" system.

Results:

Of the 253 children who were reviewed, those who have shown to have abnormal lipid metabolism with nephrotic syndrome were 35.6%, diabetes mellitus 17.8%, primary/idiopathic hyperlipidemia 19.4%, hypothyroidism 7.1%, obesity 4.3%, metabolic syndrome 2.8%, chronic liver disease 2% and chronic renal failure 1.2%. The body mass index relative to gender and age in this group of children showed that 23.2% were underweight, 38.4% were normal weight, 8.9% were overweight, and 29.5% were obese.

Conclusion:

The highest prevalence of hyperlipidemia was in nephrotic syndrome, followed by primary/idiopathic hyperlipidemia and diabetes mellitus.

Hyperlipidemia is a condition of increased lipid levels in the body. This increase imposes patients to a higher risk of diseases, primarily those involved in athersosclerotic changes to the blood vessels. Lipids are classified into several types which are; very low density lipoproteins (VLDL), low density lipoproteins (LDL), high density lipoproteins (HDL), triglycerides (TG), and total cholesterol (TC), collectively known as the lipid profile. An increase of the lipid profile is usually asymptomatic, and screening is necessary to detect it as recommended by the Expert Panel on Integrated Guidelines of National Heart, Lung and Blood institute. 1 In addition, the causes of hyperlipidemia may be classified into 2 categories; either primary causes or secondary causes. Primary causes are due to genetic disorders, which may be inherited, either as an autosomal dominant or an autosomal recessive inheritance. Secondary causes include diseases such as nephrotic syndrome, diabetes mellitus (DM), chronic renal failure (CRF), chronic liver disease (CLD), hypothyroidism, obesity or iatrogenic due to total parenteral nutrition (TPN). Minimal research has been conducted on the etiology of hyperlipidemia in Saudi Arabia, which is crucial for setting preventable measures against it. The aim of this study was to determine the multiple etiologies of hyperlipidemia and their frequencies among the pediatric population visiting the pediatric endocrine clinic.

Methods

Definitions

Nephrotic syndrome is a disease characterized by the presence of proteinuria >3.5 mg/dl, hypoalbuminemia <25g/dL, generalized edema and high serum cholesterol concentration. Hyperlipidemia is related to the hypoproteinemia and low serum oncotic pressure of nephrotic syndrome, which then leads to reactive hepatic protein synthesis, including that of lipoproteins. Next, diabetes mellitus is a disorder of hyperglycemia due to the body's inability to secret insulin, or to respond to secreted insulin appropriately or both. Diagnostic values relied upon in our study were fasting plasma glucose (FPG) value ≥126 mg/dl (7.0 mmol/l), 2-h plasma glucose (PG) value of ≥200 mg/dl (11.1 mmol/l) and an HbA1c ≥6.5% as recommended by American Diabetes Association. 2 Chronic renal disease is defined as the presence of kidney damage markers (blood, urine, or imaging) for ≥3 months, indicating structural or functional kidney abnormalities, with or without a decreased glomerular filtration rate (GFR), or a GFR <60 ml/min for ≥3 months, with or without kidney damage. 3

Hypothyroidism is a condition in which the thyroid gland is underactive and doesn't produce enough thyroid hormone, which can lead to intellectual disability and profound developmental delays if untreated. Its diagnosis was made by the presence of elevated thyroid stimulating hormone (TSH) levels, and decreased free thyroxine (T4) levels. The normal reference values used were TSH 0.36- 4.7mIU/L, free T4 12-22 pmol/L. Primary (familial) hypercholesterolemia is a heritable, single gene disorder that produces a clinical pattern of severe hypercholesterolemia due to accumulation of LDL in the plasma, and cholesterol deposition in the tendons and skin. High levels of lipid profile were defined as a TC, 4.4-5.2 mmol/l; LDL-C, 2.9-3.4 mmol/l; and TG, 0.8-1.1 mmol/l (0-9 years) or 1-1.5 mmol/l (10-19 years). High levels were defined as the following: TC, 5.2 mmol/l; LDL-C, 3.4 mmol/l; and TG, 1.1 mmol/l (0-9 years) or 1.5 mmol/l (10-19 years) as recommended by The American Academy of Pediatrics and the Expert Panel sponsored by the United States National Heart, Lung, and Blood Institute cited earlier. Metabolic syndrome was diagnosed by the presence of 2 or more of the following: insulin resistance and impaired glucose tolerance, elevated TC and TG concentrations, low circulating HDL-C concentrations, abdominal obesity, and high blood pressure. Body mass index (BMI) was calculated by dividing weight (in kilograms) by the height squared (in meters). Then, it was expressed as a percentile of the values on the Centers for Disease Control and Prevention BMI charts 4 ().

Table 1

Data collection

This retrospective, cross-sectional, cohort study was conducted by reviewing the medical records of all the children with hyperlipidemia following up at the Pediatric Endocrinology Clinic at King Abdulaziz University Hospital (KAUH), Jeddah, Kingdom of Saudi Arabia (KSA) between January 2010 and January 2015. A total of 253 children between the ages 0 and 12 years were included in the study. All laboratory data was obtained using KAUH electronic Phoenix system. Missing data from the files of the patients was obtained by directly contacting the patients or their parents, and a verbal consent was taken by the parents prior to initiating the study, which was performed according to the principles of Helsinki Declaration. The data collected compromised of age, gender, race, lipid profile (LDL, HDL, TG, TC), liver function tests (aspartate, aminotransferase [AST], alanine aminotransferase [ALT], albumin, and bilirubin concentrations), renal function tests (urea and creatinine concentrations), fasting blood glucose level (FBG), random blood glucose level, glycated hemoglobin level (HbA1c), weight, height, family medical history, drug history, and past medical history. Patients included in the study were those who have shown the presence of hyperlipidemia according to KAUH laboratory values with TC >5.2 mmol/l, LDL >3.4 mmol/l or TG >1.13 mmol/l. Exclusion criteria involved children aged >12 years, incomplete data, children on medication, or refusal to participate by the child or parent. The Research and Ethics committee at the KAUH in Jeddah approved the study.

Statistical Analysis

Statistical analysis was carried out with the help of a biostatistics specialist. The data were entered, coded, and analyzed using the Statistical Package for Social Science (SPSS Inc., Chicago, IL, USA), version 16. The correlation coefficients were calculated and the relationships BMI, TC, LDL, HDL, and TG were assessed using Pearson correlation coefficients. Simple descriptive statistics were reported as proportions for qualitative variables and as mean and standard deviation for quantitative variables, such as the mean cholesterol, LDL, HDL, and TG levels for the various BMI categories. An independent t-test was used to find the difference in BMI among males and females. p-values less than 0.05 were considered significant, unless otherwise specified.

Results

The study included 253 children of whom 114 (45.1%) were girls and 139 (54.9%) were boys. The nationality was Saudi for 94 (37.5%) children. The mean age of the boys was 3 years, and the mean age of the girls was 4 years. The frequency of children with hyperlipidemia for each disease was recorded alongside with their lipid profile (Figure 1 ). For the 45 (17.8%) children with diabetes mellitus, the mean random glucose level was 18.7 mmol/l, mean fasting glucose level was 6.1 mmol/l, and mean HbA1c was 19.6. For the 3 (1.2%) patients diagnosed with chronic renal failure, the mean blood urea nitrogen (BUN) concentration was 13.9 mmol/l, and the mean creatinine concentration was 2.10 mmol/l. For the 5 (2%) children diagnosed with chronic liver disease, the mean AST concentration was 2.5 u/l, mean ALT concentration was 1.8 u/l, mean albumin concentration was 27.5 g/l, and mean bilirubin concentration was 119.3 mmol/l. For the 21 (8.3%) children diagnosed with Hypothyroidism, the mean triiodothyronine (T3) concentration was 4.6 mmol/l, mean T4 concentration was 16.7 mmol/l, and mean TSH concentration was 8.8 mmol/l. Body mass index, relative to gender and age, indicated that 28 (14.7%) of the boys were underweight, 39 (20.5%) boys were of healthy weight, 10 (5.3%) boys were overweight, and 30 (15.8%) boys were obese. For the girls, 16 (8.4%) girls were underweight, 34 (17.9%) girls were of healthy weight, 7 (3.7%) girls were overweight, and 26 (13.7%) girls were obese.

A family history of a medical disease was present for 41 (16.2%) children, and 135 (53.4%) children had no family history of a medical disease; the data was missing for the remaining 77 (30.4%) children. A family history of hypercholesterolemia was present for 3 (1.2%) children and absent for 247 (97.6%) children; the data was missing for 3 (1.2%) children. A family history of premature death was present for 20 (8.0%) children but absent for 157 (62.1%) children, and the data for 76 (37.2%) children was missing.

Discussion

Abnormal lipid metabolism is reportedly common in patients with kidney disease, 5 particularly nephrotic syndrome (); the most common known lipid abnormalities with nephrotic syndrome are hypercholesterolemia, hyperlipidemia of LDL and hypertriglyceridemia. Decreased plasma oncotic pressure stimulates hepatic lipoprotein synthesis resulting in hypercholesterolemia, diminished clearance might also play a role in the development of hypercholesterolemia. Impaired metabolism is primarily responsible for nephrotic hypertriglyceridemia.

Table 2

In the present study, 45 children (17.8%) had diabetes mellitus. A number of lipoprotein abnormalities have been observed in the untreated, hyperglycemic patient with diabetes mellitus. In a study carried out in Egypt, 6 the lipid profiles of 60 children with type 1 diabetes mellitus were compared with those of healthy children in the general population, dyslipidemia is significantly more frequent in children and adolescents with type 1 DM compared with non-diabetic peers. In addition, HbA1c concentrations were significantly related with TC and non-HDL-C concentrations. 7 Quantitative and qualitative abnormalities occur via lipoproteins in patients with diabetes. Quantitative involve the increased level of TG and decrease in HDL cholesterol levels, whereas the qualitative abnormality occurs by increased VLDL particle size and an increase in triacylglycerol content of both LDL and HDL. 8

Dyslipidemia is a common finding among children with chronic kidney disease. It is associated with lower GFR, nephrotic proteinuria, and non-renal factors, such as age and obesity. There are various factors involved in the pathogenesis of dyslipidemia in CKD, including increased levels of triglycerides, triglyceride-rich lipoproteins, decreased levels of high-density lipoproteins, and aberrations in serum VLDL and IDL. 9, 10 Consequently, it is a cause of major concern for patients with CKD, because it has been found that the prevalence of coronary heart disease secondary to CKD is higher, and thus the mortality rates are also increased.

Hypothyroidism has previously shown to be a contributing factor to hyperlipidemia; a cross-sectional study conducted in Hail, KSA, where search of the patient database for new patients with thyroid dysfunction between January 2011 and June 2012 showed elevated serum TC, TG, and LDL-C concentrations, and decreased serum HDL-C, which predisposes patients to atherogenic changes. 11 Furthermore, the oxidation of plasma cholesterol is increased due to 2 main mechanisms that include altered binding patterns and increased cholesterol levels. 12

Regarding BMI, hyperlipidemia occurs much more frequently among overweight and obese children. The typical pattern is one of elevated serum LDL-C and TG concentrations and decreased HDL-C concentration. Our study has shown that as the BMI increases, so does the lipid profile, thus demonstrating a clear positive correlation between both.

Familial hypercholesterolemia (FH) is a genetic syndrome characterized by a high LDL-C concentration from birth. It is an autosomal dominant disorder caused by defects in the LDLR gene that encodes for the Apo B/E (LDL) receptor. 13 The associated impairment in the function of these receptors results in reduced clearance of LDL particles from the circulation and therefore elevated plasma LDL-C. In addition to LDL receptor defects, the phenotype of FH can be seen with mutations in the PCSK9 gene or mutations in the gene that codes for apolipoprotein B.

Finally, metabolic syndrome consists of several core laboratory items including a raised TG level, a decreased HDL-C level, and elevated fasting plasma glucose concentration. Clinically, it is also associated with increased abdominal obesity and an increased blood pressure. 14 Dyslipidemia in metabolic syndrome is attributed to an increased flux of free fatty acids to the liver, which promotes TG synthesis, and subsequently VLDL production. Increased VLDL, together with decreased LPL activity due to insulin resistance, causes accumulation of TG-rich lipoproteins, including proatherogenic remnants. Further increased activities of cholesteryl ester transfer protein and hepatic triglyceride lipase result in low HDL-C, and small, dense LDL concentrations. 15

In conclusion, different etiologies of hyperlipidemia have demonstrated different pathophysiology that lead to the alteration of lipid profile. The result of this study has shown that the most common cause of hyperlipidemia in children visiting the endocrinology clinic of KAUH was due to nephrotic syndrome, which according to researches cited earlier is one of the main features for diagnosing this renal disease. Diabetes mellitus was the second most common etiology for hyperlipidemia due to its various mechanisms in increasing a patient's lipid profile. The least number of patients visiting the clinic with hyperlipidemia were those with CRF. Finally, according to our study, obesity was not considered a major etiology of hyperlipidemia.

Research on Dyslipidemias in pediatric age group is very limited, and not many resources are available. This research will be a valuable resource for others who are looking further into the etiologies of hyperlipidemia, and may be used as a guide for setting preventive measures against hyperlipidemia including management guidelines and improving the lifestyle of the patients through proper diet and exercise. It will increase the public awareness regarding this disorder, and will help the community find further methods of avoiding complications brought by it.

Acknowledgment

We would like to acknowledge with thanks the Deanship of Scientific Research, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia for technical and financial support. We would also like to thank Huda Anwar Al-Sayeid, Kawther Abdulaim Al Aulami, and Esra B. Banjar (5th year medical students) for excellent assistance and support to accomplish this work.

Footnotes

Disclosure. Authors have no conflict of interest, and the work was not supported or funded by any drug company. This project was funded by the Deanship of Scientific Research, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia (Grant # G-16-140-36).

References

3. Stevens PE, Levin A. Evaluation and Management of Chronic Kidney Disease: Synopsis of the Kidney Disease: Improving Global Outcomes 2012 Clinical Practice Guideline. Ann Intern Med. 2013;158:825-830. [[ PubMed] Google Scholar]

6. Hassan M. Mona, Sharaf A. Sahar, Soliman M. Hend, Al-Wakeel A. Nanees. Dyslipidemia in type 1 diabetes mellitus: relation to diabetes duration, glycemic control, body habitus, dietary intake and other epidemiological risk factors. Gaz Egypt Paediatr Assoc. 2015;63:63-68. [ Google Scholar]

9. Khurana M, Silverstein D M. Etiology and management of dyslipidemia in children with chronic kidney disease and end-stage renal disease. Pediatric Nephrology. 2015;30:2073-2048. [[ PubMed] Google Scholar]

12. Shilpashree M K, Ravi B V. Vedavathi Serum lipoprotein (1) and lipid profile in hypothyroidism. J Clin Biomed Sci. 2014;4:235-239. [ Google Scholar]

14. Zhang H, Yang H, Lai C, Xu X, Huang K, Fu J. Quantitative relationship between liver fat content and metabolic syndrome in obese children and adolescents. Clin Endocrinol. 2015;83:43-49. [[ PubMed] Google Scholar]

# data[].attributes.attachment_link.title
Diverse etiology of hyperlipidemia among hospitalized children in Western region of Saudi Arabia

# data[].attributes.attachment_link.description
To determine the various etiologies of primary and secondary hyperlipidemia among children visiting the pediatric endocrine clinic. This is a retrospective, cross-sectional, cohort study conducted at King Abdulaziz University Hospital (KAUH), Jeddah, Kingdom of Saudi Arabia from January 2010 to 2015 that included 253 children aged from birth to 12 years old.

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TITULO:

Prevalencia de hipercolesterolemia en Nigeria: revisión sistemática y metanálisis

TIPO DE ESTUDIO:

revisión sistemática y metanálisis

AÑO: 2020
AUTOR: Adelaida, et al.
RESULTADOS: La prevalencia bruta agrupada de hipercolesterolemia en Nigeria fue del 38 % (intervalo de confianza del 95 %: 26-51), con una prevalencia en mujeres ligeramente superior (42 %, 23-63) en comparación con los hombres (38 %, 20-58). La prevalencia fue más alta en el sur-sur (53%, 38-68) y más baja en el suroeste (3%, 2-4) y noreste (4%, 2-7). Los habitantes urbanos tenían una tasa significativamente más alta (52%, 24-79) en comparación con los habitantes rurales (10%, 6-15).
CONCLUSIONES: Los hallazgos sugieren una alta prevalencia de hipercolesterolemia en Nigeria. La urbanización, los estilos de vida, las dietas y la cultura parecen estar impulsando una prevalencia cada vez mayor, especialmente entre las mujeres.

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doi: 10.1016/j.puhe.2019.09.002.

Affiliations

¹ Centre for Global Health, Usher Institute, University of Edinburgh, UK; RcDavies Evidence-based Medicine, Lagos, Nigeria. Electronic address: Davies.Adeloye@ed.ac.uk.

² Solina Centre for International Development and Research (SCIDaR), Abuja, Nigeria.

³ Department of Nursing Sciences, University of Fort Hare, East London, South Africa.

⁴ INSERM UMR 1219, Bordeaux Population Health Research Center, Bordeaux, France; Holo Healthcare Limited, Nairobi, Kenya.

⁵ WHO Nigeria Country Office, Abuja, Nigeria.

⁶ Federal Ministry of Health, Abuja, Nigeria.

⁷ International Health Consultancy, LLC, Atlanta, Georgia, USA.

⁸ Department of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine University of Pennsylvania Philadelphia, Pennsylvania, USA; Palliative and Advanced Illness Research (PAIR) Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

⁹ School of Pharmacy and Biomedical Sciences, University of Central Lancashire, Fylde Road, Preston, UK.

¹⁰ College of Medicine, University of Ibadan, Ibadan, Nigeria.

Free PMC article

Free PMC article

doi: 10.1016/j.puhe.2019.09.002.

Affiliations

¹ Centre for Global Health, Usher Institute, University of Edinburgh, UK; RcDavies Evidence-based Medicine, Lagos, Nigeria. Electronic address: Davies.Adeloye@ed.ac.uk.

² Solina Centre for International Development and Research (SCIDaR), Abuja, Nigeria.

³ Department of Nursing Sciences, University of Fort Hare, East London, South Africa.

⁴ INSERM UMR 1219, Bordeaux Population Health Research Center, Bordeaux, France; Holo Healthcare Limited, Nairobi, Kenya.

⁵ WHO Nigeria Country Office, Abuja, Nigeria.

⁶ Federal Ministry of Health, Abuja, Nigeria.

⁷ International Health Consultancy, LLC, Atlanta, Georgia, USA.

⁸ Department of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine University of Pennsylvania Philadelphia, Pennsylvania, USA; Palliative and Advanced Illness Research (PAIR) Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

⁹ School of Pharmacy and Biomedical Sciences, University of Central Lancashire, Fylde Road, Preston, UK.

¹⁰ College of Medicine, University of Ibadan, Ibadan, Nigeria.

Abstract

Objectives: Elevated blood cholesterol (hypercholesterolemia) is a significant cause of cardiovascular disease. We aimed to estimate national and zonal prevalence of hypercholesterolemia in Nigeria to help guide targeted public health programs.

Study design: This is a systematic review and synthesis of publicly available epidemiologic data on hypercholesterolemia in Nigeria.

Methods: We systematically searched MEDLINE, EMBASE, Global Health, and Africa Journals Online for studies on the prevalence of hypercholesterolemia in Nigeria published between 1990 and 2018. We used a random-effects meta-analysis (Freeman-Tukey double arcsine transformation) and meta-regression model to estimate the prevalence of hypercholesterolemia in Nigeria in 1995 and 2015.

Results: In total, 13 studies (n = 16,981) were retrieved. The pooled crude prevalence of hypercholesterolemia in Nigeria was 38% (95% confidence interval: 26-51), with prevalence in women slightly higher (42%, 23-63) compared with men (38%, 20-58). The prevalence was highest in the South-south (53%, 38-68) and lowest in the South-west (3%, 2-4) and North-east (4%, 2-7). Urban dwellers had a significantly higher rate (52%, 24-79) compared with rural dwellers (10%, 6-15). We estimated over 8.2 million persons (age-adjusted prevalence 16.5%) aged 20 years or more had hypercholesterolemia in Nigeria in 1995, increasing to 21.9 million persons (age-adjusted prevalence 25.9%) in 2015.

Conclusions: Our findings suggest a high prevalence of hypercholesterolemia in Nigeria. Urbanization, lifestyles, diets, and culture appear to be driving an increasing prevalence, especially among women. Population-wide awareness and education on reducing elevated cholesterol levels and associated risks should be prioritized.

Keywords: Dyslipidemia; Hypercholesterolemia; Ischemic heart disease; Nigeria; Prevalence.

Conflict of interest statement

Disclosure statement: The authors declare no conflicts of interest.

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national center for biotechnology information

# data[].attributes.attachment_link.title
Prevalence of hypercholesterolemia in Nigeria: a systematic review and meta-analysis - PubMed

# data[].attributes.attachment_link.description
Our findings suggest a high prevalence of hypercholesterolemia in Nigeria. Urbanization, lifestyles, diets, and culture appear to be driving an increasing prevalence, especially among women. Population-wide awareness and education on reducing elevated cholesterol levels and associated risks should b ...

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AUTOR: Rajeev Gupta , ravinder s rao , Anoop Misra , Samin K Sharma

TITULO DE ESTUDIO:  Tendencias recientes en la epidemiología de las dislipidemias en India

AÑO Y TIPO DE ESTUDIO: 2017, Estudio Transversal.

RESULTADOS: Estudios Prospectivos con sede en la Universidad de Oxford recopiló información de 61 estudios observacionales prospectivos, principalmente en Europa occidental y América del Norte, que consistieron en más de 900,000 adultos sin cardiopatía coronaria previa o enfermedad vascular con mediciones iniciales de colesterol total y presión arterial. El seguimiento de personas entre las edades de 40 y 89 años, hubo más de 55.000 muertes vasculares (CHD 34.000, accidente cerebrovascular 12.000, otros 10.000). La información sobre el colesterol HDL estuvo disponible para 150 000 participantes, entre los cuales hubo 5000 muertes vasculares (CHD 3000, accidente cerebrovascular 1000, otros 1000). Se informó que 39 mg/dl de colesterol total más bajo se asoció con aproximadamente la mitad menos de mortalidad por CI (índice de riesgo 0,44 [IC del 95 %: 0,42–0,48]) en el grupo de edad de 40–49 años, un tercio más bajo de mortalidad por CI (0,66 [0,65–0,68]) en el grupo de edad de 50 a 69 años, y una sexta menor mortalidad por cardiopatía coronaria (0,83 [0,81 a 0,85]) a la edad de 70 a 89 años en ambos sexos.

CONCLUSIONES: Esta revisión muestra que solo hay estudios limitados sobre la epidemiología de la hipercolesterolemia y otras dislipidemias en la India. Los informes publicados en la segunda mitad del siglo pasado revelaron tendencias crecientes en los niveles altos de colesterol total. Estudios multicéntricos recientes han informado que la hipercolesterolemia, definida como colesterol total ≥200 mg/dl, está presente en el 25-30% de los sujetos urbanos y en el 15-20% de los rurales. Estos son mucho más bajos que en los países de ingresos altos.

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Recent trends in epidemiology of dyslipidemias in India - PubMed

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Dyslipidemia is the most important atherosclerotic risk factor. Review of population based studies in India shows increasing mean total cholesterol levels. Recent studies have reported that high cholesterol is present in 25-30% of urban and 15-20% rural subjects. This prevalence is lower than high-i…

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5485409/TITULO: Tendencias recientes en la epidemiología de las dislipidemias en India
AÑO:2017
RESULTADOS:Estudios recientes han informado que el colesterol alto está presente en el 25-30% de los sujetos urbanos y en el 15-20% de los rurales. Esta prevalencia es inferior a la de los países de ingresos altos. La dislipidemia más común en la India es el colesterol LDL alto en el límite, el colesterol HDL bajo y los triglicéridos altos. Los estudios han informado que durante un período de 20 años los niveles de colesterol total, colesterol LDL y triglicéridos han aumentado entre las poblaciones urbanas. Los estudios de casos y controles han informado que existe una asociación significativa de eventos coronarios con apolipoproteína B elevada, colesterol total, colesterol LDL y colesterol no HDL y una asociación inversa con apolipoproteína A alta y colesterol HDL.
CONCLUSIONES:

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Abstract

Dyslipidemia is the most important atherosclerotic risk factor. Review of population based studies in India shows increasing mean total cholesterol levels. Recent studies have reported that high cholesterol is present in 25-30% of urban and 15-20% rural subjects. This prevalence is lower than high-income countries. The most common dyslipidemia in India are borderline high LDL cholesterol, low HDL cholesterol and high triglycerides. Studies have reported that over a 20-year period total cholesterol, LDL cholesterol and triglyceride levels have increased among urban populations. Case-control studies have reported that there is significant association of coronary events with raised apolipoproteinB, total cholesterol, LDL cholesterol and non-HDL cholesterol and inverse association with high apolipoproteinA and HDL cholesterol. Prevalence of suspected familial hypercholesterolemia in urban subjects varies from 1:125 to 1:450. Only limited studies exist regarding lipid abnormalities in children. There is low awareness, treatment and control of hypercholesterolemia in India.

Keywords: Hypercholesterolemia, Cholesterol, Lower middle income countries, Cardiovascular disease, Coronary heart disease, Lipids

1. Prologue

Abnormalities of various cholesterol lipoprotein lipids such as high total cholesterol, low density lipoprotein (LDL) cholesterol, very low density lipoprotein (VLDL) cholesterol and triglycerides and low high density lipoprotein (HDL) cholesterol are important coronary heart disease (CHD) risk factors. There is a strong pathophysiological association of raised LDL cholesterol with initiation and progression of coronary atherosclerosis. Robust data are available that shows that lowering its levels can regress and stabilize atherosclerotic vascular disease. Similar, though not as robust, data are also available for raised triglycerides and low HDL cholesterol.

