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O diabetes é uma doença crônica grave, acometendo e gerando disfunções em vários órgãos, o diagnóstico é simples, mas ainda é tardio para muitos pacientes que demoram a ter assistência e acompanhamento médico adequado. A ação silenciosa da doença trará prejuízos em longo prazo de difícil solução. Do ponto de vista ortopédico, relembro aos colegas a Neuroartropatia de Charcot.

A artropatia neuropática de Charcot é uma doença degenerativa de destruição óssea e articular, não infecciosa e progressiva, que ocorre pela disfunção sensitiva periférica. Foi descrita inicialmente por Jean-Martin Charcot, em 1868, em uma série de casos com pacientes portadores de sífilis terciária. Em 1936, foi descrita por Jordan, em pacientes portadores de diabetes mellitus.

A incidência da NC entre os diabéticos é em torno de 1.4%, no entanto essa incidência já foi menor, o que pode indicar um aumento do surgimento da patologia ou aumento da conscientização dos médicos e com isso mais diagnósticos. Em revisões mais recentes sobre o tema, a prevalência variou de 0.08-7.5% entre os diabéticos, enquanto a população geral com 0.16%. Em grupo de pacientes diabéticos de difícil controle, a prevalência pode chegar a 13% de neuroartropatia de Charcot. Os homens são mais acometidos do que as mulheres, e a bilateralidade entre os membros é de 30%.

A patogênese não é bem clara, e é aceito que vários mecanismos ocorrem para o desenvolvimento da artropatia neuropática de Charcot. Dentre eles, valoriza-se muito a teoria neurotraumática, em que o paciente por disfunção sensitiva, deixa de adotar mecanismos protetores normais de descarga do membro durante a marcha e suas atividades diárias, com isso, lesões únicas ou microtraumas repetitivos por sobrecarga ocorrerão. No entanto, essa teoria gera dúvida, quando observamos a patologia em articulações que não são de carga, como, por exemplo, no ombro.
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O diagnóstico é feito a partir do momento que conheço a patologia e sua apresentação clínica. E mesmo assim não é simples, o seu quadro inicial simula quadros inflamatórios e por vezes quadros infecciosos, sendo necessário fazer diagnóstico diferencial com celulites, infecção profunda, trombose, vasculites e outros.

Devemos lembrar-nos dessa patologia principalmente nos pacientes com quadros mais avançados de diabetes, com obesidade, nefropatias ou retinopatias. No DM tipo 1, ocorre principalmente na quinta década de vida, após aproximadamente 20 anos de doença; na DM tipo 2 ocorre principalmente na 6ª década de vida após 5-9 anos de doença.

As manifestações agudas iniciais: eritema, calor, edema difusa em pé e tornozelo, e dor. Um equívoco acreditar que devido às alterações da sensibilidade, a patologia é indolor. Brodsky, em seu estudo, relata dor presente em 50% dos seus pacientes. É descrito elevar o membro por alguns minutos e observar a redução desses sinais, o que irá nos auxiliar em afastar o diagnóstico de infecção.

As manifestações tardias da doença: o paciente já não se encontra nas fases inflamatórias, na maioria das vezes sem dor. No entanto, haverá padrões diferentes de destruição óssea, com subluxações e luxações articulares, formação de deformidades e ulceras de pressão. Dentre as deformidades do pé e tornozelo mais encontradas, observamos o desabamento do arco plantar, rigidez ou instabilidade do pé e tornozelo, proeminências ósseas gerando ulcerações da pele.

Radiograficamente, veremos basicamente aspectos de erosão óssea até destruição óssea grave com incongruência articular.

Separei duas classificações mais utilizadas para o Pé de Charcot: a primeira, os estágios de Eichenholtz que se baseia nos estágios de apresentação da doença; e o segundo, a classificação de Brodsky, que classifica de acordo com a região anatômica do pé acometida.

ESTÁGIOS MODIFICADOS DE EICHENHOLTZ

Estágio 0: Sem alterações radiográficas; alterações clínicas presentes (eritema, calor e edema).

Estágio 1: Fase de fragmentação.

Radiografias com evidências de osteopenia, fragmentação periarticular e subluxações.

Estágio 2: Fase de coalescência.

Fase de cicatrização, em que o edema e calor regridem, e radiograficamente passa a surgir sinais de fusão óssea e esclerose óssea.

Fase 3: Fase de reconstrução.

Fase da ausência de sinais de inflamação, com sinais sugestivos de que não há destruição ósseo ou articular em progressão. Fase em que encontramos frequentemente deformidades nos pés e tornozelos, como sequela da fase de fragmentação.

Tipo 1: colapso tarsometatarsal; é a localização mais comum com 60% dos casos.

Tipo 2: o colapso afeta o retropé (chopart e subtalar); ocorre em 10%.

Tipo 3A: acomete a tibiotársica; ocorre em 20% dos casos;
Tipo 3B: acomete a tuberosidade posterior do calcâneo resultando em fraturas.

Tipo 4: acometimento em múltiplas regiões.

Tipo 5: Acomete somente o antepé. É raro.

O tratamento é variável, dependendo do estágio de doença em que o paciente se encontra e da região acometida. O importante deve ser sair da fase inflamatória e proteger o pé das deformidades.

Nas fases mais avançadas, pode ser necessário o uso de órtese tipo AFO ou tratamento cirúrgico ortopédico.

Espero ter contribuído para relembrar essa patologia, que não é comum, mas pode surgir em seu consultório ou clinica