University of Oxford-based Prospective Studies Collaboration gathered information from 61 prospective observational studies, mostly in Western Europe and North America, consisting of more than 900,000 adults without previous CHD or vascular disease with baseline measurements of total cholesterol and blood pressure. 1 During 12 million person years of follow-up of persons between the ages of 40 and 89 years, there were more than 55,000 vascular deaths (CHD 34,000, stroke 12,000, others 10,000). Information regarding HDL cholesterol was available for 150,000 participants, among whom there were 5000 vascular deaths (CHD 3000, stroke 1000, other 1000). It was reported that 39 mg/dl lower total cholesterol was associated with about a half lower IHD mortality (hazard ratio 0.44 [95% CI 0.42-0.48]) at age-group 40-49 years, a third lower IHD mortality (0.66 [0.65-0.68]) at age-group 50-69 years, and a sixth lower CHD mortality (0.83 [0.81-0.85]) at age 70-89 years in both sexes (). 1 This was observed throughout the main range of cholesterol in most developed countries, with no apparent threshold. Of various simple indices involving HDL cholesterol, the ratio total/HDL cholesterol was the strongest predictor of CHD mortality (40% more informative than non-HDL cholesterol and more than twice as informative as total cholesterol).

The Cambridge University based Emerging Risk Factors Collaboration obtained individual records on 302,430 people without initial vascular disease from 68 long-term prospective studies, again, mostly in Europe and North America. 2 During 2.79 million person-years of follow-up, there were 8857 nonfatal myocardial infarctions, 3928 CHD deaths, 2534 ischemic strokes, 513 hemorrhagic strokes, and 2536 unclassified strokes. It was reported that rates of CHD per 1000 person-years in the bottom and top thirds of baseline lipid distributions, respectively, were 2.6 and 6.2 with triglyceride, 6.4 and 2.4 with HDL cholesterol, and 2.3 and 6.7 with non-HDL cholesterol. Adjusted hazard ratios (HRs) for CHD were 0.99 (95% CI, 0.94-1.05) with triglyceride, 0.78 (95% CI, 0.74-0.82) with HDL cholesterol, and 1.50 (95% CI, 1.39-1.61) with non-HDL cholesterol. For the subset with apolipoproteins or directly measured LDL cholesterol, HRs were 1.50 (95% CI, 1.38-1.62) with the ratio non-HDL/HDL cholesterol, 1.49 (95% CI, 1.39-1.60) with the ratio apo B/apo AI, 1.42 (95% CI, 1.06-1.91) with non-HDL cholesterol, and 1.38 (95% CI, 1.09-1.73) with directly measured LDL cholesterol. This study highlighted the importance of LDL cholesterol as well as non-HDL cholesterol.

The Cholesterol Treatment Trialists' Collaboration reported efficacy and safety of LDL lowering therapy among 174,000 men and women who participated in 27 randomized trials. 3 In this study the researchers performed meta-analyses on data from 22 trials of statin therapy versus control (n = 134,537) and five trials of more-intensive versus less-intensive statin therapy (n = 39,612). Effects on major vascular events, major coronary events, stroke, coronary revascularization and mortality were weighted per 38.7 mg/dl (1.0 mmol/L) reduction in LDL cholesterol and effects in men and women compared with a Cox model that adjusted for non-sex differences. The proportional reductions per 38.7 mg/dl reduction in LDL cholesterol in major vascular events were similar overall for women (rate ratio [RR] 0.84, 99% CI 0.78-0.91) and men (RR 0.78, 99% CI 0.75-0.81, adjusted p value for heterogeneity by sex = 0.33) and also for those women and men at less than 10% predicted 5 year absolute cardiovascular risk (adjusted heterogeneity p = 0.11). Likewise, the proportional reductions in major coronary events, coronary revascularization, and stroke did not differ significantly by sex. No adverse effect on rates of cancer incidence or non-cardiovascular mortality was noted for either sex. These net benefits translated into all-cause mortality reductions with statin therapy for both women (RR 0.91, 99% CI 0.84-0.99) and men (RR 0.90, 99% CI 0.86-0.95; adjusted heterogeneity p = 0.43). This study clearly demonstrated efficacy and safety of statin therapy and, along with many other studies, supported its widespread use in men and women at high risk for coronary events. 4

Global Burden of Metabolic Risk Factors Study reported trends in total cholesterol levels in different countries and various regions of the world from the years 1980-2008. 5 It was estimated that total cholesterol levels increased in India as well as many other low-income and lower-middle income countries over this period. 6 On the other hand, cholesterol levels declined in most high-income countries. 6 These trends were derived using mathematical modeling from sparse epidemiological studies in a number of countries. Good quality data were available from high-income countries due to periodic nationwide surveys (e.g., USA, UK, Germany, Japan, etc.). On the other hand, in low and lower-middle countries, including India, high quality epidemiological data are not available and trends were determined using probabilistic estimations. 6

In the present article we have reviewed recent studies of prevalence of dyslipidemias and levels of cholesterol lipoproteins and triglycerides in India. Epidemiological studies of other important cardiovascular risk factors, including determinants of dyslipidemias, such as body mass index and obesity, 7 abdominal obesity and metabolic syndrome 8, blood pressure and hypertension 9, 10, diabetes 11, 12 and various lifestyle factors 13 have been reviewed recently and are not included in the present report.

2. Indian epidemiological studies

We reviewed prevalence and trends in cholesterol levels in India using studies from 1960′s to 1990′s. 14 Heterogeneous data using different methodologies were available and although there was an increasing secular trend in total cholesterol levels (R ² = 0.13, ), in view of various limitations and biases in data, robustness of this trend could not be confirmed.

In India only limited studies exist on epidemiology of cholesterol and other lipoprotein lipids on large samples in the last 20 years 14, 15, 16. We reviewed all the recent large population based epidemiological studies that focused on cardiovascular risk factors including cholesterol levels and found that there were only six multisite studies with sample size ranging from 2000-15,000. 17, 18, 19, 20, 21, 22 None of these studies is nationally representative (). Studies that had a large sample size were Indian Industrial Population Surveillance Study (n = 10,442), 17 India Migration Study (n = 1983), 18 Indian Council of Medical Research (ICMR) Integrated Disease Surveillance Project (urban N = 15223, rural N = 13517, slum/periurban N = 15751), 19 Indian Women Health Study (n = 4624), 20 India Heart Watch (n = 6123), 21 INDIAB study (n = 2042) 22 and a nationwide industry-sponsored FitHeart Study (n = 46919) 23. Prevalence of hypercholesterolemia in these studies is shown in and varies from 10 to 15% in rural to 25-30% in urban populations. These prevalence rates are much lower than in studies from the US and other developed countries. 5In NHANES studies prevalence of borderline and high cholesterol (≥200 mg/dl) and corresponding borderline and high LDL cholesterol (≥130 mg/dl) varies from 50 to 70% which is much more than in India. 24

Table 1

An important shortcoming of Indian epidemiological studies is lack of large studies with details of patterns of dyslipidemia. 25 When compared with the western populations, Indians and migrant South Asians tend to have higher triglycriede levels and lower HDL cholesterol while total cholesterol levels are lower than in the US and the UK. 26, 27, 28 Migrant cross-sectional studies have reported that compared to Caucasians and migrant south Asians, Indians in India have lower total cholesterol and lower HDL cholesterol and greater triglyceride levels. 29, 30 Studies from India have also reported greater triglyceride levels in rural and urban populations associated with low HDL cholesterol levels. 31, 32 The low HDL cholesterol and hypertriglyceridemia are metabolically interlinked and their combination has been termed as atherogenic dyslipidemia. 33 This is also associated with increased levels of small-dense LDL particles and insulin resistance. 34 Atherogenic dyslipidemia is particularly common in South Asians and has been shown to have a strong association with type 2 diabetes mellitus, metabolic syndrome and CHD. 35 This could be related to high carbohydrate diets in South Asian populations. 36 Prognostic implications of this finding have not been well studied in South Asians or in India. 37

Only a few large studies have reported prevalence of different forms of lipid abnormalities among Indians. India Heart Watch study was conducted among urban middle class subjects in 11 cities of India with fasting lipid estimation. 21 Prevalence of various cholesterol lipoprotein abnormalities after age-adjustment in men and women, respectively were, total cholesterol ≥200 mg/dl in 25.1% and 24.9%, LDL cholesterol ≥130 mg/dl in 16.3% and 15.1% and ≥ 100 mg/dl in 49.5% and 49.7%, HDL cholesterol <40 mg/dl (men) and <50 mg/dl (women) in 33.6% and 52.8%, total:HDL cholesterol ratio ≥4.5 in 29.4% and 16.8% and triglycerides ≥150 mg/dl in 42.1% and 32.9% (). The prevalence rates of various fasting dyslipidemia in the first phase of ICMR INDIAB study 22 restricted to urban and rural populations in 4 states in India was hypercholesterolemia in 13.9%, high triglycerides in 29.5%, low HDL cholesterol in 72.3% and high LDL cholesterol in 11.8%. 79% men and women had abnormalities in at least one of the lipid parameters.

In a study utilizing hospital administrative database of more than 67,000 participants we reported prevalence of various dyslipidemias using a fasting sample. 38 In this cohort of mostly middle class men and women there was a high prevalence of various dyslipidemias (). Although the most prevalent dyslipidemia in this group was borderline and high LDL cholesterol (>100 mg/dl), low HDL cholesterol (men 54.9%, women 64.4%) also was highly prevalent. Another large study (FitHeart) has reported prevalence of various cholesterol lipoprotein and triglyceride levels in more than 20 states of India utilizing a camp approach to obtain fasting blood samples and uniform laboratory methodology. 23 This was an industry-sponsored pan-India primary prevention project and used data obtained from lipid evaluation screening camps conducted at 212 locations in urban Indian populations, as part of a primary prevention program conducted by a pharmaceutical company during the year 2012. Fasting blood samples from 46,919 subjects aged 18-96 years were obtained. The mean (±1 SD) age was 49.6 ± 13.2 years. The pan-India averages (mg/dl) were: total cholesterol 176.7 ± 42.1 mg/dl, LDL cholesterol 110.5 ± 34.0 mg/dl, HDL cholesterol 43.2 ± 11.7 mg/dl, non-HDL cholesterol 133.5 ± 41.3 mg/dl and triglycerides 162.3 ± 106.7 mg/dl. There were large inter-state variations in various cholesterol lipoproteins in this study (). Prevalence of various dyslipidemias was also determined. High total cholesterol ≥200 mg/dl was observed in 26.9% (men 24.0%, women 30.8%), LDL cholesterol ≥100 mg/dl in 60.0% (men 57.6%, women 63.1%), HDL cholesterol ≤40/50 mg/dl in men/women in 56.0% (men 49.9%, women 64.5%), non-HDL cholesterol ≥130 mg/dl in 50.8 (men 49.5%, women 52.6%) and triglycerides ≥150 mg/dl in 42.6% (men 45.6%, women 38.6%) (). This study reported large inter-state variation in mean levels of various cholesterol lipoproteins and lipids as well as prevalence of various lipid abnormalities. The prevalence of high total cholesterol varied from 13.8-48.2%, high LDL cholesterol 46.9-82.6%, low HDL cholesterol 42.2-69.4%, high non-HDL cholesterol 38.0-71.8% and high triglycerides 34.2-60.5%. Indian states were divided into tertiles of Human Development Index. There was a significant association of state-level Human Development Index with prevalence of various dyslipidemias (). Better developed states had greater prevalence of cholesterol-related dyslipidemias such as hypercholesterolemia, high LDL cholesterol and high non-HDL cholesterol while states with low Human Development Index had greater prevalence of hypertriglyceridemia. These data are similar to India Heart Watch study which reported similar differences in geographic distribution of lipids and other cardiovascular risk factors. 39

3. Lipid trends in india

India is undergoing a rapid epidemiological transition with increasing population, economic prosperity, urbanization and aging with associated risk factor transition. 40Increase in cardiovascular risk and hypercholesterolemia is also associated with increase in adverse lifestyles such as greater smoking and tobacco use, change in nutritional habits with greater intake of unhealthy diets and increasing sedentary lifestyle. 41, 42 All have contributed to the rising burden of non-communicable diseases, especially CHD. Even in rural areas of India non-communicable and chronic diseases have become the leading causes for death. 15 The INTERHEART study has reported that apolipoproteins such as high ApoB and low ApoA1 as well as high total and LDL cholesterol are the most important risk factor for CHD globally as well as in South Asian countries. 43 Trends in these metabolic risk factors have not been well studied.

Jaipur Heart Watch (JHW), a series of cross sectional studies in an Indian urban population, reported secular trends in cholesterol and other lipoproteins over a 20-year period. 32, 44 The first review was performed to determine secular trends in prevalence of various lipid abnormalities in an urban Indian population over a 12-year period. 32 Data from successive epidemiological studies performed in Jaipur were analyzed. The studies evaluated adults ≥20 years for multiple coronary risk factors using standardized methodology (JHW-1, 1993-94, n = 2212; JHW-2, 1999-2001, n = 1123; JHW-3, 2002-03, n = 458, and JHW-4 2004-2005, n = 1127). Data of subjects 20-59 years (n = 4136, men 2341, women 1795) were included. In successive studies, fasting measurements for cholesterol lipoproteins (total cholesterol, LDL cholesterol, HDL cholesterol) and triglycerides were performed in 193, 454, 179 and 252 men (n = 1078) and 83, 472, 195, 248 women (n = 998) (total 2076). Trends in age-adjusted prevalence (%) of dyslipidemias in JHW-1, JHW-2, JHW-3 and JHW-4, respectively, showed insignificant changes in high total cholesterol (26.3, 35.1, 25.6, 26.0, R = 0.034), high LDL cholesterol (24.2, 36.2, 31.0, 22.2, R = 0.062), and low HDL cholesterol (46.2, 53.3, 55.4, 33.7, R = 0.136) while increase was observed in prevalence of high non-HDL cholesterol (23.0, 33.5, 27.4, 26.6, R = 0.026), high VLDL cholesterol (40.1, 40.3, 30.1, 60.6, R = 0.143), high total:HDL cholesterol ratio >5.0 (22.2, 47.6, 53.2, 26.3, R = 0.031), and high triglycerides (25.7, 28.2, 17.5, 34.2, R = 0.047). It was concluded that in this cohort the prevalence of subjects with high total cholesterol did not change significantly while those with high non-HDL cholesterol, VLDL cholesterol and triglycerides as well as with high total:HDL cholesterol increased. The study also reported a significant association of increasing dyslipidemias with increasing truncal obesity and obesity. 32

In the second review of JHW studies, 20-year trends in mean cholesterol and various lipid parameters were evaluated. 44 The number of subjects aged 20-59 years evaluated were 712 in JHW-1, 558 in JHW-2, 374 in JHW-3, 887 in JHW-4, 530 in JHW-5 and 1100 in JHW-6. Across the studies, there was high prevalence of overweight, hypertension, and lipid abnormalities. Age- and sex-adjusted trends showed significant increases in mean body mass index, fasting glucose, total cholesterol, HDL cholesterol and triglycerides (quadratic and log-linear regression, p < 0.001). 44 Categorical trends showed increase in overweight and obesity (p < 0.05) while insignificant changes were observed in truncal obesity, hypertension, hypercholesterolaemia and diabetes. On the other hand the prevalence of hypertriglyceridemia increased ().

Although there are no studies that evaluated trends in hypercholesterolemia in rural populations, review of previous studies shows increasing trends in these populations also (). The prevalence of total cholesterol >200 mg/dl in early 1990′s was 16% ¹⁵ and has increased to 25-35% in more recent Andhra Pradesh Rural Health Initiative and India Migration Study 18.

4. Lipids and heart disease in india

The relative importance of different lipid components in acute coronary syndrome in different ethnic groups has been highlighted in the INTERHEART study () 43. In this study, apolipoprotein A-1 was a better marker of protection (odds ratio, OR, 0.72, CI 0.66-0.78) than HDL cholesterol (OR 0.97, CI 0.90-1.05) while raised apo B:apo A-1 was the best indicator of risk. However, the risk associated with 1 standard deviation change in total cholesterol, non-HDL cholesterol, apolipoprotein B ₁₀₀, total:HDL cholesterol ratio apolipoprotein B ₁₀₀:apolipoprotein A-1 ratio was similar in South Asians to other ethnic groups.

Table 2

Smaller case-control studies in India have reported strong association of high total cholesterol, low HDL cholesterol and raised triglycerides with CHD or acute myocardial infarction. 14 A large study of case control study of premature CHD in Bikaner, Rajasthan (cases 165, controls 199) used multivariate logistic regression (odds ratio, 95% confidence intervals) to identify risk factors of importance. 45 It was reported that smoking (19.41, 6.82-55.25), hypertension (8.95, 5.42-14.79), high LDL cholesterol (2.49, 1.62-3.84), low HDL cholesterol (10.32, 6.30-16.91), high triglycerides (3.62, 2.35-5.59), high total:HDL cholesterol (3.87, 2.35-5.59), high fibrinogen (2.87, 1.81-4.55) and high homocysteine (10.54, 3.11-35.78) were significant factors.

There are no studies that have prospectively evaluated importance of various cholesterol lipoproteins in India. In a small prospective observational study, 502 patients with pre-existing CHD were evaluated for long-term cardiovascular mortality. 46 The study was performed in the pre-statin era with limited availability of cholesterol lowering medications. It was observed that there was a linear relationship of increasing total cholesterol levels with increasing mortality in various age-groups (). A borderline high total cholesterol (200-239 mg/dl) as well as high total cholesterol (>240 mg/dl) was associated with a greater hazard of mortality at a mean of 5 years of follow-up. Recent studies of this type could all be vitiated with widespread use of statins and we may not be able to obtain similar data in secondary prevention setting.

There are a number of population based epidemiological studies available in India that have evaluated age-related cardiovascular mortality. 47 However, no study has evaluated roles of various cholesterol lipoproteins and triglycerides. The ongoing Prospective Urban Rural Epidemiology (PURE) study can provide some insights into this important question. The first follow-up of this study has reported that there is a strong association of INTERHEART Risk Score with cardiovascular outcomes, globally, as well as in India. 48 Further results are awaited.

5. Severe hypercholesterolemia

Familial hypercholesterolemia is an important coronary risk factor. Its prevalence varies from 1:200 to 1:500 in individuals of Caucasian descent among populations in Europe and North America. 49 Familial hypercholesterolemia is common in individuals who had a myocardial infarction at a young age. As many as one in 200 people could have heterozygous familial hypercholesterolemia, and up to one in 300 000 individuals could be homozygous. 49 The phenotypes of heterozygous and homozygous familial hypercholesterolemia overlap considerably; the response to treatment is also heterogeneous.

The prevalence of suspected familial hypercholesterolemia in India is unknown. To determine prevalence of severe hypercholesterolemia (suspected familial), we evaluated its prevalence in a population-based study and a hospital-based database. 21, 38 In the population-based India Heart Watch, 21 we evaluated urban middle-class participants in 11 cities in different regions of India using cluster sampling. Participants (n = 5350, men 2935, women 2415) were evaluated for demographic, biophysical, and fasting biochemical risk factors. In the hospital-based study, all consecutive fasting blood lipid tests performed over a seven-year period were analyzed (n = 67347, men 49866, women 17481). 38 The age-adjusted prevalence of severe hypercholesterolemia in population vs hospital based studies was total cholesterol 240-269 mg/dl in 5.0% vs 5.5%, 270-309 mg/dl in 2.3% vs 1.8% and ≥310 mg/dl in 0.3% vs 0.0.5%. Prevalence of severely high LDL cholesterol in population vs hospital based studies was 160-189 mg/dl in 3.6% vs 7.4%, 190-220 mg/dl in 1.1% vs 1.7% and ≥220 mg/dl in 0.3% vs 0.5% (). Severe hypercholesterolemia (LDL cholesterol ≥220 mg/dl) in population-based study was 1:357 (men 1:326, women 1:402) and in hospital-based subjects was 1:209 (men 1:271, women 1:126). These studies show that although there is a low prevalence of mild to moderate hypercholesterolemia in both population- and hospital-based subjects in India, the prevalence of severe hypercholesterolemia is high and is similar to studies from many high-income countries. 49 Larger studies are required to exactly assess the prevalence of suspected familial hypercholesterolemia in India.

A few genetic studies on identification of DNA patterns and single nucleotide polymorphisms for familial hypercholesterolemia in India have been performed. 50, 51 Results of larger registry-based studies are awaited. Studies to identify epigenetic associations of lipid abnormalities with adiposity are also needed. A recent epigenome-wide association study of body mass index and adverse outcomes of adiposity have reported significant disturbances of DNA methylation with type 2 diabetes and in prediction of CHD risk. 52

6. Hypercholesterolemia in childhood

There is limited information on prevalence of lipid abnormalities and hypercholesterolemia in childhood in India. 37 In a study at Jaipur, 237 school children aged 13-17 years were evaluated using serum cholesterol. 53 Borderline hypercholesterolemia (170-199 mg/dl) was in 33% and definite hypercholesterolemia was in 6.8%. Madhavan et al. evaluated lipid levels in 1201 adolescents 14-18 years in Delhi and reported centile values for various lipids. 54 Prevalence of various dyslipidemias was not reported. In another study in Delhi, Gupta et al. evaluated 1236 adolescents and young adults for dietary, anthropometric and biochemical risk factors 55. Dyslipidemia was defined using >95% percentile values using the same cohort. In male and female adolescents, respectively, high total cholesterol was in 14% and 15%, high LDL cholesterol was in 12% and 13%, high triglycerides in 14% and 16% and low HDL cholesterol was in 5%.

A study in South India reported that prevalence of either high waist circumference, hyperinsulinemia or dyslipidemia was present in 67.7% of 12-19 years old children (n = 2640), more in overweight vs normal weight children (85% vs 65%). 56 Prevalence of high triglycerides in this study was in 24% and low HDL cholesterol was in 57%. In Kashmir valley, a study of 5-19 year old children reported that the commonest lipid abnormality in these children was hypertriglyceridemia and low HDL cholesterol, prevalence being 82% in males, 48% in females, and 37% in males and 19% in females, respectively. 57 These data show that hypertriglyceridemia and low HDL cholesterol, both markers of atherogenic dyslipidemia, are highly prevalent in Indian children.

Pune Children's Study evaluated serum lipid levels in 477 children at age 8 years and reported high cholesterol in 5.6% and high triglycerides in 7.6%. 58 These children were tracked to age of 21 years and reported significant tracking of raised cholesterol levels at age 21 years (kappa = 0.36). Positive tracking was also observed for body mass index and systolic blood pressure. More studies to track lipid abnormalities in children in India are required as evidence suggests that type of dyslipidemia in children and adults is similar.

7. Awareness, treatment and control

Epidemiological studies of hypercholesterolemia and dyslipidemia are important for developing strategies for prevention of CHD. Unfortunately there are limited data on population level prevention for high cholesterol in India using lifestyle and drug therapies. The PURE study reported a very low use of secondary prevention drugs 59 and healthy lifestyle practices 60 in low income countries including India.

We evaluated awareness of hypercholesterolemia (total cholesterol >200 mg/dl), its treatment with statins and control (total cholesterol <200 mg/dl in patients on statins) in the Indian Heart Watch study (). 21 Awareness was in 17.5% men and 13.2% women with high cholesterol, treatment with statins was in 7.5% men and 6.7% women, while control to targets of total cholesterol <200 mg/dl was in 4.5% men and 3.7% women. There are no similar data available from the country. In clinical practices a low use of statins among patients with CHD 61 as well as in diabetics 62 has been reported. A study has also reported that despite widespread availability the use of statins is low in India compared to many developed countries. 63

8. Epilogue

In conclusion, this reviews shows that there are only limited studies on epidemiology of hypercholesterolemia and other dyslipidemias in India. Reports published in latter half of the last century revealed increasing trends in high total cholesterol levels. Recent multi-centric studies have reported that hypercholesterolemia, defined as total cholesterol ≥200 mg/dl, is present in 25-30% of urban and 15-20% rural subjects (). These are much lower than in high-income countries. 5 Studies have also reported that most common dyslipidemias in India are borderline high LDL cholesterol (>100 mg/dl), low HDL cholesterol and high triglycerides (atherogenic dyslipidemia). There are no national studies that have reported trends in various cholesterol lipids in India. Jaipur Heart Watch studies reported 20-year trends in various lipid levels and showed increase in mean total cholesterol, LDL cholesterol and triglyceride levels. 44 There are no large prospective studies in India that have determined association of various cholesterol fractions with CHD outcomes. Case-control studies have reported that there is significant association of acute coronary events with raised apolipoprotein B, total cholesterol, LDL cholesterol and non-HDL cholesterol and inverse association with high apolipoprotein A and HDL cholesterol. 43 Prevalence of severe hypercholesterolemia has not been well studied. There is very low awareness, treatment and control of hypercholesterolemia in India. Population-based strategies to control dyslipidemia include focus on social determinants of cardiovascular health for prevention and efficient healthcare systems to screen, treat and control various types of dyslipidemias, specifically hypercholesterolemia and hypertriglyceridemia. 25, 37, 64 Clinic based management of dyslipidemias in India can be improved with better physician education, improved access to medicines as well as patient empowerment for better cholesterol self-management. 37 Focus on dyslipidemia management is urgently required in India to halt the rising tide of coronary heart disease.

References

# data[].attributes.attachment_link.title
Recent trends in epidemiology of dyslipidemias in India

# data[].attributes.attachment_link.description
Dyslipidemia is the most important atherosclerotic risk factor. Review of population based studies in India shows increasing mean total cholesterol levels. Recent studies have reported that high cholesterol is present in 25-30% of urban and 15-20% rural subjects. This prevalence is lower than high-income countries.

# data[].attributes.body
https://pubmed.ncbi.nlm.nih.gov/29204622/
TITULO: DISLIPIDEMIA
AÑO: 2017

La dislipidemia es un factor de riesgo importante para la enfermedad cardiovascular aterosclerótica (ECV). Según datos de 2009 a 2012, más de 100 millones de adultos estadounidenses de 20 años o más tienen niveles de colesterol total de 200 mg/dL (5,17 mmol/L) o más, y casi 31 millones tienen niveles de 240 mg/dL (6,20 mmol/L) o mayor. Solo en 2016, aproximadamente 660 000 personas en los Estados Unidos tuvieron un nuevo evento coronario y aproximadamente 305 000 tuvieron un evento recurrente ( 1 ). Los datos epidemiológicos sugieren que la dislipidemia puede contribuir al riesgo de accidente cerebrovascular isquémico ( 2 ). Además, cada vez hay más pruebas de que la resistencia a la insulina, que está asociada con el síndrome metabólico, es un factor de riesgo importante para la ECV aterosclerótica, el accidente cerebrovascular y la enfermedad arterial periférica.3 ) porque tiende a aumentar los niveles plasmáticos de triglicéridos y colesterol unido a lipoproteínas de baja densidad (LDL-C) y a reducir los niveles de colesterol unido a lipoproteínas de alta densidad (HDL-C)

# data[].attributes.attachment_link.description
Dyslipidemia is an important risk factor for coronary artery disease and stroke. Long-term, prospective epidemiologic studies have consistently shown that persons with healthier lifestyles and fewer risk factors for coronary heart disease, and particularly those with favorable lipid profiles, have r…

# data[].attributes.body
https://pubmed.ncbi.nlm.nih.gov/30103999/
Titulo:

Prevalencia de dislipidemia entre adultos en África: una revisión sistemática y metanálisis

Autor: Noubiap Jean y colaboradores
Año: 2018
Tipo de estudio: Revisión sistemática y metanálisis
Resultado: 181 estudios con 309 207 participantes fueron incluidos en este metanálisis, donde se evaluó la calidad metodológica de todos los estudios que informaron sobre la prevalencia de concentraciones elevadas de colesterol total, colesterol LDL o triglicéridos, o concentraciones bajas de colesterol HDL en adultos que residen en países africanos, en el cual tuvieron como resultado una prevalencia combinada de dislipidemia en la población general de los estudios basados ​​en la población fue del 23,6 % (IC del 95 %: 18,4-29,2) para concentraciones elevadas de colesterol total con un punto de corte de al menos 5,2 mmol/L, 41,1 % (33,0-49,4) para concentraciones bajas de colesterol HDL con un punto de corte de menos de 1,0 mmol/L, 25,7 % (16,2-36,6) para concentraciones elevadas de LDL colesterol con un punto de corte de al menos 3,3 mmol/L, y 16,5% (11,8-21,6) para concentraciones elevadas de triglicéridos con un punto de corte de al menos 1,7 mmol/L, Para que finalmente lleguen a la conclusión que la prevalencia de dislipidemia es alta en la población adulta general de África y para que se reduzca la tasa de muertes por enfermedades cardiovasculares en África deben integrar la detección y el tratamiento efectivos de la dislipidemia.

# data[].attributes.attachment_link.title
Prevalence of dyslipidaemia among adults in Africa: a systematic review and meta-analysis - PubMed

# data[].attributes.body
SciELO - Brasil - Factores de Riesgo Cardiovascular en Cardiólogos Especialistas por la Sociedad Brasileña de Cardiología Factores de Riesgo Cardiovascular en Cardiólogos Especialistas por la Sociedad Brasileña de Cardiología
Titulo:

Cardiovascular Risk Factors in Specialist Cardiologists by the Brazilian Society of Cardiology

Tipo de Estudio: estudio multicéntrico nacional transversal
Autor: María Emilia Figueiredo,  et al.
Año: 2021
Resultados : Se evaluaron un total de 555 cardiólogos, 67,9% varones, edad media de 47,2±11,7 años. La mayoría eran no fumadores (88,7%), físicamente activos (77,1%), consumidos alcohol (78,2%), circunferencia abdominal normal (51,7%) y sobrepeso (56,1%). La prevalencia de hipertensión arterial sistémica (HSA), diabetes mellitus (DM) y dislipidemia (DLP) fue de 32,4%, 5,9% y 49,7%, respectivamente, y de estas, solo el 57,2%, 45,5% y 49,6% sabían que tenían las enfermedades.
Conclusiones: Los cardiólogos brasileños que participaron en el estudio presentaron prevalencias significativas de HSA, DM y DLP, pero solo la mitad de los participantes sabían cómo tener estas condiciones y, entre ellas, las tasas de control fueron bajas para SAH y DLP, aunque los cardiólogos eran profesionales con conocimiento diferenciado sobre estos FRCV. Los hallazgos representan una advertencia para el abordaje de los FRCV en cardiólogos brasileños y estimulan futuros estudios

# data[].attributes.attachment_link.title
Fatores de Risco Cardiovascular em Cardiologistas Especialistas pela Sociedade Brasileira de Cardiologia

# data[].attributes.attachment_link.description
Resumo Fundamento: Principal causa de morte em todo o mundo, as doenças cardiovasculares (DCV) e...

# data[].attributes.body
TITULO: Dislipidemias
TIPO: ARTÍCULO DE REVISIÓN
AÑO: 2009
AUTOR: Pedro Enrique Miguel Soca
CONCLUSIONES:
Las dislipidemias son trastornos frecuentes de los lípidos sanguíneos que favorecen la aterosclerosis y sus secuelas, principalmente las cardiopatías isquémicas. Se relacionan con hábitos de vida dañinos como el consumo de dietas hipercalóricas, y escasa actividad física que originan incremento del peso corporal y de adiposidad y aparece con más frecuencia en determinadas enfermedades. Las causas también pueden ser genéticas provocadas por alteraciones del material genético. La hipercolesterolemia y la hipertrigliceridemia, solas o combinadas, representan importantes factores de riesgo de morbilidad y muerte en quienes la padecen, por lo que es un imperativo el tratamiento agresivo de estos trastornos, sea con modificaciones en los estilos de vida o medicamentos hipolipemiantes.
http://scielo.sld.cu/scielo.php?script=sci_arttext&pid=S1024-94352009001200012

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Citado por SciELO

Similares en SciELO

Dyslipidemias

Pedro Enrique Miguel Soca

Máster en Bionergética y Medicina Natural. Departamento de Ciencias Fisiológicas. Universidad Médica "Mariana Grajales Coello". Holguín, Cuba.

El aumento de los lípidos en sangre o dislipidemias, sobre todo del colesterol y los triglicéridos, es un factor de riesgo de aterosclerosis y enfermedades cardiovasculares. Se clasifican en primarias o genéticas y secundarias. Se diagnostican con la determinación de la colesterolemia, trigliceridemia o ambas, además de las lipoproteínas séricas, como las lipoproteínas de alta densidad o HDL, y de baja densidad o LDL. Se tratan en principio con cambios en los estilos de vida, con dietas sanas, ejercicios físicos y eliminación de los hábitos tóxicos. Los principales medicamentos empleados son las estatinas, secuestrantes de ácidos biliares y los fibratos.

Palabras clave: Dislipidemia, hipercolesterolemia, hipertrigliceridemia, cambios en estilos de vida.

The increase of the lipids in blood or dyslipidemias, mainly of the cholesterol and the triglycerides, it is a factor of atherosclerosis risk and cardiovascular illnesses. They are classified in primary or genetic and secondary. They are diagnosed with the determination of the cholesterolemia, trigliceridemia or both, besides the serum lipoproteins like high density lipoprotein or HDL and low density lipoprotein or LDL. It treatment consist in principle to changes in the lifestyles with healthy diets, physical exercises and elimination of the toxic habits. The main used medications are the statins, secuestrants and the fibrates.
Key words: Dyslipidemia, hypercholesterolemia, hipertrigliceridemia, lifestyle changes.

Las dislipidemias o hiperlipidemias son trastornos en los lípidos en sangre caracterizados por un aumento de los niveles de colesterol o hipercolesterolemia (el sufijo emia significa sangre) e incrementos de las concentraciones de triglicéridos (TG) o hipertrigliceridemia. Son entidades frecuentes en la práctica médica, que acompañan a diversas alteraciones como la diabetes mellitus tipo 2 (DM-2), la gota, el alcoholismo, la insuficiencia renal crónica, el hipotiroidismo, el síndrome metabólico (SM) y el empleo de algunos fármacos. La prevalencia es variable. En sujetos sanos se reportan cifras de 57,3 % para la hipertrigliceridemia y de 48,7 % para la hipercolesterolemia; valores más altos en pacientes con resistencia a la insulina (RI). ¹ Un estudio en Cuba en pacientes mayores de 60 años encontró 56,9 % con dislipidemias. ²

Las dislipidemias aumentan el riesgo de aterosclerosis porque favorecen el depósito de lípidos en las paredes arteriales, con la aparición de placas de ateromas, y en los párpados (xantelasma) y en la piel con la formación de xantomas. ³ El aumento excesivo de los triglicéridos (TG) por encima de 11,3 mmol/L incrementa las probabilidades de pancreatitis aguda, caracterizada por un intenso dolor abdominal con vómitos que constituye una urgencia médica.

Las dislipidemias, por su elevada prevalencia, aumenta el riesgo de morbilidad y muerte por diversas enfermedades y el carácter tratable de sus afecciones, y se convierten en un problema de salud en el mundo y en nuestro país por los graves daños que provoca en los pacientes afectados. En esta contribución se describirán los aspectos básicos de las hiperlipidemias con énfasis en el metabolismo de las lipoproteínas, la clasificación de las dislipidemias y su tratamiento.

Los lípidos son insolubles en el plasma sanguíneo, por lo que circulan en la sangre unidos a proteínas en forma de lipoproteínas. La albúmina, una proteína plasmática, transporta los ácidos grasos (AG). La superficie de las lipoproteínas contiene las proteínas denominadas apoproteínas y lípidos antipáticos (con dos porciones, una polar y otra apolar) con su parte polar hacia la parte exterior de la partícula. En el núcleo de la lipoproteína se encuentran los lípidos apolares, como el colesterol esterificado (CE) y los TG. La densidad de las lipoproteínas se debe a la proporción relativa de lípidos y proteínas. Las lipoproteínas más ricas en lípidos son los quilomicrones y las abundantes en proteínas son las lipoproteínas de alta densidad (HDL). La composición de las lipoproteínas varía por el intercambio de lípidos y lipoproteínas que sufren.

Los lípidos de la dieta, principalmente los TG y en menor proporción el colesterol y otros, son digeridos en el tracto gastrointestinal por acción de enzimas como las lipasas, con la ayuda de las sales biliares y absorbidos por la mucosa del intestino delgado. En el duodeno, primera porción del intestino delgado, se originan los quilomicrones que pasan a la circulación linfática y son las lipoproteínas responsables de transportar en la sangre los TG de origen exógeno o dietético.

Otra lipoproteína, la lipoproteína de muy baja densidad o VLDL, transporta los TG sintetizados en el hígado, es decir, de origen endógeno. El aumento en sangre de estas dos lipoproteínas, los quilomicrones y las VLDL, elevan las concentraciones circulantes de TG después de las comidas grasas (hipertrigliceridemia posprandial) o en ayunas.

Las HDL al principio no contienen colesterol; se sintetizan en el hígado e intestino delgado y presentan un metabolismo complejo. ⁴ El flujo de colesterol libre desde las células es mediado por el transportador casete ligado al ATP A1 (ABCA 1) que se combina con la apoproteína A-I para producir las HDL nacientes. El colesterol de las HDL se esterifica con los AG por la enzima lecitina colesterol acil transferasa (LCAT) y se convierte en un compuesto apolar que se sitúa hacia el núcleo de la lipoproteína, y produce las HDL maduras. ⁵

Los TG de los quilomicrones y de las VLDL son degradados en los tejidos por una enzima que se encuentra adosada a la superficie interna de los vasos sanguíneos o endotelio: la lipasa de lipoproteína (LLP), una enzima dependiente de la insulina que convierte estas partículas en remanentes o partículas residuales. La apoproteína C-II de las VLDL y los quilomicrones activan a la LLP. El glicerol y los AG liberados por la acción de la LLP son captados por tejidos como el tejido adiposo y muscular que los almacenan o utilizan para obtener energía. ⁵ Los remanentes de los quilomicrones son adquiridos por el hígado y reciclados en otras lipoproteínas y los remanentes de VLDL o partículas de densidad intermedia (IDL) y pueden seguir dos destinos: se convierten en lipoproteínas de baja densidad (LDL) por acción de la lipasa hepática (LH) o son captados por el hígado. Las LDL,ricas en colesterol, se encargan de transportar el colesterol hacia los diferentes tejidos, que lo emplean en la síntesis de hormonas esteroides, vitamina D y sales biliares. El aumento de las LDL en sangre provoca un aumento del colesterol y eleva considerablemente el riesgo de aterosclerosis.

A diferencia de las LDL, las HDL intervienen en el transporte inverso del colesterol desde los tejidos y las paredes arteriales hasta el hígado, donde se excreta por la bilis al intestino, que constituye una vía de eliminación del exceso del colesterol en el organismo. Esto explica parte del efecto beneficioso de estas lipoproteínas; por eso el colesterol, unido a las HDL, se le llama "colesterol bueno" y el unido a las LDL "colesterol malo". 6

La proteína de transferencia de ésteres de colesterol (CETP) facilita la remoción del CE desde las HDL y, por tanto, reduce los niveles de HDL. ⁷ Esto contribuye al transporte de lípidos a sus lugares de destino cuando el metabolismo lipídico es normal. Cuando hay un retraso del aclaramiento de las VLDL, la permanencia prolongada de estas partículas en el plasma favorece el intercambio, lo que tiene varias consecuencias adversas: las LDL se enriquecen en TG, lo que las convierte en un buen sustrato para la LH, que hidroliza los TG, y forma LDL densas y pequeñas; estas LDL penetran fácilmente en la pared arterial y son muy susceptibles a la oxidación; las HDL pierden colesterol y adquieren TG, que son hidrolizados por la LH, y las VLDL enriquecidas en colesterol por este aumento del intercambio lipídico también son aterogénicas, ya que no se captan por los receptores hepáticos y sí por los macrófagos de la pared arterial. ⁸ Estas alteraciones justifican la aterogenicidad de la hipertrigliceridemia (es decir, su influencia sobre la ateroesclerosis), por lo que debe tratarse como la hipercolesterolemia para reducir el riesgo cardiovascular. ⁸

Las VLDL se forman en el hígado y participan en la exportación del exceso de TG derivados de los AG plasmáticos y de los residuos de quilomicrones. La síntesis de estas partículas se incrementa cuando aumentan los AG en el hígado, como resultado de una dieta rica en grasas, o en situaciones como la obesidad o la DM-2 en que se liberan grandes cantidades de AG a la circulación. La LLP también degrada los TG de las VLDL hasta glicerol y AG. ⁵

La clásica clasificación de Fredrickson divide a las hiperlipidemias en seis grupos según los patrones de aumento de lípidos y de lipoproteínas: I, IIa, IIb, III, IV y V (). Una clasificación más práctica distribuye las dislipidemias en dos grupos, primarias o secundarias. Las dislipidemias primarias responden a mutaciones genéticas (cambios en la secuencia de bases nitrogenadas del ADN) y se sospechan cuando se producen signos de dislipidemia en niños, en enfermedades ateroscleróticas prematuras (en menores de 60 años) y con niveles de colesterol en sangre por encima de 6,2 mmol/L. ⁵

Las dislipidemias secundariasconstituyen la mayoría de los casos de dislipidemia en adultos. La causa más frecuente es el estilo de vida sedentario con ingesta elevada de grasas saturadas (como la mantecas de origen animal, la carne de cerdo y otras) y colesterol; otras causas son la DM-2, el consumo excesivo de alcohol, la insuficiencia renal crónica, el hipotiroidismo, la cirrosis hepática primaria y algunos fármacos como las tiacidas, los â bloqueantes, retinoides, antirretrovirales, estrógenos, progestágenos y glucocorticoides.

Como se expresó antes, la hipercolesterolemia es el aumento de colesterol en sangre asociado frecuentemente con un incremento de las LDL en la circulación. La hipercolesterolemia esencial familiar es un trastorno genético frecuente de carácter dominante, relacionado con una deficiencia de receptores de LDL o de apo C-II que provoca un incremento de los niveles en circulación de las LDL, lipoproteínas ricas en colesterol, lo que produce hipercolesterolemia. El incremento de estas partículas en sangre favorece el depósito de placas de ateromas en el interior de las arterias y explica gran parte del riesgo cardiovascular (CV) que presentan estos pacientes.

El aumento de los TG en sangre, unido a bajos valores de colesterol de HDL, es la dislipidemia de presentación más frecuente en la práctica médica. ⁴ La hipertrigliceridemia se produce por un aumento de la formación hepática de las VLDL, sobre todo por exceso de grasa visceral o un déficit de eliminación de estas partículas por una actividad reducida de LLP. ⁸ El aumento de TG se asocia también con la síntesis de partículas de LDL pequeñas densas, que son muy aterogénicas. Actualmente, se recomiendan como valores deseables de TG niveles por debajo de 1,70 mmol/L. ⁸

Las dislipidemias se tratan con modificaciones en los estilos de vida y medicamentos. Las personas con dislipidemias, en especial con DM-2 y SM, presentan un marcado riesgo de morbilidad y mortalidad CV. Las guías actuales de tratamiento se dirigen a la disminución de las LDL con el tratamiento de estatinas, además de la modificación en los estilos de vida y dietéticos. ⁹⁻¹⁰

Las dislipidemias se tratan en primera instancia con cambios en los estilos de vida. Aunque existen distintos puntos de vista, hay consenso en que deben consumirse preferentemente frutas y vegetales frescos, que son ricos en nutrientes como vitaminas y minerales, y abundantes en fibra dietética que comprende la parte de los carbohidratos que no se absorben y, por tanto, aportan pocas calorías. 11-13 La dieta equilibrada sana comprende alrededor de un 50-60 % de carbohidratos, sobre todo complejos, menos del 30 % de grasas y un 15 % de proteínas. Las grasas ingeridas deben ser insaturadas en forma de aceites vegetales. Los aceites vegetales que no se deben consumir son los de coco y de palma porque son muy ricos en ácidos grasos saturados que aumentan los niveles de colesterol en sangre. Los pacientes con exceso de peso corporal se animan a bajar de peso con dietas hipocalóricas y los sujetos hipertensos necesitan reducir el consumo de sodio (sal de mesa). También debe limitarse la cantidad de vísceras consumidas, sobre todo el seso (cerebro) y el hígado, que son ricas en colesterol. La leche y sus derivados se deben consumir sobre todo desnatados.

Otro cambio importante en estos pacientes es el incremento de la actividad física que aumenta el gasto de energía y, por tanto, reduce el peso corporal; por otro lado, incrementa los niveles de HDL en sangre, lo que disminuye las probabilidades de padecer de enfermedades cardíacas.

Se debe promover el abandono del hábito de fumar que incrementa el riesgo de cánceres y favorece la aterosclerosis. Los pacientes con dislipidemias que fuman presentan mayores probabilidades de muerte por enfermedades cardiovasculares.

El tratamiento farmacológico comprende el uso de estatinas, fibratos, secuestradores de ácidos biliares, ecetimiba, ácido nicotínico, entre otros. Las estatinas representan un conjunto de medicamentos muy efectivos en el tratamiento de las dislipidemias, que inhiben la enzima HMG CoA reductasa que interviene en la síntesis de colesterol en las células. ¹⁰ Al reducirse la formación de colesterol, las células utilizan el colesterol que transportan las LDL, lo que disminuye la concentración de estas partículas en sangre, y como estas lipoproteínas son las más abundantes en este compuesto, se produce una disminución de la colesterolemia.

Las estatinas comprenden el tratamiento de elección para reducir las LDL y la mortalidad CV y producen pequeños aumentos de las HDL con disminución modesta de los TG. 5 Los efectos adversos son poco frecuentes y se producen principalmente en ancianos y en personas con varias enfermedades, comprenden aumento de enzimas hepáticas (TGP) e inflamación del músculo o miositis.

Los fibratos disminuyen los TG en alrededor del 50 % y aumentan las HDL hasta 20 %. Producen efectos adversos como trastornos digestivos y dolor abdominal. ⁵ Sus efectos sobre los lípidos sanguíneos se producen por la activación del receptor alfa activado por el proliferador del peroxisoma (PPAR-a). Esto promueve la oxidación de los AG y estimula la actividad LLP, lo cual reduce los TG y aumenta la síntesis de apoproteínas de las HDL, lo que incrementa las cifras de colesterol de HDL. ⁸

Los secuestradores de ácidos biliares disminuyen la reabsorción intestinal de ácidos biliares, por lo que incrementan la captación hepática del colesterol de las LDL para la síntesis de ácidos biliares y reducen los niveles de colesterol en sangre; además disminuyen la mortalidad CV. En general se asocian con las estatinas y el ácido nicotínico en pacientes refractarios (que no responden al tratamiento). Son los fármacos de elección en niños y mujeres que desean tener embarazos. Tienen un uso limitado por sus efectos adversos: meteorismo (gases), náuseas, cólicos y estreñimiento. No deben utilizarse cuando hay hipertrigliceridemia porque aumentan los TG en sangre. ⁵

La ecetimiba disminuye la absorción intestinal de colesterol, reduce las LDL 15-20 % y ligeramente los TG, además de aumentar las HDL. Se emplean en monoterapia o con estatinas en pacientes con LDL altas que no responden a dosis máximas de estatinas. No están bien establecidos sus efectos adversos. ⁵

El ácido nicotínico es el fármaco más eficaz para aumentar las HDL en las dosis recomendadas hasta en 29 % y reduce sustancialmente las LDL y los TG, aunque no se conoce bien su mecanismo de acción. ⁹ Produce rubor (enrojecimiento), prurito o picazón y náuseas; efectos que se previenen con bajas dosis de ácido acetilsalicílico. Otros efectos adversos menos frecuentes son aumento de las enzimas hepáticas, aumento del ácido úrico y gota. Su uso en individuos diabéticos es seguro. ⁹

Otros medicamentos son los ácidos grasos omega 3 y el PPG. En dosis altas, los ácidos grasos de origen marino son tan eficaces como los fibratos en la reducción de TG y carecen de efectos secundarios. ⁸ Los AG omega 3 también son ligandos de PPAR-a pero reducen la síntesis de AG por mecanismos independientes, lo cual justifica que su efecto en la reducción de los TG sea complementario de los fibratos. Se ha demostrado la eficacia de estos ácidos grasos en la disminución de TG y en la prevención de las enfermedades cardiovasculares. ¹⁴ Un resumen de las dosis de los medicamentos hipolipemiantes puede observarse en la .

CONCLUSIONES

Las dislipidemias son trastornos frecuentes de los lípidos sanguíneos que favorecen la aterosclerosis y sus secuelas, principalmente las cardiopatías isquémicas. Se relacionan con hábitos de vida dañinos como el consumo de dietas hipercalóricas, y escasa actividad física que originan incremento del peso corporal y de adiposidad y aparece con más frecuencia en determinadas enfermedades. Las causas también pueden ser genéticas provocadas por alteraciones del material genético. La hipercolesterolemia y la hipertrigliceridemia, solas o combinadas, representan importantes factores de riesgo de morbilidad y muerte en quienes la padecen, por lo que es un imperativo el tratamiento agresivo de estos trastornos, sea con modificaciones en los estilos de vida o medicamentos hipolipemiantes.

1. Munguía-Miranda C, Sánchez-Barrera RG, Hernández-Saavedra D, Cruz-López M. Prevalencia de dislipidemias en una población de sujetos en apariencia sanos y su relación con la resistencia a la insulina. Salud Publica Mex. 2008;50(5):375-82.

2. López Pérez JE, Villar Novell AL. Dislipidemia en personas mayores de 60 años. Rev Cubana Med Gen Integr. 2005;21(3-4). Disponible en http://www.bvs.sld.cu/revistas/mgi/vol21_3-4_05/mgi043-405.htm [Consultado: 27 de octubre de 2009].

3. Miguel Soca PE. El síndrome metabólico: un alto riesgo para individuos sedentarios. Acimed. 2009;20(2). Disponible en http://bvs.sld.cu/revistas/aci/vol20_2_09 /acisu809.htm [Consultado: 22 de octubre de 2009].

4. Millán J, Pintó X, Muñoz A, Zúñiga M, Rubiés-Prat J, Pallardo LF, et al. Lipoprotein ratios: Physiological significance and clinical usefulness in cardiovascular prevention. Vasc Health Risk Manag. 2009;5:757-65.

5. Beers MH, Porter RS, Jones TV, Kaplan JL, Berkwits M (eds.). El Manual Merck de Diagnóstico y Tratamiento. Madrid: Elsevier; 2007.

6. Sharma RK, Singh VN, Reddy HK. Thinking beyond low-density lipoprotein cholesterol: strategies to further reduce cardiovascular risk. Vasc Health Risk Manag. 2009;5:793-9.

7. Masson D, Jiang XC, Lagrost L, Tall AR. The role of plasma lipid transfer proteins in lipoprotein metabolism and atherogenesis. J Lipid Res. 2009;50 (Suppl):S201-6.

8. Ros E, Laguna JC. Tratamiento de la hipertrigliceridemia: fibratos frente a ácidos grasos omega-3. Rev Esp Cardiol.2006;6(Suppl):52D-61D.

9. Shepherd J, Betteridge J, Van Gaal L; European Consensus Panel. Nicotinic acid in the management of dyslipidaemia associated with diabetes and metabolic syndrome: a position paper developed by a European Consensus Panel. Curr Med Res Opin. 2005;21(5):665-82.

10. Becker DJ, Gordon RY, Morris PB, Yorko J, Gordon YJ, Li M, et al. Simvastatin vs therapeutic lifestyle changes and supplements: randomized primary prevention trial. Mayo Clin Proc. 2008;83(7):758-64.

11. Jenkins DJ, Wong JM, Kendall CW, Esfahani A, Ng VW, Leong TC, et al. The effect of a plant-based low-carbohydrate("Eco-Atkins") diet on body weight and blood lipid concentrations in hyperlipidemic subjects. Arch Intern Med. 2009;169(11):1046-54.

12. Radhika G, Ganesan A, Sathya RM, Sudha V, Mohan V. Dietary carbohydrates, glycemic load and serum high-density lipoprotein cholesterol concentrations among South Indian adults. Eur J Clin Nutr. 2009;63:413-20.

13. Holvoet P, De Keyzer D, Jacobs DR. Oxidized LDL and the metabolic syndrome. Future Lipidol. 2008;3(6):637-49.

14. Houston MC, Fazio S, Chilton FH, Wise DE, Jones KB, Barringer TA, et al. Nonpharmacologic treatment of dyslipidemia. Prog Cardiovasc Dis. 2009;52(2):61-94.

Recibido: 29 de octubre de 2009.
Aprobado: 8 de noviembre de 2009.

Dr. Pedro Enrique Miguel Soca. Departamento de Morfofisiología. Universidad Médica "Mariana Grajales Coello". Avenida Vladimir I. Lenin No. 4 e/ Aguilera y Agramonte, CP: 80100, Holguín. Correo electrónico:

Ficha de procesamiento

Términos sugeridos para la indización

DISLIPIDEMIAS; HIPERCOLESTEROLEMIA; COLESTEROL; COLESTEROL HDL; COLESTEROL LDL; COLESTEROL VLDL; TRIGLICÉRIDOS; HIPERTRIGLICERIDEMIA; SÍNDROME X METABÓLICO; ATEROSCLEROSIS; ENFERMEDADES CARDIOVASCULARES.
DYSLIPIDEMIAS; HYPERCHOLESTEROLEMIA; CHOLESTEROL; CHOLESTEROL, HDL; CHOLESTEROL, HDL; CHOLESTEROL, VLDL; HYPERTRIGLYCERIDEMIA; TRIGLYCERIDES; METABOLIC SYNDROME X; ATHEROSCLEROSIS; CARDIOVASCULAR DISEASES.

Copyright: © ECIMED. Contribución de acceso abierto, distribuida bajo los términos de la Licencia Creative Commons Reconocimiento-No Comercial-Compartir Igual 2.0, que permite consultar, reproducir, distribuir, comunicar públicamente y utilizar los resultados del trabajo en la práctica, así como todos sus derivados, sin propósitos comerciales y con licencia idéntica, siempre que se cite adecuadamente el autor o los autores y su fuente original.

Cita (Vancouver): Miguel Soca PE. Dislipidemias. Acimed. 2009;20(6). Disponible en: Dirección electrónica de la contribución [Consultado: día/mes/año].

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Citado por SciELO Similares en SciELO Dyslipidemias Pedro Enrique Miguel Soca Máster en Bionergética y Medicina Natural. Departamento de Ciencias Fisiológicas. Universidad Médica "Mariana Grajales Coello". Holguín, Cuba. El aumento de los lípidos en sangre o dislipidemias, sobre todo del colesterol y los triglicéridos, es un factor de riesgo de aterosclerosis y enfermedades cardiovasculares.

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Título: Dislipidemias
Año: 2017
Estudio: Revisión Sistemática
Autor: Laurie Kopin , Charles Lowenstein
Resultados:
Etiología
Primarios:
LDL aumentado
HDL disminuido
Secundarias:
Incluyen hipotiroidismo, enfermedad hepática obstructiva, síndrome nefrótico, insuficiencia renal, diabetes mellitus no controlada y consumo de tabaco o alcohol. Varios medicamentos también pueden causar dislipidemia
Medicamentos que pueden causar dislipidemia
Corticoesteroides
esteroides androgénicos
progestágenos
diuréticos tiazídicos
betabloqueantes
Derivados del ácido retinoico
Estrógenos orales

https://www.acpjournals.org/doi/10.7326/AITC201712050

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https://bmccardiovascdisord.biomedcentral.com/articles/10.1186/s12872-020-01825-2
TITULO:

La prevalencia de la hipercolesterolemia y los factores de riesgo asociados en la población de Al-Kharj, Arabia Saudita: una encuesta transversal

TIPO DE ESTUDIO: Estudio transversal
AÑO: 2021
RESULTADOS: La prevalencia de hipercolesterolemia en la muestra (1019 personas) fue del 12,5%. Hubo una asociación positiva moderada significativa entre el aumento de la edad y la prevalencia de HC (r = 0,240, P <0,0001). Los hombres tenían una prevalencia significativamente mayor de HC (56,7%) en comparación con sus contrapartes femeninas (43,3%) ( X ² = 23,093, P ≤ 0,0001). El IMC se asoció positiva y significativamente con el estado de colesterol alto. Los participantes en la categoría de sobrepeso tenían un riesgo significativamente mayor de HC (OR = 1,727; IC del 95 % = 1,58–1,914; P = 0,046). Los participantes no obesos (< 25 kg/m ² ) tuvieron una asociación inversa significativa con el riesgo de hipercolesterolemia. (OR = 0,411; IC 95 % = 0,216–0,783;P = 0,007).
CONCLUSIONES: En este estudio poblacional, los factores de riesgo predominantes de hipercolesterolemia (HC) en la región de Al-Kharj fueron ser de nacionalidad saudita, hombre, tener obesidad, estar desempleado y ser un trabajador civil. Existe una clara necesidad de futuros estudios de detección de HC, ya que la mayoría de los estudios anteriores informaron datos de prevalencia contradictorios (porque se realizaron en diferentes regiones de KSA).

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Research article

Open Access

Published:

BMC Cardiovascular Disorders 21, Article number: 22 (2021) Cite this article

Abstract

Background

Hypercholesterolemia (HC) is an important precursor to many cardiovascular, cerebrovascular, and peripheral vascular diseases. A report conducted by the American Heart Association showed the prevalence of HC to be 11.9%, with around 28.5 million adults age ≥ 20 years having high cholesterol levels. This study aimed to evaluate the prevalence of HC and its associated risk factors among the general population of Al-Kharj, Saudi Arabia.

Method

A cross-sectional study was conducted on the general population of Al-Kharj, Saudi Arabia in 2016. The representative sample consisted of 1019 individuals, who all participated on a voluntary basis. The statistical analysis was performed using SPSS version 25.

Results

The results of this study showed the prevalence of HC in the sample to be 12.5%. There was a significant moderate positive association between increasing age and the prevalence of HC (r = 0.240, P < 0.0001). Males had a significantly higher prevalence of HC (56.7%) compared to their female counterparts (43.3%) ( X ² = 23.093, P ≤ 0.0001). BMI was positively and significantly associated with high cholesterol status. Participants in the overweight category had a significantly higher risk of HC (OR = 1.727; 95% CI = 1.58-1.914; P = 0.046). The non-obese (< 25 kg/m ²) participants had an inverse significant association with the risk of hypercholesterolemia. (OR = 0.411; 95% CI = 0.216-0.783; P  = 0.007).

Conclusion

In this population-based study, the predominant risk factors of HC in Al-Kharj region were being of a Saudi nationality, male, having obesity, being unemployed, and being a civilian worker. There is a clear need for future screening studies of HC, as most previous studies have reported contradictory prevalence data (because they were conducted in different regions of KSA). Furthermore, well-designed prospective cohort studies are needed in the future to assess how the association between lifestyle behavioural factors such as dietary intake patterns and levels of physical activity may affect the relative risk of HC status.

Peer Review reports

Background

Elevated blood cholesterol level better known as hypercholesterolemia (HC) is an well-established risk factor for cardiovascular, cerebrovascular, and peripheral vascular diseases [ 1]. Hypercholesterolemia can be either due to primary (genetic or familial), or secondary (acquired) causes. Genetic mutations of the LDL receptor gene account for 85% of familial causes. Other factors include defective apolipoprotein B, proprotein convertase subtilisin/kexin type 9 gene gain-of-function mutation, LDL receptor adaptor protein mutation and polygenic HC [ 2, 3, 4]. Acquired causes include medical conditions which include hypothyroidism, diabetes mellitus, nephrotic syndrome, and cholestasis. Some medications such as cyclosporine and thiazide diuretics, as well as excessive intake of dietary cholesterol and smoking have been linked with increased risk of HC [ 1, 5, 6].

Age is also a strong risk factor for HC; more advanced age has been associated with higher risk of HC for both sexs [ 7, 8, 9]. In people who are in younger age groups (teenagers, young adults 18-25 years of age), HC can go undetected [ 10]. In a study by Basulaiman et al., it was reported that 65% of Saudis with HC were undiagnosed [ 9]. Another study reported that the prevalence of HC was 23.7% in the young age group [ 10]. There is currently a gap in the literature when it comes to HC, as there is a very limited number of studies which include young adults (18-25 years of age) [ 9, 11, 12]. This age group seems to be at a relatively lower risk of having HC; however, according to the National Cholesterol Education Program (NCEP), adults 20 years of age and older should be screened for HC at least once every 5 years [ 13]. Additionally, in a surprising cross-sectional study conducted in children (9-12 years)-not even young adults-in Riyadh showed a prevalence of HC of 32.7% [ 14].

Sex is a risk factor for HC which requires more extensive research. While some studies reported greater numbers of HC among males [ 7, 8], other investigations have on the contrary reported higher levels in females [ 12, 15]. Furthermore, there were other 'unusual' factors that showed some association with HC, including insomnia and early menopause [ 16, 17].

Globally, the prevalence of HC is relatively high. The World Health Organization (WHO) reported a global prevalence of 39% in 2008 [ 18]. Recent estimates have shown that around 28.5 million people from the adult population (aged 20 years or older) have high levels of total serum cholesterol, with the reported prevalence being 11.9% [ 19]. Data on HC levels in the Middle East are very limited. In a study conducted in 14 African and Middle Eastern (AFME) countries, the dyslipidemia level was as high as 70%. However, the prevalence of HC was not mentioned [ 20]. In Saudi Arabia, the prevalence of HC ranges widely from 8.5 to 54.9% in both the general population and the stable clinic visitors in different regions of the Kingdom [ 11, 12, 21].

This wide range of HC prevalence figures could be due to the fact that HC is an asymptomatic condition. It could also be a result of the differences between the studied age groups, sex, ethnic heterogeneity, and many other factors. Given that studies on HC are scarce in the Middle East and in Saudi Arabia, there is a significant need for a thorough cross-sectional population-based study in the region. Therefore, the current study aims to provide reliable data on the prevalence of hypercholesteremia at a population level. In order to have a comprehensive view of the topic, the study investigated the relationship between hypercholesteremia and its associated factors, including age, sex, marital status, body mass index (BMI), education level, employment status, diabetes status, and smoking status.

Methods

This was a cross-sectional study conducted in Al-Kharj region of Saudi Arabia. The study's duration was six months, starting from January to June 2016. The estimated total population of the city at the time of the study was reported to be slightly over 0.3 million (n = 300,000). Al-Kharj is one of the Kingdom's major hubs, having great economic importance and up-to-date administration. It also possesses significant natural resources, an important geographical location, and population diversity (a population with a variety of ethnic backgrounds). Moreover, published studies showed that among the population of Al-Kharj, the prevalence of hypertension was 30.3%, the prevalence of obesity was 49.6%, and the risk of coronary heart disease (CHD) was 2.5% [ 22]. Given the increased prevalence of these chronic conditions (hypertension, obesity, and CHD), the assessment of hypercholesterolemia and its association to certain risk factors for CHD in the current study is warranted.

Study population

Figure 1 represents the inclusion and exclusion criteria of the study population.

Flowchart of inclusion and exclusion criteria

Data collection procedure and tools

A total of 1200 respondents participated in the study, with a response rate of 85%. All incomplete questionnaires in which more than 5 responses were missing were excluded. In the final analysis, the data of a total of 1019 respondents were included. A multistage sampling technique was utilized for the collection of the data. Samples were selected from different governmental and private institutions through a cluster sampling technique. Afterwards, cluster lists were made, and seven clusters were randomly selected by the investigators for inclusion in the study. Another round of cluster sampling was performed on the selected cluster, and two clusters of that were then included. The total population of the selected clusters was then divided into different sampling units using the list of participants obtained from each department of the selected institutes. Study respondents were then selected using simple random sampling from each of the selected groups through a computer-generated list. Finally, the eligible subjects among them were recruited in the study. The aforementioned sample population has also been used in previously published studies [ 23, 24, 25].

Material and measures

Data were collected from the participants using a structured questionnaire. The questionnaire used in this study has been published previously [ 23, 26]. Information about sociodemographic factors such as age, sex, marital status, and education levels was obtained via the same questionnaire. Anthropometric measurements like body weight (kilograms), height (meters), Body Mass Index (BMI) and waist circumference (centimeters) were taken at the time of the interview by trained nurses. All the procedures were performed based on the standards for anthropometric measurements. In addition to this, a blood sample was drawn for a fasting (10-12 h fast) lipid profile from each respondent.

Operational definition

Hypercholesterolemia (HC) is defined as a blood cholesterol level of > 200 mg/dL or > 5 mmol/L [ 27]. Non-obese or normal weight is defined as a BMI of < 25 kg/m ², and overweight denotes a BMI of ≥ 25 kg/m ², while a BMI of ≥ 30 kg/m ² falls within the obese category [ 28].

Data analyses

Data were analyzed using SPSS version 25.0 (SPSS Inc., Chicago, Illinois, USA) for Windows. A simple chi-square test was used to examine the association between HC and different categorical variables. Univariate analysis was conducted using the bivariate correlation coefficient (Pearson's r), while a multinomial regression model was used to test the relationship (adjusted odds ratio) between HC and all other possible risk factors. The confidence interval was 95%, and a P value of less than 0.05 was set to establish a statistical significance.

Results

Data related to the description of the study population were previously published [ 23, 26]. Figure 2 shows the normal distribution (Bell curve/Histogram) of the original continuous serum cholesterol variable, with a mean of 4.63 mmol/L and a standard deviation (SD) of 0.855 for the entire sample (n = 1019). There were no outliers in the normal distribution of the serum cholesterol levels.

Normal distribution of serum cholesterol in Al-Kharj population (n = 1019)

Univariate analysis

Bivariate correlation coefficient (Pearson's r) was conducted between age of respondents.

(continuous variable) and binary HC status (1 = no HC; 2 = yes.

hypercholesterolemia).

The bivariate correlation coefficient (Pearson's r) was conducted between the ages of the respondents (continuous variable) and binary HC status (1 = no HC; 2 = yes HC). The results showed that there was a significant moderate positive association between increasing age and the prevalence of HC (r = 0.240, P < 0.0001). Another Pearson's r correlation coefficient test revealed that a high body mass index (BMI), as a continuous variable, was positively and significantly associated with the presence of HC (r = 0.181, P  < 0.0001).

The prevalence of HC as a binary variable (1 = no HC; 2 = yes HC) was contrasted with sociodemographic and other risk factors. Seven (n = 7) cross-tabulation ( X ²) tests were conducted to assess the relationship between HC status and each of: sex, marital status, educational attainment, job type, diabetes status, smoking status, and body mass index (BMI) class/category.

The results are summarized in Table 1. A higher proportion of males (56.7%) had a significantly higher prevalence of HC compared with their female counterparts (43.3%). The Chi-Squared test was ( X ²) = 23.093, P ≤ 0.0001. Married individuals were significantly more likely to have HC (67.7%) in comparison to individuals who had never married (32.2%). The Chi-Squared test was ( X ²) = 68.086, P ≤ 0.0001. When HC status was examined according to educational attainment, it was found that secondary school students (23.6%) and university students (63.8%) had the highest prevalence of HC. The Chi-Squared test was ( X ²) = 27.177, P ≤ 0.000. In regard to job/employment type, a significant proportion of civilian workers had HC (84.3%) compared with those who were unemployed or were soldiers. The Chi-Squared test was ( X ²) = 56.683, P  ≤ 0.0001.

Table 1 Univariate analysis regarding HC status in the Al Kharj population sample (n = 1019)

The relationship between HC and diabetes status showed that individuals with diabetes had a higher prevalence of HC (91.3%) than non-diabetic individuals with HC (8.7%). The Chi-Squared test was ( X ²) = 6.195, P = 0.013 (Table 1). There was a significant increase in the proportion of current smokers who had high cholesterol levels (15.7%), as opposed to only 5.5% of ex-smokers who had high cholesterol levels. The Chi-Squared test was ( X ²) = 9.044, P ≤ 0.011. Across the BMI categories, the results revealed that the overweight category showed a significantly higher proportion (33.1%) which had high cholesterol levels, followed by the class I obese category (27.6%), and then the class II/III obese group (18.9%). The Chi-Squared test was ( X ²) = 41.090, P  ≤ 0.0001.

Multiple logistic regression analyses

A first multiple logistic regression analysis was conducted by using the dichotomous HC status (outcome variable) with BMI (continuous independent variable) and other sociodemographic and lifestyle risk factors (Table 2). The results showed that BMI was positively and significantly associated with high cholesterol status. The odds ratio (OR) was 1.64 (95% CI = 1.610-1.671; P = 0.008). Marital status showed a significant inverse association with HC, in that married individuals had a significantly lower risk of having high cholesterol levels. The OR was 0.396 (95% CI = 0.236-0.664; P ≤ 0.0001). Moreover, job type/status-whether 'not working' (unemployed) or 'civilian'-was positively and significantly associated with HC. The OR for the 'not working' status was 3.988 (95% CI = 2.051-5.139; P = 0.042), while the OR for a 'civilian' job status was 3.385 (95% CI = 1.722-6.652; P  ≤ 0.0001).

Table 2 Logistic regression model using BMI (continuous variable) as a predictor for hypercholesterolemia status (binary outcome), after adjusting for sociodemographic and other variables (n = 1019)

A second multiple logistic regression analysis was further carried out to examine the association between BMI class (categorical variable) and the relative risk of HC, after adjusting for sociodemographic and lifestyle risk factors (Table 3). The results showed that overweight respondents had a significantly higher risk of HC. The odds ratio (OR) was 1.727 (95% CI = 1.58-1.914; P = 0.046). Non-obese (< 25 kg/m ²) participants had an inverse significant association with the risk of HC. The OR was 0.411 (95% CI = 0.216-0.783; P = 0.007). Marital status and job type/status were also significantly inversely and positively associated with HC respectively (Table 3).

Table 3 Logistic regression model using BMI class (categorical variable) as a predictor for hypercholesterolemia status (binary outcome), after adjusting for sociodemographic and other variables (n = 1019)

Discussion

The study findings show that increasing age and high BMI have significant positive associations with HC. While evaluating sociodemographic and other risk factors, it was found that HC was significantly associated with being male, married, a university graduate, a civilian worker, diabetic, a smoker, overweight or obese. On the other hand, in the multiple regression analysis, being overweight, unemployed and being a civilian worker were significant positive predictors. Whereas non-obese (< 25 kg/m ²) and married individuals had a significant inverse association with HC.

The prevalence of HC in this study population is around 12.5%. A recent study conducted in Al-Hofuf region showed findings that were nearly consistent with those of this analysis [ 15]. In previously published studies with large sample sizes, it was reported that the prevalence of HC was 54% (in 2008) and 8.5% (in 2013) among Saudis [ 7, 9]. However, the prevalence of HC varies between different populations. The prevalence of HC appears to be increasing over time in developing countries [ 29]. For instance, the reported prevalence among the Nigerian population is 38% [ 30], while Taiwan has an estimated prevalence of 44% [ 31], and Korea reported a prevalence of 19.5% in 2015 [ 32]. Data from WHO's Global Health Observatory showed that HC was highest in Europe (54%), followed by America (48%), South East Asia (29%), and Africa (22.6%) [ 18].

It was found that males had a higher prevalence of HC than females. Likewise, a recent university survey reported that HC and hypertriglyceridemia were more common among males [ 8]. The recent Africa Middle East Cardiovascular Epidemiological (ACE) Study reported significant differences between males (81%) and females (63%) [ 20]. In a Japanese prospective cohort study, unemployed men with fewer than 13 years of education had higher risk of HC [ 33]. However, contrasting results were found in some studies, in which HC was more frequently found in females [ 7, 30, 34], while other studies reported no differences in the prevalence of HC of both sexs [ 7].

Similarly, being overweight, unemployed, and being a civilian worker were positively associated with HC. Another Saudi study reported a higher prevalence of HC, with the main cause being a combination of unhealthy dietary habits and a lack of physical activity [ 7]. In one study, the estimated prevalence of physical inactivity was 96%, which increased with age and decreased with higher education level [ 35]. The key drivers for these findings are urbanization and the ubiquity of unhealthy diets and processed food across the entire Kingdom of Saudi Arabia [ 36]. Nonetheless, one study found no association between BMI and HC [ 29].

Furthermore, the current study found a higher prevalence of hypercholesterolemia among diabetic participants. A recently published Berlin Aging Study II (BASEII) found that elderly individuals on lipid lowering medication had a higher prevalence of diabetes [ 10]. However, most published studies have reported a higher prevalence of HC among diabetic individuals [ 27, 37]. A study conducted in Jeddah among primary healthcare employees reported that diabetic participants had a significant nine-fold increased risk of developing HC (OR = 9.27; 95% CI = 1.68-52.19, P = 0.019)[ 29]. Another Saudi study reported that the risk of having HC was doubled for diabetic individuals [ 9].

Naturally, there were few limitations to the current study. First, this was a cross-sectional study; therefore, causal inferences for observed significant associations cannot be made. Second, some risk factors were not explored, such as dietary habits, daily consumption of fat, physical activity/inactivity, family history, and drug/medication history, which could all be plausible contributory factors impacting the prevalence of HC. Third, the findings of the current study cannot be generalizable to some other countries due to differences in geographic location, lifestyle factors, and medical healthcare facilities. On the other hand, the major strength of the current study is its utilization of cluster sampling techniques, which, according to WHO's recommendation, assures that the recruited sample accurately represents the entire population. The study also included common risk factors and evaluated their association with HC. Hypercholesterolemia (HC) and BMI were not self-reported but were measured through blood samples, while height, weight and all other data were collected by trained staff to ensure the reliability of the data.

Conclusion

In a population-based study, the prevalence of HC in Saudi Arabia was found to be 12.5%, which is lower than what was reported in previous studies. Regarding the predominant risk factors, it was found that being Saudi, male, having obesity, being unemployed, and being a civilian worker were factors associated with HC in Al-Kharj region. These findings indicate that many non-communicable diseases, particularly cardiovascular disease (CVD), can be prevented by targeting high risk populations. Community-based awareness and education campaigns should be directed towards increasing individuals' knowledge of the risk factors for HC. There is also a need for more screening studies, as most of the studies conducted in different regions of KSA show different prevalence rates. Furthermore, well-designed prospective cohort studies are warranted in the future in order to assess how the relationship between dietary intake patterns and physical activity/inactivity levels my affect the risk of HC.

Availability of data and materials

The data used in this study is only available upon request by the corresponding author of Prince Sattam Bin Abdulaziz University.

References

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Funding

This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.

Author information

Affiliations

1. Family and Community Medicine Department, College of Medicine, Prince Sattam Bin Abdulaziz University, Al-Kharj, 11942, Saudi Arabia

Jamaan Al-Zahrani, Sameer Al-Ghamdi & Khaled K. Aldossari

2. School of Health Sciences, University of Northern British Columbia (UNBC), 3333 University Way, Prince George, BC, V2N 4Z9, Canada

Mamdouh M. Shubair

3. Family and Community Medicine Department, College of Medicine, King Saud University, Riyadh, Saudi Arabia

Abdullah A. Alrasheed

4. Internal Medicine Department, College of Medicine, Jouf University, Sakaka, Saudi Arabia

Abdulrahman A. Alduraywish

5. Family and Community Medicine Department, College of Medicine, University of Hail, Hail, Saudi Arabia

Fayez Saud Alreshidi

6. College of Applied Medical Sciences, King Khalid University, Abha, Saudi Arabia

Saeed Mastour Alshahrani

7. Department of Emergency Medicine, King Abdulaziz Medical City, College of Public Health and Health Informatics, King Saud Bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia

Majid Alsalamah

8. Department of Family Medicine, King Abdulaziz Medical City, College of Public Health and Health Informatics, King Saud Bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia

Badr F. Al-Khateeb

9. Clinical Nutrition, Community Health Department, Applied Medical Science, King Saud University, Riyadh, Saudi Arabia

Aljawharah Ibraheem Ashathri

10. College of Public Health and Health Informatics, King Saud Bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia

Ashraf El-Metwally

Contributions

AA, JMAZ, KKA, AAA, MAS and AEM were involved in the design of the study. SG contributed to the data collection for this study. AIA and KKA wrote the first draft of the manuscript, after, AAA, FSA, AEM, KKA and BFA read and contributed to the revision of the manuscript. MMS did the statistical analysis, results, and contributed to the final revisions of the manuscript. AEM, AA, JMAZ, KKA, MAS, BFA and SMA contributed to the final revisions of the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Jamaan Al-Zahrani.

Ethics declarations

Ethics approval and consent to participate

Ethical approval was obtained for this study from the local Institutional Review board of College of the Medicine, Prince Sattam Bin Abdulaziz University, Al-Kharj, Saudi Arabia. Consent was taken both verbally and in written form after a thorough explanation of the study procedures was given to the voluntarily recruited participants. Confidentially of the study participants was carefully maintained through data de-identification.

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Not applicable. This manuscript did not contain any individual personal data.

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The authors declare that they have no competing interests.

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Al-Zahrani, J., Shubair, M.M., Al-Ghamdi, S. et al. The prevalence of hypercholesterolemia and associated risk factors in Al-Kharj population, Saudi Arabia: a cross-sectional survey. BMC Cardiovasc Disord 21, 22 (2021). https://doi.org/10.1186/s12872-020-01825-2
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Keywords

Hypercholesterolemia

Obesity

Cross-sectional

Al-kharj

Saudi arabia

# data[].attributes.attachment_link.title
The prevalence of hypercholesterolemia and associated risk factors in Al-Kharj population, Saudi Arabia: a cross-sectional survey - BMC Cardiovascular Disorders

# data[].attributes.attachment_link.description
Background Hypercholesterolemia (HC) is an important precursor to many cardiovascular, cerebrovascular, and peripheral vascular diseases. A report conducted by the American Heart Association showed the prevalence of HC to be 11.9%, with around 28.5 million adults age ≥ 20 years having high cholesterol levels.

# data[].attributes.body
Título:Prevalencia, concienciación, tratamiento y control de la dislipidemia entre adultos en China

Año:2016
Conclusiones: La prevalencia de dislipidemia entre los adultos chinos fue alta, pero la conciencia, el tratamiento y el control de la dislipidemia fueron bajos. Las personas urbanas de ingresos altos y las rurales de ingresos medios muestran una mayor prevalencia. Las personas de bajos ingresos en la población urbana y rural tienen el peor tratamiento de conciencia y tasa de control. Existe una mayor necesidad de monitorear y controlar de cerca los factores de alto riesgo en las poblaciones, incluidas las mujeres posmenopáusicas, las personas con estilos de vida poco saludables y los pacientes con enfermedades crónicas no transmisibles.

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doi: 10.1016/j.atherosclerosis.2016.02.006.

Affiliations

¹ Renal Division, Department of Medicine, First Affiliated Hospital of Guangxi Medical University, China; Guangxi Medical University Institute of Urinology, Nanning, 530021, Guangxi Zhuang Autonomous Region, China.

² Cardiology Division, Department of Medicine, First Affiliated Hospital of Guangxi Medical University, China.

³ Renal Division, Department of Medicine, First Affiliated Hospital of Guangxi Medical University, China; Guangxi Medical University Institute of Urinology, Nanning, 530021, Guangxi Zhuang Autonomous Region, China. Electronic address: yunhualiao1989@sina.com.

⁴ Renal Division, Department of Medicine, Peking University First Hospital, Beijing, China; Peking University Institute of Nephrology, Peking University Health Science Center, Beijing, China.

doi: 10.1016/j.atherosclerosis.2016.02.006.

Affiliations

¹ Renal Division, Department of Medicine, First Affiliated Hospital of Guangxi Medical University, China; Guangxi Medical University Institute of Urinology, Nanning, 530021, Guangxi Zhuang Autonomous Region, China.

² Cardiology Division, Department of Medicine, First Affiliated Hospital of Guangxi Medical University, China.

³ Renal Division, Department of Medicine, First Affiliated Hospital of Guangxi Medical University, China; Guangxi Medical University Institute of Urinology, Nanning, 530021, Guangxi Zhuang Autonomous Region, China. Electronic address: yunhualiao1989@sina.com.

⁴ Renal Division, Department of Medicine, Peking University First Hospital, Beijing, China; Peking University Institute of Nephrology, Peking University Health Science Center, Beijing, China.

Abstract

Objectives: To analyze the prevalence, awareness, treatment, control and epidemiological characteristics of dyslipidemia in Chinese adults.

Methods: In this cross-sectional study, we adopted a multi-stage, stratified sampling method to obtain representative samples of the general population aged >18 years from different urban and rural regions in China. All subjects completed a lifestyle and medical history questionnaire and were examined for risk factors. Dyslipidemia was defined according to criteria of the 2007 Chinese Guidelines on Prevention and Treatment of Dyslipidemia in Adults. Continuous variables were compared using variance analysis. Multivariate logistic regression analysis was performed to explore the risk factors of dyslipidemia.

Results: The prevalence of dyslipidemia was 34.0% overall, and 35.1%, and 26.3% in urban and rural areas, respectively. The prevalence of dyslipidemia was significantly higher in men than women (41.9% vs 32.5%; P < 0.001). Rates of awareness, treatment, and control were 31.0%, 19.5%, and 8.9%, respectively. Increasing age (OR = 1.012; 95% CI:1.010, 1.014), male sex (OR = 1.411; 95% CI:1.318, 1.510), obesity (OR = 1.424; 95% CI:1.345, 1.507), cardiovascular disease (OR = 1.343; 95% CI:1.125, 1.603), diabetes (OR = 1.955; 95% CI:1.751, 2.182), hypertension (OR = 1.481; 95% CI:1.391, 1.577) and hyperuricemia (OR = 2.223; 95% CI:2.060, 2.399) were independent risk factors of dyslipidemia.

Conclusion: The prevalence of dyslipidemia among Chinese adults was high but awareness, treatment, and control of dyslipidemia were low. Urban high income earners and rural medium income earners show higher prevalence. Low income earners in urban and rural population have the worst awareness treatment, and control rate. There is an increased need for closely monitoring and controlling high risk factors in the populations including postmenopausal women, unhealthy lifestyle peoples and patients with chronic non-communicable diseases.

Keywords: China; Dyslipidemia; Epidemiology; Prevalence.

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Affiliations

¹ Section of Emergency Medicine, Department of Pediatrics, Baylor College of Medicine, The Children's Hospital of San Antonio, San Antonio, TX.

² Office of Student Affairs, Baylor College of Medicine, Houston, TX.

³ Section of Emergency Medicine, Department of Pediatrics, Baylor College of Medicine, Texas Children's Hospital, Houston, TX.

Affiliations

¹ Section of Emergency Medicine, Department of Pediatrics, Baylor College of Medicine, The Children's Hospital of San Antonio, San Antonio, TX.

² Office of Student Affairs, Baylor College of Medicine, Houston, TX.

³ Section of Emergency Medicine, Department of Pediatrics, Baylor College of Medicine, Texas Children's Hospital, Houston, TX.

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Tipo de estudio: Estudio de cohorte retrospectivo
Año: 2019
Resultados: En todas las etiologías, los niveles de colesterol total fueron significativamente más bajos en ACLD, en comparación con los no ACLD. En consecuencia, los niveles de colesterol LDL fueron significativamente más bajos en ACLD debido a la hepatitis C, la hepatitis B, la enfermedad del hígado graso/metabólico y la hepatitis autoinmune. Los niveles de triglicéridos no difirieron debido a la gravedad de la enfermedad en ninguna etiología. A pesar de los niveles más bajos de colesterol total y LDL en ACLD, los patrones de dislipidemia específicos de etiología se mantuvieron similares a los de no ACLD. Contrariamente a este estado lipídico “mejorado” en ACLD, las comorbilidades cardiovasculares fueron más prevalentes en ACLD: la hipertensión arterial estuvo presente en el 26,6% de los pacientes sin ACLD y en el 55,4% de los pacientes con ACLD ( p < 0,001), y la diabetes estuvo presente en el 8,1% de pacientes sin ACLD y 25,6% de pacientes con ACLD ( p < 0,001).
Conclusión: La etiología de la enfermedad hepática es un determinante importante de los patrones y la prevalencia de la dislipidemia. La progresión a ACLD “mejora” los niveles de lípidos séricos mientras que la hipertensión arterial y la diabetes mellitus son más prevalentes. Los estudios futuros deberían evaluar los eventos cardiovasculares después de la "mejoría" de la dislipidemia inducida por ACLD.

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Summary

Background

Liver disease impacts on hepatic synthesis of lipoproteins and lipogenesis but data on dyslipidemia during disease progression are limited. We assessed the patterns of dyslipidemia in (i) different liver disease etiologies and discriminated (ii) non-advanced (non-ACLD) from advanced chronic liver disease (ACLD) as it is unclear how progression to ACLD impacts on dyslipidemia-associated cardiovascular risk.

Methods

Patients with alcoholic liver disease ( n = 121), hepatitis C ( n = 1438), hepatitis B ( n = 384), metabolic/fatty liver disease ( n = 532), cholestatic liver disease ( n = 119), and autoimmune hepatitis ( n  = 114) were included. Liver stiffness ≥15 kPa defined ACLD. Dyslipidemia was defined as total cholesterol >200 mg/dL, low-density lipoprotein (LDL)-cholesterol >130 mg/dL and triglycerides >200 mg/dL.

Results

Across all etiologies, total cholesterol levels were significantly lower in ACLD, when compared to non-ACLD. Accordingly, LDL-cholesterol levels were significantly lower in ACLD due to hepatitis C, hepatitis B, metabolic/fatty liver disease and autoimmune hepatitis. Triglyceride levels did not differ due to disease severity in any etiology. Despite lower total and LDL cholesterol levels in ACLD, etiology-specific dyslipidemia patterns remained similar to non-ACLD. Contrary to this "improved" lipid status in ACLD, cardiovascular comorbidities were more prevalent in ACLD: arterial hypertension was present in 26.6% of non-ACLD and in 55.4% of ACLD patients ( p < 0.001), and diabetes was present in 8.1% of non-ACLD and 25.6% of ACLD patients ( p  < 0.001).

Conclusion

Liver disease etiology is a major determinant of dyslipidemia patterns and prevalence. Progression to ACLD "improves" serum lipid levels while arterial hypertension and diabetes mellitus are more prevalent. Future studies should evaluate cardiovascular events after ACLD-induced "improvement" of dyslipidemia.

Introduction

Dyslipidemia, among other factors, is a major risk factor for cardiovascular disease (CVD) development and progression [ 1] and therefore, guidelines recommend lipid-lowering therapy in patients at increased risk for CVD. As the liver plays a central role in lipid metabolism [ 2], lipid profiles are altered by chronic liver disease (CLD) severity. Although a vast body of literature exists on the effect of CLD on lipid profiles in several etiologies, state of the art assessment of CLD severity by, e.g. grading fibrosis severity is lacking in many studies and advanced CLD (ACLD)/cirrhosis is usually classified as a distinct etiology [ 2]. This classification is insufficient, as dyslipidemia patterns change during ACLD, and baseline values are strongly dependent on the underlying etiology. In addition, concomitant CVD risk factors such as arterial hypertension and diabetes mellitus must be taken into account when assessing the overall CVD risk.

Nowadays, non-invasive methods such as transient elastography are available to reliably assess the severity of fibrosis and guide/monitor CLD severity [ 3]. Therefore, evaluation of fibrosis severity in large patient cohorts is feasible and allows correlation with readily available lipid profiles. Actual real-life data are therefore warranted as treatment in chronic liver disease has evolved and most patients are exposed to an altered lipid profile for an extensive period of time as progression to ACLD can be halted in many cases. In addition, although cut-off levels for initiation of lipid-lowering treatment/statin treatment are well-established and stratified by clinical atherosclerotic cardiovascular disease risk, no specific guidelines for CLD and concomitant CVD are available.

Despite altered metabolism of statins, the most common drug class used as lipid-lowering therapy, and an increased risk of rhabdomyolysis [ 4, 5], hepatotoxic effects and severe adverse events are lower than suggested in the past [ 4]. Nevertheless, statins remain underutilized in patients with non-ACLD [ 6]. This gap in clinical implementation of guidelines might further impair outcome in CLD as several studies have shown beneficial effects on portal hypertension of statin therapy in CLD irrespective of low-density lipoprotein (LDL)-cholesterol levels [ 7]. Until further evidence from prospective randomized controlled trials is available, real-life data in dyslipidemia patterns and severity with respect to CLD etiology and severity is needed. Therefore, this study aimed to investigate differences among the most common CLD etiologies, namely alcoholic liver disease (ALD), non-alcoholic fatty liver disease (NAFLD), hepatitis C (HCV), hepatitis B (HBV), cholestatic liver diseases, primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) as well as autoimmune hepatitis (AIH).

Patients, material and methods

Study design and patient selection

All patients with (i) a clinically established diagnosis of ALD, HCV, HBV, NAFLD, cholestatic liver disease or AIH, (ii) available and valid liver stiffness measurements (LSM) by transient elastography (TE) with controlled attenuation parameter (CAP) values, (iii) available information on total serum cholesterol laboratory values within 3 months of TE-based liver stiffness measurement, and (iv) age >18 years presenting in the liver outpatient clinic of the Medical University of Vienna between October 2013 and October 2016 were included. After exclusion of patients that did not fulfil the inclusion criteria, 2708 patients were identified for further analysis. A patient flow chart and distribution according to liver disease severity is presented in Fig. 1.

Patient consort flow chart. AIH autoimmune hepatitis, ALD alcoholic liver disease, CAP controlled attenuation parameters, HBV hepatitis B virus infection, HCV hepatitis C virus infection, NAFLD non-alcoholic fatty liver disease, PBC primary biliary cholangitis, PSC primary sclerosing cholangitis

Assessment of liver fibrosis and hepatic steatosis

The assessment of liver stiffness using TE was carried out by experienced operators using the FibroScan® (EchoSens, Paris, France) device, as previously described [ 8]. Overnight fasting was a prerequisite for TE measurements and a total number of 10 valid measurements were required [ 9]. A cut-off value of ≥15 kPa defined ACLD, as suggested by the Baveno VI faculty consensus [ 10].

Definition of dyslipidemia

Total cholesterol levels of >200 mg/dL, LDL cholesterol levels >130 mg/dL or triglyceride levels >200 mg/dL were considered as dyslipidemia, according to the American Association of Clinical Endocrinologists and American College of Endocrinology 2017 guidelines [ 11]. Low high-density lipoprotein (HDL) cholesterol was not considered as dyslipidemia since there exists no treatment specifically indicated for low HDL cholesterol levels. In cases of intake of any lipid-lowering drug, the patients were excluded from the analyses of plasma lipid profiles, since lipid lowering therapy would have been a significant confounder. For the epidemiological analysis on dyslipidemia prevalence, patients on lipid-lowering therapy were considered as suffering from dyslipidemia, except patients with cholestatic liver disease and fibrates as second line therapy.

Evaluation of concomitant metabolic disorders

To evaluate concomitant CVD and, therefore, additional CVD risk factors, arterial hypertension as well as antihypertensive treatment and prescribed drug classes were assessed. Notably, non-selective beta blocker treatment that was solely administered for preventing portal hypertensive bleeding was not considered as antihypertensive medication.

Statistical analysis

Differences in proportions between groups were evaluated using χ ²-test or Fisher's exact test whenever appropriate. For normally distributed numerical variables and comparisons between two groups, Student's t‑test or Mann-Whitney U-test was used, as applicable. For visualization of liver stiffness, total cholesterol levels, as well as for linear regression and D'Agostino's K ²-test, GraphPad Prism Version 8.1.2 (GraphPad Software, La Jolla, CA, USA) was used. SPSS Version 24 (IBM, Armonk, NY, USA) was used for all other statistical analyses. A p-value <0.05 denoted statistical significance.

Institutional review board

The retrospective cohort study was conducted according to the Declaration of Helsinki and was approved by the Medical University of Vienna's institutional review board (EK-Nr. 2013/2016; https://ekmeduniwien.at/core/catalog/2016/).

Results

Differences in patient characteristics according to underlying liver disease in patients with non-ACLD and ACLD

In order to investigate differences in chronic liver disease severity, Fig. 1 presents proportions of patients with non-ACLD and ACLD. The vast majority of patients were non-ACLD patients with <15 kPa in TE except for ALD where the majority of patients suffered from ACLD. In order to assess differences between various etiologies of CLD, the characteristics of patients with non-ACLD (Table 1) as well as ACLD were compared (Table 2). Baseline characteristics were significantly different between etiologies, with the most profoundly increased concomitant CVD risk factors, namely body mass index (BMI), diabetes mellitus and arterial hypertension, in NAFLD. This pattern was preserved in ACLD, although arterial hypertension was even more prevalent in cholestatic liver disease and markedly elevated in patients suffering from HBV.

Table 1 Patient characteristics in non-ACLD patients (liver stiffness <15 kPa)

Table 2 Patient characteristics in ACLD patients (liver stiffness ≥15 kPa)

Differences in serum lipid levels in non-ACLD and ACLD

For analysis of systemic lipid levels, patients on lipid lowering therapy were excluded from the analysis. Fig. 2 shows lipid levels in the respective etiologies in non-ACLD and ACLD patients. Scatter plots showing correlation of total cholesterol levels with liver stiffness values of individual patients are provided as Supp. Fig. 1, both for the overall cohort as well as for subgroups of patients with different etiologies of liver disease.

Scatter plots depicting individual total cholesterol levels for the respective etiology in non-ACLD ( blue, left) and ACLD ( red, right) patients. * p < 0.05, ** p < 0.01, *** p < 0.001. AIH autoimmune hepatitis, ALD alcoholic liver disease, CAP controlled attenuation parameters, HBV hepatitis B virus infection, HCV hepatitis C virus infection, NAFLD non-alcoholic fatty liver disease

When lipid status was analyzed according to etiology, total cholesterol was significantly lower in patients with ACLD compared to non-ACLD patients in ALD (191 (IQR 54) mg/dL vs. 160 (IQR 62) mg/dL; p = 0.015), HCV (170 (IQR 47) mg/dL vs. 149 (IQR 52) mg/dL; p < 0.001), HBV (172 (IQR 45) mg/dL vs. 161 (IQR 33) mg/dL; p = 0.031), NAFLD (197 (IQR 54) mg/dL vs. 172 (IQR 50) mg/dL; p < 0.001), cholestatic liver disease (205 (IQR 56) md/dL vs. 184 (IQR 70) mg/dL; p = 0.049) and in AIH (191 (IQR 47) mg/dL vs. 160 (IQR 69) mg/dL; p = 0.037), respectively; however, LDL values did not significantly differ in ALD (102 (IQR 44) mg/dL vs. 83 (IQR 41) mg/dL; p = 0.059) and cholestatic liver diseases (118 (IQR 50) mg/dL vs. 111 (IQR 49) mg/dL; p = 0.341) while LDL was significantly lower in ACLD patients with viral hepatitis (HCV: 93 (IQR 41) mg/dL vs. 79 (IQR 46) mg/dL; p < 0.001; HBV: 106 (IQR 59) mg/dL vs. 81 (IQR 50) mg/dL; p = 0.012), NAFLD (115 (IQR 43) mg/dL vs. 94 (IQR 54) mg/dL; p = 0.001) and AIH (125 (IQR 46) mg/dL vs. 85 (IQR 41) mg/dL; p  = 0.034).

The HDL levels were significantly lower in HCV (50 (IQR 25) mg/dL vs. 44 (IQR 25) mg/dL; p < 0.001) and NAFLD-associated ACLD (51 (IQR 23) mg/dL vs. 42 (IQR 17) mg/dL; p < 0.001) in ACLD while it was not decreased in the other etiologies (ALD: 58 (IQR 35) mg/dL vs. 51 (IQR 24) mg/dL; p = 0.295; HBV: 46 (IQR 23) mg/dL vs. 42 (IQR 20) mg/dL; p = 0.271; cholestatic: 54 (IQR 35) mg/dL vs. 53 (IQR 51) mg/dL; p = 0.276; AIH: 58 (IQR 16) mg/dL vs. 40 (IQR 55) mg/dL; p  = 0.524).

The presence of ACLD had no effect on triglyceride levels (ALD: 99 (IQR 74) mg/dL vs. 88 (IQR 53) mg/dL; p = 0.116; HCV: 97 (IQR 59) mg/dL vs. 90 (IQR 52) mg/dL; p = 0.077; HBV: 82 (IQR 66) mg/dl vs. 107 (IQR 97) mg/dL; p = 0.093; NAFLD: 119 (IQR 81) mg/dL vs. 108 (IQR 96) mg/dL; p = 0.626; cholestatic: 86 (IQR 56) mg/dL vs. 99 (IQR 50) mg/dL; p = 0.841; AIH: 100 (IQR 56) mg/dL vs. 86 (IQR 42) mg/dL; p  = 0.417, respectively).

Prevalence of hypercholesterolemia, increased LDL levels and hypertriglyceridemia in patients without lipid-lowering therapy

As cut-off-values for increased CVD risk are well-defined in the AACE 2017 guidelines [ 11], we investigated the prevalence of hypercholesterolemia (total cholesterol >200 mg/dL), increased LDL levels (LDL >130 mg/dL) and hypertriglyceridemia (>200 mg/dL). There were important differences in the prevalence of hypercholesterolemia, increased LDL levels and hypertriglyceridemia between etiologies (Fig. 3). Interestingly, etiology-specific patterns of dyslipidemia remained similar between patient with and without ACLD. Cholestatic liver disease, AIH and NAFLD had the highest prevalence of dyslipidemia while patients with viral hepatitis and ALD showed the lowest prevalence of dyslipidemia.

Percentages of patients with an increased total cholesterol level ( white bar), increased LDL levels ( light grey) or increased fasting triglyceride levels ( dark grey), as indicated by the 2017 American Association of Clinical Endocrinologists and American College of Endocrinology guidelines. a non-ACLD patients; b ACLD patients. AIH autoimmune hepatitis, ALD alcoholic liver disease, CAP controlled attenuation parameters, HBV hepatitis B virus infection, HCV hepatitis C virus infection, NAFLD non-alcoholic fatty liver disease

Discussion

Hyperlipidemia promotes atherosclerosis via endothelial cell activation and dysfunction. Due to ingestion of LDL by foam cells, plaques develop and subsequently lead to atherosclerotic lesions [ 12]. This leads to further secretion of inflammatory cytokines and accelerates plaque development [ 13]. While the mechanisms involved in plaque formation are relatively well-studied and the beneficial effects of pharmacologic intervention aiming at decreasing LDL levels in patients at risk for CVD/CVD patients are well-established, less evidence is available for the impact of dyslipidemia in patients with CLD and especially for the respective different etiologies of liver disease.

Certain etiologies, e.g. hepatitis C, may directly impact on CVD risk. The hepatitis C virus particles require LDL (and VLDL) receptors to enter hepatocytes [ 14] and cure of hepatitis C virus infection is associated with altered total cholesterol and LDL levels [ 15]. On the other hand, HBV does not seem to alter CVD risk [ 16]; however, the data on prevalence and severity of dyslipidemia are insufficiently comparable to other liver disease etiologies and differences in liver disease severity does not allow a fair comparison across different studies and patient cohorts. The data therefore add important insights as all patients were analyzed according to liver disease etiology and liver disease severity by reliable LSM. Nevertheless, patient numbers are low in some subgroups of patients with rare etiologies of liver disease, such as cholestatic or autoimmune liver disease. Although the numbers reflect the prevalence of these diseases, greater numbers would be favorable.

Although the risk for CVD in alcoholic liver disease seems to considerably depend on the actual amount of ingested alcohol, dyslipidemia has not been reported to represent an additional risk factor for CVD in ALD [ 17]. In cholestatic liver disease, where LDL cholesterol concentrations are usually elevated, CVD risk is not proportionally increased. These findings are explained by elevated lipoprotein X levels, which cannot be distinguished from LDL by standard laboratory tests but does not exert the same risk for atherosclerosis and thus, CVD events [ 18, 19]. These differences are of immense importance, as they implicate a more differentiated approach in treatment strategies. Even within the etiology of viral hepatitis, HCV and HBV have different risk profiles. The HCV-RNA circulates in large spherical particles, which bind in a competitive way with LDL and VLDL [ 20] and inhibition of microsomal triglyceride transfer protein by HCV infection leads to reduced VLDL secretion by hepatocytes, ultimately leading to decreased serum concentrations of VLDL and LDL [ 21]. In HBV, on the other hand, serum lipid levels are not affected [ 22], leading to higher absolute serum cholesterol levels than in HCV. Based on the findings in this large patient cohort, further research on the association between dyslipidemia, steatosis and CLD of different etiologies is warranted. While recent studies focused on NAFLD and NASH, dyslipidemia and its impact on the course of liver disease and cardiovascular risk should not be neglected in other etiologies of CLD. While the underlying mechanisms and associations between dyslipidemia, hepatic steatosis and CVD risk are being explored, a recent study by Corey and Chalasani showed that aggressive lipid lowering therapy reduces the high risk of CVD in NAFLD [ 23]; however, no specific recommendations are given for concomitant dyslipidemia and/or steatosis in other etiologies [ 23]. Importantly, the change of pathological lifestyle remains a management priority in patients with metabolic diseases [ 24].

In this study, patients with ACLD showed a relatively high prevalence of arterial hypertension and diabetes of >50% and 15%, respectively. Notably, however, patients with ACLD were on average older than non-ACLD patients, which may represent a potential confounder. These differences in baseline characteristics highlight the complexity of CVD risk in CLD. Future studies evaluating statin therapy in the CLD setting should therefore focus on CVD risk factors and take into account that CVD accounts for significant morbidity in CLD. Clinical guidelines should take these interactions into account and adapted cut-off values for recommendations to initiate lipid-lowering therapy might be necessary.

While we demonstrated differences in baseline characteristics between different etiologies including distinct patterns of dyslipidemia, we could demonstrate that the dyslipidemia patterns remain to be present when CLD progresses to ACLD. Nevertheless, it was observed that absolute cholesterol levels are lower in all etiologies after ACLD develops, reflecting impaired liver synthetic function. In this study, hepatic steatosis as assessed by CAP, increased in patients with ACLD, which is paralleled by an increase in metabolic comorbidities. Notably, few patients with any CLD other than NAFLD had a CAP ≥284 dB/m, implicating significant steatosis [ 25]. In theory, portal hypertension with increased bile acid levels and subsequent increased Takeda G‑protein-coupled receptor 5 (TGR5) activation might result in reduced steatosis in cirrhosis [ 26]. These findings highlight the fragile metabolic condition of NAFLD patients. Interestingly, also patients with HBV and cholestatic liver disease, who are thought to have no increased CVD risk compared to the general population [ 16, 27], still had a high prevalence of concomitant metabolic diseases that in turn may affect CVD risk profile. In summary, available studies that pool together different stages of CLD might underestimate the effect of stage-specific changes as well as etiology-specific risk modifications.

Conclusion

Dyslipidemia is common in patients with CLD and significantly varies between different etiologies of liver disease. Progression of liver disease significantly alters lipid profiles, although etiology-specific patterns remain. It is warranted to systematically assess cardiovascular events after ACLD-induced "improvement" of dyslipidemia. Future studies should evaluate the impact of dyslipidemia and respective treatment on long-term outcome specifically in patients with CLD.

Abbreviations

ACLD:

Advanced chronic liver disease

AIH:

Autoimmune hepatitis

ALD:

Alcoholic liver disease

ALP:

Alkaline phosphatase

ALT:

Alanine aminotransferase

ASCVD:

Atherosclerotic cardiovascular disease

AST:

Aspartate aminotransferase

BMI:

Body mass index

CAP:

Controlled attenuation parameters

CLD:

Chronic liver disease

CVD:

Cardiovascular disease

GGT:

Gamma-glutamyl transferase

HBV:

Hepatitis B virus

HDL:

High-density lipoprotein

HCV:

Hepatitis C virus

IQR:

interquartil range

LDL:

Low-density lipoprotein

LSM:

Liver stiffness measurement

NAFLD:

Non-alcoholic fatty liver disease

TE:

Transient elastography

Funding

Open access funding provided by Medical University of Vienna.

Author information

Affiliations

1. Division of General Surgery, Department of Surgery, Medical University of Vienna, Währinger Gürtel 18-20, Vienna, Austria

Lukas W. Unger, Bernadette Forstner, Stephan Schneglberger & Moritz Muckenhuber

2. IT-Systems & Communications, Medical University of Vienna, Währinger Gürtel 18-20, Vienna, Austria

Ernst Eigenbauer

3. Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria

Bernhard Scheiner, Mattias Mandorfer, Michael Trauner & Thomas Reiberger M.D.

4. Vienna Hepatic Hemodynamic Laboratory, Medical University of Vienna, Währinger Gürtel 18-20, Vienna, Austria

Lukas W. Unger, Bernhard Scheiner, Mattias Mandorfer & Thomas Reiberger M.D.

Corresponding author

Correspondence to Thomas Reiberger M.D..

Ethics declarations

Conflict of interest

L.W. Unger, B. Forstner, S. Schneglberger, M. Muckenhuber, E. Eigenbauer, and B. Scheiner, declare that they have no competing interests. M. Mandorfer has served as a speaker and/or consultant and/or advisory board member for AbbVie, Bristol-Myers Squibb, Gilead, W. L. Gore & Associates, and Janssen. M. Trauner has served as speaker for BMS, Falk Foundation, Gilead and MSD; advisory boards for Albireo, Falk Pharma GmbH, Genfit, Gilead, Intercept, MSD, Novartis, Phenex and Regulus. He further received travel grants from Abbvie, Falk, Gilead and Intercept and unrestricted research grants from Albireo, Cymabay, Falk, Gilead, Intercept, MSD and Takeda. He is also coinventor of patents on the medical use of norUDCA filed by the Medical University of Graz. T. Reiberger has served as a speaker and/or consultant and/or advisory board member for AbbVie, Bayer, Boehringer Ingelheim, Gilead, W. L. Gore & Associates, and MSD and has received research funding from AbbVie, Boehringer Ingelheim, Gilead, MSD, Phenex Pharmaceuticals, and Philips.

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Unger, L.W., Forstner, B., Schneglberger, S. et al. Patterns and prevalence of dyslipidemia in patients with different etiologies of chronic liver disease. Wien Klin Wochenschr 131, 395-403 (2019). https://doi.org/10.1007/s00508-019-01544-5
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Keywords

Portal hypertension

Serum lipid levels

Hypercholesterolemia

Hypertriglyceridemia

Cirrhosis

# data[].attributes.attachment_link.title
Patterns and prevalence of dyslipidemia in patients with different etiologies of chronic liver disease - Wiener klinische Wochenschrift

# data[].attributes.attachment_link.description
Background Liver disease impacts on hepatic synthesis of lipoproteins and lipogenesis but data on dyslipidemia during disease progression are limited. We assessed the patterns of dyslipidemia in (i) different liver disease etiologies and discriminated (ii) non-advanced (non-ACLD) from advanced chronic liver disease (ACLD) as it is unclear how progression to ACLD impacts on dyslipidemia-associated cardiovascular risk.

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https://pubmed.ncbi.nlm.nih.gov/31698139/
TITULO: Prevalencia de hipercolesterolemia en Nigeria: revisión sistemática y metanálisis.
TIPO DE ESTUDIO: Revisión sistemática
AÑO: 2020
RESULTADO: En total, se recuperaron 13 estudios (n = 16 981). La prevalencia agrupada de hipercolesterolemia en Nigeria fue del 38 % (intervalo de confianza del 95 %: 26-51), con una prevalencia en mujeres ligeramente superior (42 %, 23-63) en comparación con los hombres (38 %, 20-58). La prevalencia fue más alta en el sur-sur (53%, 38-68) y más baja en el suroeste (3%, 2-4) y noreste (4%, 2-7). Los habitantes urbanos tenían una tasa significativamente más alta (52%, 24-79) en comparación con los habitantes rurales (10%, 6-15).
CONCLUSIÓN: Los hallazgos sugieren una alta prevalencia de hipercolesterolemia en Nigeria. La urbanización, los estilos de vida, las dietas y la cultura parecen estar impulsando una prevalencia cada vez mayor, especialmente entre las mujeres. Se debe priorizar la concientización y educación de toda la población sobre la reducción de los niveles elevados de colesterol y los riesgos asociados.

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doi: 10.1016/j.puhe.2019.09.002.

Affiliations

¹ Centre for Global Health, Usher Institute, University of Edinburgh, UK; RcDavies Evidence-based Medicine, Lagos, Nigeria. Electronic address: Davies.Adeloye@ed.ac.uk.

² Solina Centre for International Development and Research (SCIDaR), Abuja, Nigeria.

³ Department of Nursing Sciences, University of Fort Hare, East London, South Africa.

⁴ INSERM UMR 1219, Bordeaux Population Health Research Center, Bordeaux, France; Holo Healthcare Limited, Nairobi, Kenya.

⁵ WHO Nigeria Country Office, Abuja, Nigeria.

⁶ Federal Ministry of Health, Abuja, Nigeria.

⁷ International Health Consultancy, LLC, Atlanta, Georgia, USA.

⁸ Department of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine University of Pennsylvania Philadelphia, Pennsylvania, USA; Palliative and Advanced Illness Research (PAIR) Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

⁹ School of Pharmacy and Biomedical Sciences, University of Central Lancashire, Fylde Road, Preston, UK.

¹⁰ College of Medicine, University of Ibadan, Ibadan, Nigeria.

Free PMC article

Free PMC article

doi: 10.1016/j.puhe.2019.09.002.

Affiliations

¹ Centre for Global Health, Usher Institute, University of Edinburgh, UK; RcDavies Evidence-based Medicine, Lagos, Nigeria. Electronic address: Davies.Adeloye@ed.ac.uk.

² Solina Centre for International Development and Research (SCIDaR), Abuja, Nigeria.

³ Department of Nursing Sciences, University of Fort Hare, East London, South Africa.

⁴ INSERM UMR 1219, Bordeaux Population Health Research Center, Bordeaux, France; Holo Healthcare Limited, Nairobi, Kenya.

⁵ WHO Nigeria Country Office, Abuja, Nigeria.

⁶ Federal Ministry of Health, Abuja, Nigeria.

⁷ International Health Consultancy, LLC, Atlanta, Georgia, USA.

⁸ Department of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine University of Pennsylvania Philadelphia, Pennsylvania, USA; Palliative and Advanced Illness Research (PAIR) Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

⁹ School of Pharmacy and Biomedical Sciences, University of Central Lancashire, Fylde Road, Preston, UK.

¹⁰ College of Medicine, University of Ibadan, Ibadan, Nigeria.

Abstract

Objectives: Elevated blood cholesterol (hypercholesterolemia) is a significant cause of cardiovascular disease. We aimed to estimate national and zonal prevalence of hypercholesterolemia in Nigeria to help guide targeted public health programs.

Study design: This is a systematic review and synthesis of publicly available epidemiologic data on hypercholesterolemia in Nigeria.

Methods: We systematically searched MEDLINE, EMBASE, Global Health, and Africa Journals Online for studies on the prevalence of hypercholesterolemia in Nigeria published between 1990 and 2018. We used a random-effects meta-analysis (Freeman-Tukey double arcsine transformation) and meta-regression model to estimate the prevalence of hypercholesterolemia in Nigeria in 1995 and 2015.

Results: In total, 13 studies (n = 16,981) were retrieved. The pooled crude prevalence of hypercholesterolemia in Nigeria was 38% (95% confidence interval: 26-51), with prevalence in women slightly higher (42%, 23-63) compared with men (38%, 20-58). The prevalence was highest in the South-south (53%, 38-68) and lowest in the South-west (3%, 2-4) and North-east (4%, 2-7). Urban dwellers had a significantly higher rate (52%, 24-79) compared with rural dwellers (10%, 6-15). We estimated over 8.2 million persons (age-adjusted prevalence 16.5%) aged 20 years or more had hypercholesterolemia in Nigeria in 1995, increasing to 21.9 million persons (age-adjusted prevalence 25.9%) in 2015.

Conclusions: Our findings suggest a high prevalence of hypercholesterolemia in Nigeria. Urbanization, lifestyles, diets, and culture appear to be driving an increasing prevalence, especially among women. Population-wide awareness and education on reducing elevated cholesterol levels and associated risks should be prioritized.

Keywords: Dyslipidemia; Hypercholesterolemia; Ischemic heart disease; Nigeria; Prevalence.

Conflict of interest statement

Disclosure statement: The authors declare no conflicts of interest.

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Lipid abnormalities beyond elevated low-density lipoprotein (LDL) cholesterol contribute
to increased risk of atherosclerotic cardiovascular disease (ASCVD) in type 2 diabetes.
We searched for English language randomized controlled trials of lipid-lowering therapies
primarily since 2012 that include…

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https://pubmed.ncbi.nlm.nih.gov/25333861/
Título:

Perfil lipídico en pacientes con enfermedad coronaria de nuevo diagnóstico: estudio transversal 2012 y 2013 en el Hospital Luis Vernaza, Ecuador.

Autor y año: Vásquez-Cedeño, D
Intervencion: Se calcularon estadísticas descriptivas (media y desviación estándar) para todas las variables y se realizaron pruebas de comparación de medias. Se desarrollaron árboles de clasificación relacionando los valores de lípidos con los resultados de gSPECT, identificando puntos de corte óptimos para su uso como indicadores de isquemia miocárdica silente en la población total del estudio y para cada sexo por separado.
Resultados: Los diabéticos gSPECT positivos tenían niveles más altos de colesterol total, LDL y triglicéridos (p < 0,05). Los niveles de HDL fueron más bajos en este grupo (p < 0,05). Los árboles de clasificación mostraron puntos de corte óptimos, indicadores de isquemia silente, para: HDL ≤44 mg/dL, LDL >119,9 mg/dL y triglicéridos >107,2 mg/d; El 80,4% de los diabéticos con estos valores de HDL y triglicéridos tenían isquemia. HDL fue la variable normalizada más importante cuando se analizó toda la población.

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Affiliations

¹ Universidad Católica de Santiago de Guayaquil, Ecuador. Address: Avenida Carlos Julio Arosemena Tola Km 1.5, Guayaquil, Ecuador. Email: diegoavasquez@gmail.com.

² Universidad Católica de Santiago de Guayaquil, Ecuador.

Affiliations

¹ Universidad Católica de Santiago de Guayaquil, Ecuador. Address: Avenida Carlos Julio Arosemena Tola Km 1.5, Guayaquil, Ecuador. Email: diegoavasquez@gmail.com.

² Universidad Católica de Santiago de Guayaquil, Ecuador.

Introduction: Endothelial dysfunction is an early event in the progression of atherosclerosis, and it appears in pathologies such as dyslipidemias. Certain pro-inflammatory enzymes are associated negatively with high-density lipoproteins (HDL) and positively with low-density lipoproteins (LDL). Calculating the atherogenic index greatly complements the study of these diseases. Lipid alterations have a high prevalence in Ecuadorian and Latin American populations. Better knowledge of which lipid alteration is the most prevalent would bring more attention to the subject, leading to early treatment. The goal of this study is to describe the complete lipid profile alterations in patients recently diagnosed with ischemic heart disease and find which of these is the most prevalent.

Methods: We designed a cross-sectional, descriptive study that included patients from the Cardiology Service of the "Hospital Luis Vernaza" who presented with the first episode of ischemic heart disease between January 2012 and 2013. There were 220 patients with that diagnosis. One-hundred and thirty-one were excluded because they did not meet inclusion criteria. The final sample comprised 89 patients.

Results: We found 41 (46.06%) patients with low HDL levels, 49 (55.05%) with high LDL levels, 28 (31.46%) with high triglycerides, 24 (26.96%) with high cholesterol levels, 25 (28.08%) with high VLDL levels, 26 (29.21%) had values over 5 in the Castelli index, and 32 (35.95%) had LDL/HDL values higher than 3.

Discussion: It is of great importance to have a complete lipid profile from patients recently diagnosed with ischemic heart disease in order to work on secondary prevention. The most prevalent alteration found in our study was high LDL levels. The percentage of patients with low HDL was similar to other Latin American populations. More studies are needed to gain a more accurate idea of the status of the general population in this regard.

Introducción: La disfunción endotelial es un evento temprano en el proceso de la aterosclerosis y suele darse en patologías como las dislipidemias. Ciertas enzimas proinflamatorias se asocian negativamente a lipoproteínas de alta densidad (HDL) y positivamente a las de baja densidad (LDL). El cálculo del índice aterogénico es un complemento de gran utilidad para el estudio de estas patologías. Las alteraciones lipídicas tienen gran prevalencia en el medio ecuatoriano y latinoamericano en general. El mejor conocimiento sobre qué alteración lipídica tiene mayor prevalencia generaría mayor atención sobre dicha condición, llevando a su pronto tratamiento. El principal objetivo del presente estudio fue describir las alteraciones del perfil lipídico entre pacientes con diagnóstico reciente de cardiopatía isquémica y encontrar la más prevalente.

Métodos: Se realizó un estudio transversal y descriptivo. Se incluyeron pacientes atendidos en el servicio de cardiología del Hospital Luis Vernaza, entre enero de 2012 e igual mes de 2013, que hayan padecido su primer evento de cardiopatía isquémica. De 220 pacientes con dicho diagnóstico, se excluyeron 131 que no cumplían los criterios de inclusión. La muestra final fue de 89 pacientes.

Resultados: Cuarenta y un pacientes (46,06%) mostraban HDL bajo, 49 (55,05%) LDL alto, 28 (31,46%) triglicéridos altos, 24 (26,96%) colesterol elevado, 25 (28,08%) VLDL alto, 26 (29,21%) valores superiores a 5 del índice de Castelli y 32 (35,95%) presentaban valores superiores a 3 de la razón LDL/HDL.

Discusión: Es de enorme importancia contar con un perfil lipídico completo en pacientes con diagnóstico reciente de cardiopatía isquémica para la prevención secundaria. La alteración del perfil lipídico más prevalente entre los pacientes estudiados fue el colesterol LDL. El porcentaje de pacientes con HDL anormal fue similar al de otras poblaciones latinoamericanas. Es necesario realizar estudios descriptivos similares en la población general.

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national center for biotechnology information

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[Lipid profile in patients with newly diagnosed coronary heart disease: 2012 and 2013 cross-sectional study in Luis Vernaza Hospital, Ecuador] - PubMed

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It is of great importance to have a complete lipid profile from patients recently diagnosed with ischemic heart disease in order to work on secondary prevention. The most prevalent alteration found in our study was high LDL levels. The percentage of patients with low HDL was similar to other Latin A ...

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TITULO: Prevalencia de hipercolesterolemia familiar en población general y pacientes con enfermedad cardiovascular aterosclerótica.
TIPO DE ESTUDIO: Revisión sistemática y metaanálisis.
AÑO: 2020
OBJETIVO: Proporcionar una evaluación integral y una estimación más confiable de la prevalencia de Hipercolesterolemia familiar (HF)que hasta ahora es posible en la población general (GP) y entre pacientes con ASCVD.
RESULTADOS: La heterogeneidad entre los estudios fue grande ( I ² >95%). Las pruebas que evaluaron el sesgo no fueron significativas ( P > 0,3).
CONCLUSIONES: Con una prevalencia general de 1:311, la HF se encuentra entre los trastornos genéticos más comunes en el médico de cabecera, se presenta de manera similar en diferentes regiones del mundo y es más frecuente entre aquellos con ASCVD.

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Prevalence of Familial Hypercholesterolemia Among the General Population and Patients With Atherosclerotic Cardiovascular Disease: A Systematic Review and Meta-Analysis - PubMed

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With an overall prevalence of 1:311, FH is among the commonest genetic disorders in the GP, similarly present across different regions of the world, and is more frequent among those with ASCVD. The present results support the advocacy for the institution of public health policies, including screenin…

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5946253/
TITULO: Almendras y Salud Cardiovascular: Una Revisión
AÑO: 2017
RESULTADOS: Un análisis de 101 estudios encontró una relación causal entre la hipertrigliceridemia y la EAC
CONCLUSIONES:Se ha demostrado que las almendras reducen el LDL-C, que es un factor de riesgo conocido para la enfermedad coronaria en varios ensayos clínicos bien realizados. Los estudios también han analizado el efecto de las almendras en el HDL-C y se ha descubierto que el consumo de almendras ha ayudado a mantener o incluso aumentar los niveles de HDL-C. El consumo diario de alrededor de 45 g de almendras puede ayudar a reducir uno de los factores de riesgo más importantes de ECV en los indios, a saber. dislipidemia. La adición de almendras enteras en la dieta es una estrategia nutricional segura y práctica que se puede recomendar para controlar la dislipidemia. Es necesario realizar más estudios para investigar el mecanismo de acción responsable del efecto de las almendras sobre la dislipidemia, así como su efecto sobre el tamaño de las partículas lipídicas y la salud vascular.

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Almonds and Cardiovascular Health: A Review

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Several preventive strategies to reduce dyslipidemia have been suggested, of which dietary modification features as an important one. Dyslipidemia is a major risk factor for coronary heart disease and strategies to manage dyslipidemia have been shown ...

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Título :Prevalencia de dislipidemias y consumo de alimentos: un estudio de base poblacional
Tipo de estudio y año: ECA,2021
Resultado : La muestra estuvo compuesta por 884 individuos, de los cuales el 52,31% eran hombres y con una edad media de 37,7 años. De acuerdo con los datos presentados , la mayor parte pertenecía a individuos entre 20 y 29 años (31,80%) y el 46,32% del exceso de peso presentado. Los dislipidémicos presentan mayor escolaridad, mayor IMC y perímetro de cintura elevado en comparación con los dislipidémicos (p<0,001).La prevalencia de dislipidemia fue del 64,25%. Sin embargo, no hubo diferencia estadística en la adecuación de la ingesta de grasas y carbohidratos entre individuos con y sin dislipidemia.
Conclusión: Se concluye que en esta muestra representativa de la población de Viçosa-MG, Brasil, existe alta prevalencia de dislipidemia, ingesta excesiva de grasas saturadas, grasas trans y carbohidratos, además de ingesta subóptima de grasas monoinsaturadas. La ingesta alta de grasas saturadas y trans fue mayor entre los individuos con HDL-c y proporciones altas de TG/HDL, CT/HDL y LDL/HDL, y los individuos con colesterol total normal tenían un mayor porcentaje de adecuación de la ingesta de omega-3.

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Prevalência de dislipidemias e consumo alimentar: um estudo de base populacional

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Resumo O presente artigo objetivou estimar a prevalência de dislipidemias e sua associação e...

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http://bonga.unisimon.edu.co/handle/20.500.12442/4607

TITULO: Comportamiento epidemiológico de las dislipidemias en pacientes del Instituto de Investigaciones Endocrino-Metabólicas Dr. Félix Gómez, Venezuela.

OBJETIVO: Estudiar las alteraciones lipídicas en individuos adultos de un centro de atención endocrino-metabólico.

TIPO DE ESTUDIO: Estudio descriptivo, no experimental, y transversal.

AÑO: 2019

RESULTADOS: El 78% de la muestra correspondió al sexo femenino. La media aritmética de la edad fue de 50,22± 16,4 años. La prevalencia general de dislipidemias fue del 86,9% (n=214), siendo del 91,6% en las mujeres y del 70,2% en los hombres; solo el 13,0% (n=28) de los individuos fueron eulipémicos. La frecuencia de las dislipidemias observadas fue: LDL-c elevado aislado 24,7%, Hipertriacilgliceridemia aislada 18,2%, Hipertriacilgliceridemia con HDL-c Bajas 13,5%, Dislipidemia Mixta 13,5%.

CONCLUSIONES: La alta prevalencia de dislipidemias en los pacientes estudiados es característica de un centro para la atención de estas patologías, observándose una prevalencia elevada de HDL-c bajas e Hipertriacilgliceridemia. Estos resultados justifican la determinación de lípidos séricos para identificar de manera temprana y oportuna este conjunto de alteraciones con la finalidad de prevenir potenciales complicaciones cardiometabólicas.

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Comportamiento epidemiológico de las dislipidemias en pacientes del Instituto de Investigaciones Endocrino-Metabólicas Dr. Félix Gómez, Venezuela

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Repositorio institucional de la Universidad Simón Bolívar.

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TÍTULO:  Prevalencia de dislipidemias en pacientes obesos

TIPO DE ESTUDIO:  estudio correlacional, retrospectivo y transversal de 150 pacientes obesos, quienes acudieron a la consulta externa de la Clínica Medina del Hospital Básico de Guayaquil, desde el 2018 hasta el 2019.
AUTOR: RUIZ LOPEZ, Juan Carlos; LETAMENDI VELASCO, Jaime Alfredo  y  CALDERON LEON, Roberto André
RESULTADOS: En la serie predominaron el sexo masculino (62,6%), los pacientes con más de 65 años de edad (42,0 %), los niveles entre rango crítico y alto riesgo (66 pacientes); 16,0 % se clasificaron de alto riesgo con niveles de colesterol superior a 240 mg/dL. Mostraron resultados anormales en cuanto a los triglicéridos 62 afectados, en un rango mayor de 150 con niveles y limítrofe altos.

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http://bonga.unisimon.edu.co/handle/20.500.12442/4607
Comportamiento epidemiológico de las dislipidemias en pacientes del Instituto de Investigaciones Endocrino-Metabólicas Dr. Félix Gómez, Venezuela

Tipo de estudio: Estudio descriptivo, no experimental, y transversal.
Año: 2019
Objetivo: Estudiar las alteraciones lipídicas en individuos adultos de un centro de atención endocrino-metabólico.
Resultados: El 78% de la muestra correspondió al sexo femenino. La media aritmética de la edad fue de 50,22± 16,4 años. La prevalencia general de dislipidemias fue del 86,9% (n=214), siendo del 91,6% en las mujeres y del 70,2% en los hombres; solo el 13,0% (n=28) de los individuos fueron eulipémicos. La frecuencia de las dislipidemias observadas fue: LDL-c elevado aislado 24,7%, Hipertriacilgliceridemia aislada 18,2%, Hipertriacilgliceridemia con HDL-c Bajas 13,5%, Dislipidemia Mixta 13,5%.
Conclusión: La alta prevalencia de dislipidemias en los pacientes estudiados es característica de un centro para la atención de estas patologías, observándose una prevalencia elevada de HDL-c bajas e Hipertriacilgliceridemia. Estos resultados justifican la determinación de lípidos séricos para identificar de manera temprana y oportuna este conjunto de alteraciones con la finalidad de prevenir potenciales complicaciones cardiometabólicas.

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Comportamiento epidemiológico de las dislipidemias en pacientes del Instituto de Investigaciones Endocrino-Metabólicas Dr. Félix Gómez, Venezuela

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Repositorio institucional de la Universidad Simón Bolívar.

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TÍTULO:  Epidemiología de la dislipidemia y los factores de riesgo cardiovascular asociados en el noreste de China: un estudio transversal
AÑO: 2020
TIPO DE ESTUDIO: Estudio transversal
Antecedentes y objetivos: El manejo de la dislipemia sigue siendo la piedra angular para la prevención de las enfermedades cardiovasculares. Nuestro objetivo fue evaluar la epidemiología de la dislipidemia en el noreste de China.
RESULTADOS:  Esta encuesta transversal se administró a 18 796 participantes de ≥40 años desde septiembre de 2017 hasta marzo de 2019 a través de un método de muestreo multietápico, estratificado y aleatorio por conglomerados.
La prevalencia estandarizada por edad de dislipidemia fue de 34,0% (urbana 47,9% y rural 28,9%; hombres 36,2% y mujeres 33,4%). Las prevalencias de colesterol total (CT) alto, triglicéridos (TG) altos, colesterol de lipoproteínas de baja densidad (LDL-C) alto y colesterol de lipoproteínas de alta densidad (HDL-C) bajo fueron 14.2%, 17.7%, 5.7% y 11.4 % respectivamente. Notablemente, la prevalencia de C-LDL alto y C-HDL bajo en las zonas urbanas mostró un aumento de 2,2 y 6,3 veces respecto de las zonas rurales (9,3 % frente a 4,2 % y 28,4 % frente a 4,5 %, respectivamente). Entre los participantes con dislipidemia, el 14,7% conocía su condición; el 5,9% tomaba medicamentos reguladores de lípidos; y solo el 2,9% tenía controlada la dislipidemia. Las comorbilidades, incluida la hipertensión (63,6 %) y la diabetes (25,2 %), fueron muy prevalentes en los pacientes con dislipidemia; sin embargo, las tasas de control de esas comorbilidades fueron solo del 40,0 % y el 6,6 %.
CONCLUSIONES: Los pacientes con dislipidemia presentaron alta carga cardiovascular con bajas tasas de control de la dislipidemia, alta prevalencia de factores de riesgo coexistentes. Por lo tanto, deben destacarse las estrategias específicas de la región y el sexo para controlar la dislipidemia y los factores de riesgo relacionados.

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Affiliations

¹ Department of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China; Department of Chronic Disease, Liaoning Provincial Center for Disease Control and Prevention, Shenyang, Liaoning, People's Republic of China.

² Department of Chronic Disease, Liaoning Provincial Center for Disease Control and Prevention, Shenyang, Liaoning, People's Republic of China.

³ Department of Chronic Disease, Disease Control and Prevention of Chao Yang City, Chaoyang, Liaoning, People's Republic of China.

⁴ Department of Chronic Disease, Disease Control and Prevention of Dan Dong City, Dan Dong, Liaoning, People's Republic of China.

⁵ Department of Chronic Disease, Disease Control and Prevention of Liao Yang City, Liaoyang, Liaoning, People's Republic of China.

⁶ Department of Cardiovascular Ultrasound, The First Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China. Electronic address: liushuang_cmu1h@163.com.

Affiliations

¹ Department of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China; Department of Chronic Disease, Liaoning Provincial Center for Disease Control and Prevention, Shenyang, Liaoning, People's Republic of China.

² Department of Chronic Disease, Liaoning Provincial Center for Disease Control and Prevention, Shenyang, Liaoning, People's Republic of China.

³ Department of Chronic Disease, Disease Control and Prevention of Chao Yang City, Chaoyang, Liaoning, People's Republic of China.

⁴ Department of Chronic Disease, Disease Control and Prevention of Dan Dong City, Dan Dong, Liaoning, People's Republic of China.

⁵ Department of Chronic Disease, Disease Control and Prevention of Liao Yang City, Liaoyang, Liaoning, People's Republic of China.

⁶ Department of Cardiovascular Ultrasound, The First Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China. Electronic address: liushuang_cmu1h@163.com.

Abstract

Background and aims: Management of dyslipidemia remains the cornerstone for prevention of cardiovascular diseases. We aimed to evaluate the epidemiology of dyslipidemia in northeast China.

Methods and results: This cross-sectional survey was administered on 18,796 participants aged ≥40 years from September 2017 to March 2019 through a multistage, stratified, and cluster random sampling method. Lipid profiles were proposed by National Cholesterol Education Program Adult Treatment Panel III. The crude prevalence of dyslipidemia was 35.8%, higher in urban and women than their counterparts (49.5% vs 30.2%, 37.6% vs 33.0%, p < 0.001). The age-standardized prevalence of dyslipidemia was 34.0% (urban 47.9%, and rural 28.9%; men 36.2%, and women 33.4%). The prevalence of high total cholesterol (TC), high triglyceride (TG), high low-density lipoprotein cholesterol (LDL-C) and low high-density lipoprotein cholesterol (HDL-C) were 14.2%, 17.7%, 5.7% and 11.4% respectively. Noticeably, the prevalence of high LDL-C and low HDL-C in urban areas showed a 2.2-fold and 6.3-fold increase over the rural areas (9.3% vs 4.2% and 28.4% vs 4.5%, respectively). Among participants with dyslipidemia, 14.7% were aware of their condition; 5.9% were taking lipid-regulating medications; and only 2.9% had their dyslipidemia controlled. Comorbidities including hypertension (63.6%), and diabetes (25.2%) were highly prevalent in patients with dyslipidemia, however, the control rates of those comorbidities were only 40.0% and 6.6%.

Conclusions: Patients with dyslipidemia showed high cardiovascular burden with low control rates of dyslipidemia, high prevalence of coexisting risk factors. Therefore, region- and sex-specific strategies to manage dyslipidemia and related risk factors should be highlighted.

Keywords: China; Control; Dyslipidemia; Prevalence; Risk factors.

Conflict of interest statement

Declaration of competing interest The authors declared they have no competing interests.

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Epidemiology of dyslipidemia and associated cardiovascular risk factors in northeast China: A cross-sectional study - PubMed

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1 Department of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning, People's Republic of China; Department of Chronic Disease, Liaoning Provincial Center for Disease Control and Prevention, Shenyang, Liaoning, People's Republic of China. 2 Department of Chronic Disease, Liaoning Provincial Center for Disease Control and Prevention, Shenyang, Liaoning, People's Republic of China.

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TÍTULO:  Estudio Descriptivo: Prevalencia de Dislipidemia en Adultos de 40 - 64 Años, Cuenca - Ecuador, Enero a Julio 2014
TIPO: Estudio descriptivo
AÑO: 2014
CONCLUSIONES: El promedio de edad de las personas con dislipidemia fue de 51 años, de los cuales el 71.9% fueron mujeres. La prevalencia de hipercolesterolemia fue 38.5%; en relación al sexo existió predominio en las mujeres con 34.4%, en los hombres el 28.7%. La prevalencia de hipertrigliceridemia fue de 58.5%.

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https://pubmed.ncbi.nlm.nih.gov/29366425/
TITULO:

Hipertrigliceridemia: causas comunes, estrategias de prevención y tratamiento

TIPO DE ESTUDIO:
Revisión sistemática
AÑO:
2018
OBJETIVO:
El objetivo de esta revisión es facilitar la traducción de las tendencias actuales en el manejo de la hipertrigliceridemia a la práctica diaria. El artículo se centra en las causas y consecuencias comunes de la hipertrigliceridemia.
CONCLUSIONES:
Esta revisión presenta las principales estrategias relacionadas con la práctica, basadas en las guías actuales para el manejo de las dislipidemias y el riesgo de ECV, según la Sociedad Europea de Cardiología (ESC), la Sociedad Europea de Aterosclerosis (EAS) y el Colegio Americano de Cardiología (ACC)/Asociación Americana del Corazón (AHA), incluidos los enfoques no farmacológicos y farmacológicos. También aborda el impacto beneficioso de las intervenciones de atención farmacéutica (AP) en los resultados clínicos de los pacientes con trastornos de lípidos y riesgo de ECV (a la luz de los datos de los ensayos controlados aleatorios (RCT)), y subraya la importancia de una estrecha cooperación entre médicos y farmacéuticos, que manejar este tipo de pacientes.

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. 2018 Mar 14;14(1):67-76.

doi: 10.2174/1573403X14666180123165542.

Affiliation

¹ Department of Family Practice, Medical University of Silesia (SUM), Katowice-Zabrze, Poland.

Free PMC article

Katarzyna Rygiel . Curr Cardiol Rev.

Free PMC article

. 2018 Mar 14;14(1):67-76.

doi: 10.2174/1573403X14666180123165542.

Affiliation

¹ Department of Family Practice, Medical University of Silesia (SUM), Katowice-Zabrze, Poland.

Abstract

Background: Prevention and treatment of dyslipidemias represent the key issues of Cardiovascular Disease (CVD) prophylaxis. Consequently, the effective management of different types of lipid disorders, including hypertriglyceridemia, should be a priority for the healthcare practitioners (e.g.: cardiology and endocrinology specialists, primary care physicians, dietitians, and pharmacists), who provide medical care, as well as for the patients, who receive this care, and need to be directly engaged in it, in order to improve their outcomes. The aim of this review is to facilitate the translation of current trends in hypertriglyceridemia management into a daily practice. The article focuses on the common causes and consequences of hypertriglyceridemia, and discusses diagnostic evaluation and therapeutic options for patients with high Triglyceride (TG) levels and CVD risk.

Conclusion: This review presents the main practice-related strategies, based on the current guidelines for the management of dyslipidemias and CVD risk, according to the European Society of Cardiology (ESC), the European Atherosclerosis Society (EAS), and the American College of Cardiology (ACC)/American Heart Association (AHA), including both non-pharmacological, and pharmacological approaches. It also addresses the beneficial impact of pharmaceutical Care (PC) interventions on clinical outcomes of patients with lipid disorders and CVD risk (in light of Randomized Controlled Trials (RCT) data), and underlines the importance of close cooperation between physicians and pharmacists, who manage such patients.

Keywords: Cardiovascular Diseases (CVD); Pharmaceutical Care (PC); Triglyceride (TG) levels.; dyslipidemia; hypertriglyceridemia; patient management.

Figures

References

Reiner Z, Catapano AL, De Backer G, et al. European Association for Cardiovascular Prevention Rehabilitation1. The Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS) ESC/EAS Guidelines for the management of dyslipidaemias. Eur Heart J. 2011;32:1769-818. - PubMed

Miller M., Stone N.J., Ballantyne C., et al. The american heart association clinical lipidology, thrombosis, and prevention committee of the council on nutrition, physical activity and metabolism, council on arteriosclerosis, thrombosis and vascular biology, council on cardiovascular nursing, and council on the kidney in cardiovascular disease. Triglycerides and cardiovascular disease: A scientific statement from the American Heart Association. Circulation. 2011;123:2292-2333. - PubMed

Stone N.J., Robinson J.G., Lichtenstein A.H., et al. The American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014;129(25) Suppl. 2:S1-S45. - PubMed

Ray K.K., Kastelein J.J., Boekholdt S.M., et al. The ACC/AHA 2013 guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular disease risk in adults: The good the bad and the uncertain: A comparison with ESC/EAS guidelines for the management of dyslipidaemias 2011. Eur. Heart J. 2014;35:960-968. - PubMed

Jellinger P.S., Smith D.A., Mehta A.E., et al. American Association of Clinical Endocrinologists' guidelines for management of dyslipidemia and prevention of atherosclerosis. Endocr. Pract. 2012;18(Suppl. 1):1-78. - PubMed

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hypertriglyceridemia* / prevention & control

# data[].attributes.attachment_link.keywords[]
national center for biotechnology information

# data[].attributes.attachment_link.title
Hypertriglyceridemia - Common Causes, Prevention and Treatment Strategies - PubMed

# data[].attributes.attachment_link.description
This review presents the main practice-related strategies, based on the current guidelines for the management of dyslipidemias and CVD risk, according to the European Society of Cardiology (ESC), the European Atherosclerosis Society (EAS), and the American College of Cardiology (ACC)/American Heart ...

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Epidemiología:
Título: Prevalencia de dislipidemia en niños y adolescentes chinos: un metanálisis
Año: 2015
Autor: Ding Wenqing, Hongbo-dong, Jie Mi
Objetivo: Cuantificar la prevalencia de dislipidemia entre niños y adolescentes en China.
Método: Búsquedas exhaustivas en la base de datos biomédica china (CBM), las bases de datos de Wanfang, la infraestructura de conocimiento nacional de China (CNKI) y PubMed. La prevalencia : software Strata 11.0. Se realizó un análisis de subgrupos sobre temas de género, edad, regiones y tendencias seculares. Se realizó un análisis de sensibilidad para evaluar el impacto de la calidad o el estándar de diagnóstico.
Muestras: 24 artículos, con un tamaño total de la muestra de 129 426
Resultado: La prevalencia global combinada de dislipidemia total se estimó en un 25,3 % (IC del 95 %: 12,7 %-37,8 %). Las tasas de prevalencia de CT alto, LDL-C, TG, HDL-C bajo e hiperlipemia fueron 4,1 % (IC 95 %: 3,4 %-4,9 %), 5,3 % (IC 95 %: 3,9 %-6,7 %), 8,5 % ( IC del 95 %:6,3 %-10,7 %), 6,8 % (IC del 95 %: 3,7 %-9,9 %), 4,8 % (IC del 95 %:0,6 %-9,1 %), respectivamente. Las niñas (3,4%) tenían menor prevalencia de TG elevados que los niños (5,6%), pero tenían mayor prevalencia de otros tipos diferentes de dislipemia. Los niños de 7 a 18 años tenían una mayor prevalencia general de dislipidemia (31,6 %) en comparación con los niños de 2 a 6 años (9,0 %). No hubo diferencias estadísticamente significativas por subgrupos de edad, región y período en cuanto a las tasas de prevalencia de TG elevados, CT y HDL-C bajos (P > 0,05).
Conclusión: La prevalencia de dislipidemia fue alta y con tendencia creciente entre niños y adolescentes en China. Deben enfatizarse y promoverse programas de prevención y detección temprana de lípidos séricos anormales.

https://pubmed.ncbi.nlm.nih.gov/25876870/

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Affiliations

¹ Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College; School of Public Health, Ningxia Medical University.

² Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College.

³ Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College. Email: jiemi@vip.163.com.

Affiliations

¹ Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College; School of Public Health, Ningxia Medical University.

² Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College.

³ Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College. Email: jiemi@vip.163.com.

Abstract

Objective: To quantify the prevalence of dyslipidemia among children and adolescents in China.

Methods: Chinese Biomedical Database (CBM), Wanfang Databases, China National Knowledge Infrastructrue (CNKI) and PubMed were comprehensively searched. Original reports were selected if data on prevalence estimates of dyslipdemia among children and adolescents in China, was provided under cross-sectional epidemiological studies. Quality of the literature was evaluated through the STROBE statement. The prevalence through Meta was estimated using the Strata 11.0 software. Subgroup analysis was undertaken on gender, age, regions and secular trends issues. Sensitivity analysis was performed to evaluate the impact of quality or standard of diagnosis.

Results: A total of 24 papers were included in this Meta-analysis, with the whole sample size as 129 426. The overall pooled-prevalence of total dsylipidemia was estimated at 25.3% (95% CI: 12.7%-37.8%). Prevalence rates of high TC, LDL-C, TG, low HDL-C and hyperlipemia were 4.1% (95% CI:3.4%-4.9%), 5.3% (95% CI:3.9%-6.7%), 8.5% (95% CI:6.3%-10.7%), 6.8% (95% CI: 3.7%-9.9%), 4.8% (95%CI:0.6%-9.1%), respectively. Girls (3.4%) had lower prevalence of high TG than boys (5.6%), but having higher prevalence of other different types dyslipidemia. Children aged 7-18 years had higher overall prevalence of dyslipidemia (31.6%) when compared to children aged 2-6 years (9.0%). There were no statistically significant differences for subgroups of age, region and period regarding the prevalence rates of high TG, TC and low HDL-C(P > 0.05).

Conclusion: Prevalence of dyslipidemia was high and with increasing trend among children and adolescents in China. Early screening and prevention programs on abnormal serum lipids should be emphasized and promoted.

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He H, Pan L, Du J, Liu F, Jin Y, Ma J, Wang L, Jia P, Hu Z, Shan G. He H, et al. Am J Hum Biol. 2019 Sep;31(5):e23286. doi: 10.1002/ajhb.23286. Epub 2019 Jun 28. Am J Hum Biol. 2019. PMID: 31254309

Maternal gestational diabetes and childhood hyperlipidemia.

Yang X, Leng J, Liu H, Wang L, Li W, Li W, Yang X, Liu M, Hu G. Yang X, et al. Diabet Med. 2021 Nov;38(11):e14606. doi: 10.1111/dme.14606. Epub 2021 Jun 2. Diabet Med. 2021. PMID: 34021927

# data[].attributes.attachment_link.keywords[]
national center for biotechnology information

# data[].attributes.attachment_link.title
[Prevalence of dyslipidemia in Chinese children and adolescents:a Meta-analysis] - PubMed

# data[].attributes.attachment_link.description
1 Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College; School of Public Health, Ningxia Medical University. 2 Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College. 3 Department of Epidemiology, Capital Institute of Pediatrics, Beijing 100020, China; Graduate School, Peking Union Medical College.

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Título:

Eficacia del entrenamiento con ejercicio físico de bajo a moderado sobre el nivel de lipoproteínas de baja densidad: una revisión sistemática

Tipo de estudio: Revisión sistemática.
Año: 2018
Resultados: El ejercicio aeróbico de intensidad baja y moderada resultó en una reducción significativa del colesterol total. Los efectos sobre los niveles de lipoproteínas de baja densidad fueron significativos y la mayoría de los estudios mostraron cambios en el nivel sin relación significativa con el tipo de ejercicio. Al mismo tiempo, el ejercicio mejoró el estado de salud y la condición física de todos los participantes en los estudios incluidos.

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Effectiveness of Low to Moderate Physical Exercise Training on the Level of Low-Density Lipoproteins: A Systematic Review

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Regular exercise reduces risk factors associated with cardiovascular disease (CVD). Elevated low-density lipoprotein (LDL) contributes to atherosclerosis formation, which is associated with an increased risk of CVD. The relationship between exercise ...

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https://www.revespcardiol.org/es-
magnitud-manejo-hipercolesterolemia-poblacion-adulta-articulo-S030089321200139X
TÍTULO: Magnitud y manejo de la hipercolesterolemia en la población adulta de España, 2008-2010, el estudio ENRICA
TIPO DE ESTUDIO: Estudio transversal
AÑO DE PUBLICACIÓN: 2012
AUTORES: Guallar P., Gil M.,  León L. etal.
RESULTADOS: De la población adulta, el 50,5% tenía hipercolesterolemia (colesterol total ≥ 200mg/dl o tratamiento farmacológico) y el 44,9% colesterol unido a lipoproteínas de baja densidad elevado (≥ 130mg/dl o tratamiento farmacológico). Además, el 25,5% de los varones tenían colesterol unido a lipoproteínas de alta densidad < 40mg/dl y el 26,4% de las mujeres, colesterol unido a lipoproteínas de alta densidad < 50mg/dl. Entre los que tenían el colesterol unido a lipoproteínas de baja densidad elevado, el 53,6% lo sabían; de ellos, el 44,1% estaba tratado con hipolipemiantes, y de estos, el 55,7% estaba controlado (el 13,2% de todos los hipercolesterolémicos). El control del colesterol unido a lipoproteínas de baja densidad elevado aumentó con la edad y con el número de visitas al especialista, pero disminuyó en personas diabéticas (odds ratio=0,38; intervalo de confianza del 95%, 0,28-0,53) o con enfermedad cardiovascular (odds ratio=0,55; intervalo de confianza del 95%, 0,33-0,92).
CONCLUSIONES: Aproximadamente la mitad de los españoles tienen colestererolemia elevada; el control del colesterol es pobre, particularmente en aquellos con mayor riesgo cardiovascular, como los diabéticos o los enfermos cardiovasculares.

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Magnitud y manejo de la hipercolesterolemia en la población adulta de España, 2008-2010, el estudio ENRICA | Revista Española de Cardiología

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Introducción y objetivosPocos estudios han reportado datos nacionales de base poblacional sobre

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EPIDEMIOLOGÍA
Título: Prevalencia de dislipidemias en pacientes obesos.
Autor: Ruiz J, Letamendi J.

Año de publicación: 2020
Objetivo: Determinar la prevalencia de dislipidemias en pacientes obesos.
Métodos: Se realizó un estudio correlacional, retrospectivo y transversal de150 pacientes obesos, quienes acudieron a la consulta externa de la Clínica Medina del Hospital Básico de Guayaquil, desde el 2018 hasta el 2019. Las variables analizadas fueron edad, sexo, índice de masa corporal y resultados de laboratorio, tales como colesterol total, triglicéridos, colesterol LDL y dislipidemia mixta (colesterol HDL y VLDL).
Resultados: En la serie predominaron el sexo masculino (62,6%), los pacientes con más de 65 años de edad (42,0 %), los niveles entre rango crítico y alto riesgo (66 pacientes); 16,0 % se clasificaron de alto riesgo con niveles de colesterol superior a 240 mg/dL. Mostraron resultados anormales en cuanto a los triglicéridos 62 afectados, en un rango mayor de 150 con niveles y limítrofe altos.
Conclusiones: Se observó una correspondencia entre las dislipidemias y la obesidad, pues todos los pacientes presentaron algún tipo de alteración en los lípidos.

http://scielo.sld.cu/scielo.php?script=sci_arttext&pid=S1029-30192020000200211

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https://pubmed.ncbi.nlm.nih.gov/32439005/
TITULO: Prevalencia mundial de hipercolesterolemia familiar: metanálisis de 11 millones de sujetos.
TIPO DE ESTUDIO: Revisión sistemática y metánalisis.
AÑO: 2020
RESULTADOS: Las estimaciones de la prevalencia de HF se agruparon mediante metanálisis de efectos aleatorios y fueron del 0,32 % (intervalo de confianza [IC] del 95 %: 0,26 % a 0,39 % [correspondiente a 1:313]) entre 10 921 310 sujetos únicos en la población general (33 036 pacientes con HF) sobre la base de 44 estudios, 3,2 % (IC del 95 %: 2,2 % a 4,3 % [1:31]) entre 84 479 sujetos únicos con cardiopatía isquémica (2103 pacientes con HF) sobre la base de 28 estudios, 6,7 % ( IC del 95 %: del 4,9 % al 8,7 % [1:15]) entre 31 316 sujetos únicos con cardiopatía isquémica prematura (1471 pacientes con HF) sobre la base de 32 estudios, y el 7,2 % (IC del 95 %: del 4,6 % al 10,8 % [1 :14]) entre 17 728 sujetos únicos con hipercolesterolemia grave (920 pacientes con HF) sobre la base de 7 estudios. La prevalencia de HF en la población general fue similar utilizando diagnósticos genéticos versus clínicos.
CONCLUSIÓN: En comparación con 1:313 entre los sujetos de la población general, la prevalencia de HF es 10 veces mayor entre aquellos con CI, 20 veces mayor entre aquellos con CI prematura y 23 veces mayor entre aquellos con hipercolesterolemia severa. La prevalencia de HF es desconocida en el 90% de los países del mundo.

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Affiliations

¹ Department of Clinical Biochemistry and the Copenhagen General Population Study, Herlev and Gentofte Hospital, Copenhagen University Hospital, Herlev, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

² Department of Clinical Biochemistry and the Copenhagen General Population Study, Herlev and Gentofte Hospital, Copenhagen University Hospital, Herlev, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Electronic address: boerge.nordestgaard@regionh.dk.

Free article

Free article

Affiliations

¹ Department of Clinical Biochemistry and the Copenhagen General Population Study, Herlev and Gentofte Hospital, Copenhagen University Hospital, Herlev, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

² Department of Clinical Biochemistry and the Copenhagen General Population Study, Herlev and Gentofte Hospital, Copenhagen University Hospital, Herlev, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Electronic address: boerge.nordestgaard@regionh.dk.

Abstract

Background: Despite the greater prevalence of familial hypercholesterolemia (FH) in subjects with ischemic heart disease (IHD), premature IHD, and severe hypercholesterolemia (low-density lipoprotein ≥190 mg/dl), overall prevalence estimates are not available.

Objectives: The aim of this study was to provide worldwide estimates of FH prevalence in subjects with IHD, premature IHD, and severe hypercholesterolemia compared with those in the general population.

Methods: In this systematic review and meta-analyses, Embase, PubMed, and the Web of Science were searched until June 3, 2019, for peer-reviewed papers and conference abstracts reporting heterozygous FH prevalence in nonfounder populations, revealing 104 studies eligible for inclusion.

Results: Estimates of FH prevalence were pooled using random-effects meta-analyses and were 0.32% (95% confidence interval [CI]: 0.26% to 0.39% [corresponding to 1:313]) among 10,921,310 unique subjects in the general population (33,036 patients with FH) on the basis of 44 studies, 3.2% (95% CI: 2.2% to 4.3% [1:31]) among 84,479 unique subjects with IHD (2,103 patients with FH) on the basis of 28 studies, 6.7% (95% CI: 4.9% to 8.7% [1:15]) among 31,316 unique subjects with premature IHD (1,471 patients with FH) on the basis of 32 studies, and 7.2% (95% CI: 4.6% to 10.8% [1:14]) among 17,728 unique subjects with severe hypercholesterolemia (920 patients with FH) on the basis of 7 studies. FH prevalence in the general population was similar using genetic versus clinical diagnoses. Seventeen of 195 countries (9%) in the world have reported FH prevalence for the general population, leaving 178 (91%) countries in the world with unknown prevalence.

Conclusions: Compared with 1:313 among subjects in the general population, FH prevalence is 10-fold higher among those with IHD, 20-fold higher among those with premature IHD, and 23-fold higher among those with severe hypercholesterolemia. The prevalence of FH is unknown in 90% of countries in the world.

Keywords: epidemiology; frequency; myocardial infarction; premature; severe hypercholesterolemia; systematic review.

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Prevalence of Familial Hypercholesterolemia Among the General Population and Patients With Atherosclerotic Cardiovascular Disease: A Systematic Review and Meta-Analysis.

Hu P, Dharmayat KI, Stevens CAT, Sharabiani MTA, Jones RS, Watts GF, Genest J, Ray KK, Vallejo-Vaz AJ. Hu P, et al. Circulation. 2020 Jun 2;141(22):1742-1759. doi: 10.1161/CIRCULATIONAHA.119.044795. Epub 2020 May 29. Circulation. 2020. PMID: 32468833

The molecular genetic basis and diagnosis of familial hypercholesterolemia in Denmark.

Efficiency and problems of statin therapy in patients with heterozygous familial hypercholesterolemia.

Korneva V, Kuznetsova T, Julius U. Korneva V, et al. Atheroscler Suppl. 2019 Dec;40:79-87. doi: 10.1016/j.atherosclerosissup.2019.08.029. Epub 2019 Aug 17. Atheroscler Suppl. 2019. PMID: 31818452

Spectrum of mutations of familial hypercholesterolemia in the 22 Arab countries.

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Two Novel Disease-Causing Mutations in the LDLR of Familial Hypercholesterolemia.

Hu H, Shu T, Ma J, Chen R, Wang J, Wang S, Lin S, Chen X. Hu H, et al. Front Genet. 2021 Dec 14;12:762587. doi: 10.3389/fgene.2021.762587. eCollection 2021. Front Genet. 2021. PMID: 34970301 Free PMC article.

# data[].attributes.attachment_link.keywords[]
hyperlipoproteinemia type ii / epidemiology*

# data[].attributes.attachment_link.keywords[]
hyperlipoproteinemia type ii / ethnology

# data[].attributes.attachment_link.keywords[]
national center for biotechnology information

# data[].attributes.attachment_link.title
Worldwide Prevalence of Familial Hypercholesterolemia: Meta-Analyses of 11 Million Subjects - PubMed

# data[].attributes.attachment_link.description
Compared with 1:313 among subjects in the general population, FH prevalence is 10-fold higher among those with IHD, 20-fold higher among those with premature IHD, and 23-fold higher among those with severe hypercholesterolemia. The prevalence of FH is unknown in 90% of countries in the world.

# data[].attributes.body
TITILO: Prevalencia mundial de hipercolesterolemia familiar: metanálisis de 11 millones de sujetos.
TIPÓ DE ESTUDIO: Metaanálisis
AÑO: 2020
OBJETIVO: Proporcionar estimaciones mundiales de la prevalencia de HF en sujetos con cardiopatía isquémica, cardiopatía isquémica prematura e hipercolesterolemia grave en comparación con la población general.
RESULTADOS: Las estimaciones de la prevalencia de hipercolesterolemia familiar (HF)  se agruparon mediante metaanálisis de efectos aleatorios y fueron del 0,32 % (IC del 95 %: 0,26 % a 0,39 % [correspondiente a 1:313]) entre 10 921 310 sujetos únicos en la población general (33 036 pacientes con HF) sobre la base de 44 estudios, 3,2 % (IC del 95 %: 2,2 % a 4,3 % [1:31]) entre 84 479 sujetos únicos con cardiopatía isquémica (2103 pacientes con HF) sobre la base de 28 estudios, 6,7 % ( IC del 95 %: del 4,9 % al 8,7 % [1:15]) entre 31 316 sujetos únicos con cardiopatía isquémica prematura (1471 pacientes con HF) sobre la base de 32 estudios, y el 7,2 % (IC del 95 %: del 4,6 % al 10,8 % [1 :14]) entre 17 728 sujetos únicos con hipercolesterolemia grave (920 pacientes con HF) sobre la base de 7 estudios.
CONCLUSIÓN: En comparación con 1:313 entre los sujetos de la población general, la prevalencia de HF es 10 veces mayor entre aquellos con CI, 20 veces mayor entre aquellos con CI prematura y 23 veces mayor entre aquellos con hipercolesterolemia severa. La prevalencia de HF es desconocida en el 90% de los países del mundo.

https://pubmed.ncbi.nlm.nih.gov/32439005/

# data[].attributes.attachment_link.readable_text
Affiliations

¹ Department of Clinical Biochemistry and the Copenhagen General Population Study, Herlev and Gentofte Hospital, Copenhagen University Hospital, Herlev, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

² Department of Clinical Biochemistry and the Copenhagen General Population Study, Herlev and Gentofte Hospital, Copenhagen University Hospital, Herlev, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Electronic address: boerge.nordestgaard@regionh.dk.

Free article

Free article

Affiliations

¹ Department of Clinical Biochemistry and the Copenhagen General Population Study, Herlev and Gentofte Hospital, Copenhagen University Hospital, Herlev, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

² Department of Clinical Biochemistry and the Copenhagen General Population Study, Herlev and Gentofte Hospital, Copenhagen University Hospital, Herlev, Denmark; Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark. Electronic address: boerge.nordestgaard@regionh.dk.

Abstract

Background: Despite the greater prevalence of familial hypercholesterolemia (FH) in subjects with ischemic heart disease (IHD), premature IHD, and severe hypercholesterolemia (low-density lipoprotein ≥190 mg/dl), overall prevalence estimates are not available.

Objectives: The aim of this study was to provide worldwide estimates of FH prevalence in subjects with IHD, premature IHD, and severe hypercholesterolemia compared with those in the general population.

Methods: In this systematic review and meta-analyses, Embase, PubMed, and the Web of Science were searched until June 3, 2019, for peer-reviewed papers and conference abstracts reporting heterozygous FH prevalence in nonfounder populations, revealing 104 studies eligible for inclusion.

Results: Estimates of FH prevalence were pooled using random-effects meta-analyses and were 0.32% (95% confidence interval [CI]: 0.26% to 0.39% [corresponding to 1:313]) among 10,921,310 unique subjects in the general population (33,036 patients with FH) on the basis of 44 studies, 3.2% (95% CI: 2.2% to 4.3% [1:31]) among 84,479 unique subjects with IHD (2,103 patients with FH) on the basis of 28 studies, 6.7% (95% CI: 4.9% to 8.7% [1:15]) among 31,316 unique subjects with premature IHD (1,471 patients with FH) on the basis of 32 studies, and 7.2% (95% CI: 4.6% to 10.8% [1:14]) among 17,728 unique subjects with severe hypercholesterolemia (920 patients with FH) on the basis of 7 studies. FH prevalence in the general population was similar using genetic versus clinical diagnoses. Seventeen of 195 countries (9%) in the world have reported FH prevalence for the general population, leaving 178 (91%) countries in the world with unknown prevalence.

Conclusions: Compared with 1:313 among subjects in the general population, FH prevalence is 10-fold higher among those with IHD, 20-fold higher among those with premature IHD, and 23-fold higher among those with severe hypercholesterolemia. The prevalence of FH is unknown in 90% of countries in the world.

Keywords: epidemiology; frequency; myocardial infarction; premature; severe hypercholesterolemia; systematic review.

Similar articles

Prevalence of Familial Hypercholesterolemia Among the General Population and Patients With Atherosclerotic Cardiovascular Disease: A Systematic Review and Meta-Analysis.

Hu P, Dharmayat KI, Stevens CAT, Sharabiani MTA, Jones RS, Watts GF, Genest J, Ray KK, Vallejo-Vaz AJ. Hu P, et al. Circulation. 2020 Jun 2;141(22):1742-1759. doi: 10.1161/CIRCULATIONAHA.119.044795. Epub 2020 May 29. Circulation. 2020. PMID: 32468833

The molecular genetic basis and diagnosis of familial hypercholesterolemia in Denmark.

Efficiency and problems of statin therapy in patients with heterozygous familial hypercholesterolemia.

Korneva V, Kuznetsova T, Julius U. Korneva V, et al. Atheroscler Suppl. 2019 Dec;40:79-87. doi: 10.1016/j.atherosclerosissup.2019.08.029. Epub 2019 Aug 17. Atheroscler Suppl. 2019. PMID: 31818452

Spectrum of mutations of familial hypercholesterolemia in the 22 Arab countries.

Alhababi D, Zayed H. Alhababi D, et al. Atherosclerosis. 2018 Dec;279:62-72. doi: 10.1016/j.atherosclerosis.2018.10.022. Epub 2018 Oct 19. Atherosclerosis. 2018. PMID: 30415195

Two Novel Disease-Causing Mutations in the LDLR of Familial Hypercholesterolemia.

Hu H, Shu T, Ma J, Chen R, Wang J, Wang S, Lin S, Chen X. Hu H, et al. Front Genet. 2021 Dec 14;12:762587. doi: 10.3389/fgene.2021.762587. eCollection 2021. Front Genet. 2021. PMID: 34970301 Free PMC article.

# data[].attributes.attachment_link.keywords[]
hyperlipoproteinemia type ii / epidemiology*

# data[].attributes.attachment_link.keywords[]
hyperlipoproteinemia type ii / ethnology

# data[].attributes.attachment_link.keywords[]
national center for biotechnology information

# data[].attributes.attachment_link.title
Worldwide Prevalence of Familial Hypercholesterolemia: Meta-Analyses of 11 Million Subjects - PubMed

# data[].attributes.attachment_link.description
Compared with 1:313 among subjects in the general population, FH prevalence is 10-fold higher among those with IHD, 20-fold higher among those with premature IHD, and 23-fold higher among those with severe hypercholesterolemia. The prevalence of FH is unknown in 90% of countries in the world.

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09-fisiopatologicas.pdf (cardiol.br)
Titulo: Bases fisiopatológicas da dislipidemia e hipertensão arterial
Autor: Ana Paula Marte, Raul Dias Santos
año: 2007
Resultados: La evidencia sugiere que la hipercolesterolemia contribuye a la progresión de la hipertensión arterial a través de la activación del sistema innina-angiotensina,la reducción de la disponibilidad de óxido nítrico y la disfunción endotelial. Otros mecanismos descritos son la sensibilidad a la sal, lasecreción de sustancias vasoactivas y el enriquecimiento de las membranas celulares con exceso de colesterol. Estos mecanismos actúan sinérgicamente en la exacerbación del proceso ateoesclerótico. Se debe lograr la optimización terapéutica en el control de la presión arterial y la reducción de los niveles de colesterol, especialmente en pacientes con alto riesgo de eventos cardiovasculares.

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Título: Prevalencia de hiperlipidemia y sus factores asociados en estudiantes universitarios de Colombia

Tipo de estudio: revisión sistemática
Año: 2017
Resultados:  La mediana de edad de los participantes fue de 21,3 ± 3,8 años. La mayoría de los participantes se clasificaron como mujeres (77%), adultos jóvenes (62,3%), personas de nivel socioeconómico medio (55,1%) y personas solteras (92,5%). Entre los hábitos saludables, el 71,7% de los estudiantes “realiza actividad física” y el 76,2% “consume comida casera”. Sin embargo, se evidenció una contradicción en los hábitos alimentarios, observándose proporciones similares en el consumo de frutas y verduras (94,5%) en relación a los alimentos ricos en carbohidratos (94,7%) y con alto contenido de aceite (88,6%). Asimismo, se identificó el alto consumo de embutidos y conservas (69,3%) como factores predisponentes a mediano plazo en el desarrollo de NDC. Por otro lado, el alto consumo de bebidas alcohólicas fue un factor de riesgo importante debido al efecto negativo que producían en el hígado, lo que conlleva una alteración en el metabolismo de los lípidos. En cuanto a los antecedentes patológicos, se observa que la mayoría de los estudiantes presentó un bajo porcentaje de preexistencia mórbida (menos del 3%).

Conclusiones:  La prevalencia de hiperlipidemia en estudiantes universitarios fue del 33,8%, siendo el sexo (masculino) y el consumo de bebidas alcohólicas los principales factores que aumentan el riesgo de desarrollar hiperlipidemia

https://www.sciencedirect.com/science/article/pii/S240584402032260X

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Título: Epidemiología de la dislipidemia en adultos chinos: metanálisis de prevalencia, conciencia, tratamiento y control.
Tipo de estudio: Metanálisis
Año: 2014
Método: Realizamos una revisión sistemática de los estudios observacionales relacionados publicados desde 2003 mediante búsquedas en bases de datos de literatura en inglés y chino. Se realizaron metanálisis en estudios elegibles utilizando un modelo de efectos aleatorios para resumir las tasas de prevalencia, conocimiento, tratamiento y control de la dislipidemia. Se analizaron la heterogeneidad y el sesgo de publicación. Se realizaron análisis de sensibilidad para explicar la heterogeneidad y examinar el impacto de la calidad del estudio en los resultados de los metanálisis.
Resultados: Se incluyeron 38 artículos para metanálisis, con un tamaño de muestra total de 387 825. Las tasas de prevalencia, conocimiento, tratamiento y control de la dislipidemia fueron 41,9 % (IC 95 %: 37,7 % - 46,2 %), 24,4 % (IC 95 %: 14,4 % - 38,4 %), 8,8 % (IC 95 %: 7,7 % - 10,0%) y 4,3% (IC 95%: 4,1% - 4,5%), respectivamente. La prevalencia de hipercolesterolemia, hipertrigliceridemia, hiperlipidemia mixta, niveles bajos de colesterol de lipoproteínas de alta densidad y niveles altos de colesterol de lipoproteínas de baja densidad fueron 10,1% (IC 95%: 5,8% - 16,9%), 17,7% (IC 95%: 14,0 % - 22,1 %), 5,1 % (95 % IC: 3,1 % - 8,2 %), 11,0 % (95 % IC: 8,0 % - 15,0 %) y 8,8 % (95 % IC: 4,1 % - 17,8 %), respectivamente. Los análisis de sensibilidad revelaron que los hombres tenían una mayor prevalencia de dislipidemia (43,2 %) que las mujeres (35,6 %). Las muestras de estudio de 30 años o más en la región oriental tendieron a tener una mayor prevalencia de dislipidemia. La calidad de los estudios tiene un ligero impacto en las estimaciones agrupadas.
Conclusión: Se estimó que la prevalencia general combinada de dislipidemia en adultos chinos era del 41,9 %, y los hombres tenían una tasa más alta que las mujeres.

https://pophealthmetrics.biomedcentral.com/articles/10.1186/s12963-014-0028-7

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Population Health Metrics 12, Article number: 28 (2014) Cite this article

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Abstract

Background

Numerous epidemiology studies on dyslipidemia have been conducted in China. However, a nationally representative estimate for dyslipidemia prevalence is lacking. The aim of this study is to appraise the nationwide prevalence, awareness, treatment, and control rates of dyslipidemia in adults in China.

Methods

We performed a systematic review of the related observational studies published since 2003 by searching English and Chinese literature databases. Meta-analyses were conducted in eligible studies using a random effect model to summarize the dyslipidemia prevalence, awareness, treatment, and control rates. Heterogeneity and publication bias were analyzed. Sensitivity analyses were performed to explain heterogeneity and examine the impact of study quality on the results of meta-analyses.

Results

Thirty-eight papers were included for meta-analyses, with a total sample size of 387,825. The prevalence, awareness, treatment, and control rates of dyslipidemia were 41.9% (95% CI: 37.7% - 46.2%), 24.4% (95% CI: 14.4% - 38.4%), 8.8% (95% CI: 7.7% - 10.0%), and 4.3% (95% CI: 4.1% - 4.5%), respectively. The prevalence of hypercholesterolemia, hypertriglyceridemia, mixed hyperlipidemia, low levels of high-density lipoprotein cholesterol, and high levels of low-density lipoprotein cholesterol were 10.1% (95% CI: 5.8% - 16.9%), 17.7% (95% CI: 14.0% - 22.1%), 5.1% (95% CI: 3.1% - 8.2%), 11.0% (95% CI: 8.0% - 15.0%), and 8.8% (95% CI: 4.1% - 17.8%), respectively. Sensitivity analyses revealed that males had a higher prevalence of dyslipidemia (43.2%) than females (35.6%). Study samples of age 30 and above in the eastern region tended to have higher prevalence of dyslipidemia. The quality of the studies has a slight impact on the pooled estimates.

Conclusions

The overall pooled prevalence of dyslipidemia in Chinese adults was estimated to be 41.9%, with males having a higher rate than females.

Peer Review reports

Introduction

Dyslipidemia represents one of the major risk factors for atherosclerosis affecting arteries of large and medium size and consequently causing ischemia in the brain, heart, or legs. Coronary artery disease and cerebral stroke represent the major causes of morbidity and mortality among elderly and middle aged subjects [ 1]. The prevalence of dyslipidemia has increased dramatically in Chinese cities with lifestyle changes over the past decade, and cardiovascular diseases have emerged as a leading cause of death in Chinese adults [ 2].

Surveys investigating the epidemiological data of dyslipidemia in Chinese adults have been published, but the results vary due to diverse populations of different regions and the use of different diagnosis criteria [ 2]. An overall appraisal of dyslipidemia epidemiology nationwide in China would potentially benefit future research and policy discussions. We therefore performed meta-analyses by a comprehensive systematic review of all available evidence to synthesize the current dyslipidemia prevalence, awareness, treatment, and control among Chinese adults.

Methods

Search strategy and eligibility criteria

Based on the MOOSE guideline [ 3], we identified epidemiological studies on dyslipidemia in Chinese adults published in English or Chinese between January 2003 and August 2013. The search strategy comprised of a search of Western electronic databases (including Medline, Embase, and CINAHL) and a search of Chinese databases (including SinoMed, CNKI, and Wanfang Data). We used the search terms "dyslipidemia", "hyperlipidemia", "epidemiology", "incidence", "prevalence", "awareness rate", "treatment rate", "control rate", "China or Chinese", and these terms' variants and combinations.

Eligible studies had to have reported any of the following epidemiological data related to dyslipidemia in sampled populations of Chinese subjects: prevalence, awareness rate, treatment rate, and control rate. The diagnosis criteria was based on the Chinese Guidelines on Prevention and Treatment of Dyslipidemia in Adults [ 2], which defined dyslipidemia as any one of the following four conditions: hypercholesterolemia (total cholesterol (TC) ≥ 6.22 mmol/L); hypertriglyceridemia (triglycerides (TG) ≥2.26 mmol/L); low levels of high-density lipoprotein cholesterol (HDL-C < 1.04 mmol/L); high levels of low-density lipoprotein cholesterol (LDL-C ≥ 4.14 mmol/L).

Dyslipidemia awareness was defined as a self-report of any prior laboratory diagnosis of dyslipidemia. Treatment was defined broadly as interventions including medication, diet, exercise, and monitoring to manage dyslipidemia. Participants were considered to have controlled dyslipidemia if their serum TC, TG, LDL-C, and HDL-C were within the normal ranges as defined above based on the 2007 Chinese guidelines.

We also applied the following exclusion criteria in filtering the identified publications:

Non-human studies

Non-research based publications such as press releases, newsletters, forum discussions, etc.

Non-epidemiological studies such as basic science research on dyslipidemia.

Studies that did not disclose when the data was collected, sample size, or denominator for each reported prevalence or rate.

Studies that investigated specific populations such as military, prisoners, specific ethnic groups, etc.

Studies that did not apply the diagnosis criteria published in the 2007 Chinese Guidelines on Prevention and Treatment of Dyslipidemia in Adults.

Study identification and data extraction

We identified relevant studies by searching electronic databases, scanning reference lists, and consulting clinical experts in dyslipidemia. Additionally, studies presented at key conference proceedings were identified. Two reviewers independently examined all the titles and abstracts of the studies retrieved from the searches for potentially eligible studies, then the full text of all potentially relevant citations were obtained and independently assessed by the reviewers to confirm whether they met the inclusion criteria. The results were checked and discussed by the two reviewers to agree upon a final list of included studies.

Using a standardized and predesigned data collection form, all relevant data in each included paper were extracted by two reviewers independently. The data extracted were cross-checked and any unresolved discrepancies were referred to a third reviewer. Where necessary, inputs of a clinical expert advisor were solicited to facilitate discussions among the reviewers.

For each included study, we extracted general information (including authors, year, title, type of publication, etc.), study characteristics (including study design, population, location, diagnosis criteria, sample size, etc.), participants' characteristics (including age, sex, type of dyslipidemia, etc.). We further recorded the numbers of people with any one type of dyslipidemia condition and reported awareness, treatment, and control rates. The data stratified by sex and dyslipidemia types, where available, were also extracted.

To inform the appropriateness of included studies in the meta-analysis and later evaluate the strength of the evidence, the two reviewers independently assessed and agreed on the quality of each included study using the quality assessment checklist for epidemiological studies [ 4]. The checklist assesses the quality of studies on a scale of 0 (the worst) to 18 (the best) using predefined criteria on both internal and external validities [ 4].

Statistical analyses and heterogeneity test

Pooled estimates of the dyslipidemia prevalence, awareness rate, treatment rate, and control rate and their corresponding 95% confidence intervals (CI) were calculated based on the random effect model [ 5] and stratified by sex and age group (over 18 or over 30 years) where applicable. Heterogeneity between studies was evaluated with the Cochran's Q test and I ² statistic, which describes the percentage of variation across studies (values of 25%, 50%, and 75% indicate low, moderate, and high degrees of heterogeneity, respectively) [ 6],[ 7]. Subgroup analyses were performed to investigate potential sources of heterogeneity from different geographical regions and types of dyslipidemia. Publication bias was evaluated by using the funnel plots method. Furthermore, sensitivity analyses were performed to evaluate the influence of particular study on a pooled estimate, which was recalculated by omitting a study each time. Independent or paired t-tests were used as appropriate, and a significant difference was reported if the p-value was less than 0.05. All statistical analyses were performed using SPSS version 20.0 (SPSS Inc, Chicago, USA) and Comprehensive Meta-Analysis software version 2.0 (Biostat, Englewood, USA).

Results

Characteristics of included studies

Our searches retrieved 7669 citations. Of these, 6800 were excluded after reading the abstracts, and 831 were further excluded after assessing the full papers, leaving 38 eligible papers for inclusion in our review and analyses (Figure 1) [ 8]-[ 45], which involved a total of 387,825 Chinese people.

Flow chart of screening and inclusion of studies for review and analysis.

Among the 38 included papers, 36 were written in Chinese and two were written in English; 33 studies were cross-sectional surveys and five studies employed census surveys or other designs; 18 studies were conducted in eastern China, 10 studies were conducted in central China, eight studies were conducted in western China, and two surveys crossed regions nationwide (Table 1) [ 8]-[ 45].

Study quality was assessed for the 38 included papers. Four papers had quality scores between eight and 10 points, 13 papers had scores between 11 and 13 points, and 21 papers had scores between 14 and 16 points. Overall study quality was upper-middle and high, and the study quality did not differ significantly among the included studies.

Prevalence of dyslipidemia

Twenty-eight papers reported the total numbers of participants in the studies and those who were diagnosed with dyslipidemia (Figure 2). The pooled prevalence of dyslipidemia in Chinese adults was 41.9% (95% CI: 37.7% - 46.2%). The t-tests showed there were no statistically significant differences between subgroups stratified by age and geographic region (Tables 2 and 3); however, the pooled prevalence of dyslipidemia in males (43.2%) was higher than in female (35.6%) with statistical significance (t = 3.08, p < 0.05).

Forest plot of 28 studies' reported prevalence of dyslipidemia.

In terms of the different types of dyslipidemia, the pooled prevalence estimates of hypercholesterolemia (TC), hypertriglyceridemia (TG), mixed hyperlipidemia (TC + TG), low levels of high-density lipoprotein cholesterol (HDL-C), and high levels of low-density lipoprotein cholesterol (LDL-C) are 10.1% (95% CI: 5.8% - 16.9%), 17.7% (95% CI: 14.0% - 22.1%), 5.1% (95% CI: 3.1% - 8.2%), 11.0% (95% CI: 8.0% - 15.0%), and 8.8% (95% CI: 54.1% - 17.8%), respectively. There were no significant differences between age groups within each type of dyslipidemia condition (Table 4 and Additional file 1).

Dyslipidemia awareness, treatment, and control

Using the dyslipidemia awareness rates reported in four studies, we arrived at a pooled estimate of 24.4% (95% CI: 14.4% - 38.4%). Based on the reported dyslipidemia treatment rates in two studies, we estimated a pooled treatment rate of 8.8% (95% CI: 7.7% - 10.0%). There were no significant differences between males and females in terms of dyslipidemia awareness and treatment rates (Table 5). Only one paper reported a dyslipidemia control rate, which was 4.3% (3.1% for males and 5.5% for females).

Sensitivity analysis, publication bias and heterogeneity

Two studies were assessed with a quality score of eight, the lowest among the included studies. In the sensitivity analysis, omitting these two studies resulted in a slight change in the pooled dyslipidemia prevalence estimate, 41.7% from 41.9%. The pooled prevalence of TC, TG, HDL-C, and LDL-C changed to 9.4%, 17.0%, 10.7%, and 8.3% from 10.1%, 17.7%, 11.0%, and 8.8%, respectively. Funnel plots were produced for the prevalence of each type of dyslipidemia (see the Additional file 1). Asymmetric funnels suggest the possibility of publication bias. A moderate degree of heterogeneity was observed in the pooled dyslipidemia prevalence (I ² = 49.9%, Q = 1.00, P < 0.001), awareness rate (I ² = 49.9%, Q = 0.99, P < 0.001), and treatment rate (I ² = 38.0%, Q = 0.721, P = 0.098).

Discussion

Our systematic review included 38 observational studies conducted in the past decade, covering most of the regions in China, and involving a total of 387,825 participants, representing the adult Chinese population. The pooled estimates from the meta-analyses showed high prevalence of dyslipidemia and low awareness, treatment, and control rates. The study and results are timely, as currently there is a lack of published up-to-date nationwide epidemiological data of dyslipidemia to support the evidence-based approach and management of dyslipidemia in China.

The pooled estimate of dyslipidemia prevalence among Chinese adults is 41.9%, which has more than doubled in the last 10 years [ 46], approaching the reported prevalence of 53% from the US National Health and Nutrition Examination Survey 2003-2006 [ 47]. The observed increase of dyslipidemia prevalence in China could possibly be attributed to the increasingly aging population and dramatic lifestyle changes coupled with economic growth, especially changes in cigarette smoking, dietary, and alcohol drinking behaviors among the general population [ 48].

The study discovered that hypertriglyceridemia (TG) was the most prevalent form of dyslipidemia, with a pooled estimate of 17.7%, followed by low levels of blood high-density lipoprotein cholesterol (HDL-C) (11.0%), hypercholesterolemia (TC) (10.1%), high levels of low-density lipoprotein cholesterol (LDL-C) (8.8%), and mixed hyperlipidemia (TC + TG) (5.1%). As dyslipidemia is one of the well-established risk factors for cardiovascular diseases [ 47], these results highlight the extensive need for appropriate interventions, both clinical and non-clinical, to treat all types of dyslipidemia. In addition, other considerations such as improving general awareness about dyslipidemia among both patients and health care professionals and promoting healthy diet and lifestyles are equally important in designing and implementing relevant public health strategies.

We calculated and compared the pooled estimates of dyslipidemia prevalence in age groups over 18 years and over 30 years. No significant difference was found between these age groups across different types of dyslipidemia conditions. However, trends of higher prevalence of TC, TG, and LDL-C abnormalities were observed in studies of older participants (≥30 years old) compared to those studies that enrolled younger participants (≥18 years old). We observed the highest estimate at 49.3% (95% CI: 39.4-59.3) among all of the pooled prevalence estimates in people over 30 years old in the eastern region of China. Another study in China concluded that greater burden of diet-related chronic conditions including dyslipidemia has been observed in economically vibrant and highly urbanized areas [ 49], which are predominantly in the eastern coastal region. More economically developed areas tend to have better access to health care facilities, which might have contributed to diagnosis and hence higher reported prevalence rates in these studies among populations in the eastern region of China.

The systematic review showed that dyslipidemia is more common in men than in women, which is consistent with the findings from American population-based studies [ 50],[ 51]. There were no significant differences in awareness, treatment, and control rates between the groups of men and women in China. However, studies conducted in the US showed that dyslipidemia was treated and controlled less often in men than in women [ 50]. A possible explanation for the higher dyslipidemia prevalence observed in men could be their higher probability of cigarette smoking, alcohol, and consumption of foods high in cholesterol.

The quality of studies included in our systematic review were generally good, thus the sensitivity analysis did not demonstrate much difference in the results of meta-analyses when the studies with the lowest quality scores were removed in the analyses. We believe our searches were comprehensive, although the asymmetric funnel plots suggested the possibility of publication bias. The moderate heterogeneity observed could come from the different study settings and populations. We investigated possible sources and performed subgroup analyses, but that still inadequately explained the heterogeneity findings in this study. The recent research of heterogeneity suggested that I ² estimates need to be interpreted with caution when a meta-analysis only includes a limited number of events or trials, in particular when the number of studies for further subgroup analyses is small [ 52]. Nevertheless, these uncertainties indicate the need of a higher-quality national survey with larger samples with better represented coverage across China.

Our study has some limitations. First, all the included studies were published after 2007 as we used the Chinese Guidelines on Prevention and Treatment of Dyslipidemia in Adults, published in 2007, as the diagnosis criteria [ 2]. Studies published before 2007 were based on a different set of diagnosis criteria, and therefore have not been included in our meta-analyses. Secondly, we could not investigate the differences in dyslipidemia prevalence between rural and urban areas due to the limited information reported in the included studies. Furthermore, we would like to highlight that the meta-analysis results on awareness, treatment, and control rate need to be interpreted with caution, as the number of studies reporting the relevant data are relatively small.

Conclusions

The pooled estimate of dyslipidemia prevalence among Chinese adults was 41.9%, and hypertriglyceridemia (TG) is the most prevalent dislipidemia condition. The prevalence of dyslipidemia in males was higher than in females. Our study also showed low dyslipidemia awareness, treatment, and control rates in China.

References

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Funding

This study has been funded by Pfizer Investment Co. Ltd., Beijing, China, including all costs associated with the development and the publishing of the present manuscript. Funding was not contingent upon publication of the manuscript.

Author information

Affiliations

1. School of Public Health, Central South University, Changsha, China

Yuanxiu Huang & Lin Gao

2. Pfizer Investment Co. Ltd, Outcomes Research, Beijing, China

Xiaoping Xie

3. IMS Health Asia Pacific, 8 Cross Street, #21-01/02/03 PWC Building, Singapore, Health Economics & Outcomes Research, 048424, Singapore

Seng Chuen Tan

Corresponding author

Correspondence to Seng Chuen Tan.

Additional information

Competing interests

X. Xie is currently employed as a researcher in health outcomes by Pfizer Investment Co. Ltd., at Beijing. The other authors declare that they have no competing interests.

Authors' contributions

YH, LG, and XX developed the study objective and scope, search strategy, and conducted the literature search, selection of included studies, and endpoints. YH and LG completed data extraction and statistical analyses. XX and SCT reviewed the analyses and contributed to the discussion of the study. The manuscript was drafted, reviewed, and agreed by all co-authors. All authors approved the final version of the manuscript.

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Huang, Y., Gao, L., Xie, X. et al. Epidemiology of dyslipidemia in Chinese adults: meta-analysis of prevalence, awareness, treatment, and control. Popul Health Metrics 12, 28 (2014). https://doi.org/10.1186/s12963-014-0028-7
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Keywords

Dyslipidemia

Prevalence

Awareness rate

Treatment rate

Control rate

Meta-analysis

# data[].attributes.attachment_link.title
Epidemiology of dyslipidemia in Chinese adults: meta-analysis of prevalence, awareness, treatment, and control - Population Health Metrics

# data[].attributes.attachment_link.description
Background Numerous epidemiology studies on dyslipidemia have been conducted in China. However, a nationally representative estimate for dyslipidemia prevalence is lacking. The aim of this study is to appraise the nationwide prevalence, awareness, treatment, and control rates of dyslipidemia in adults in China.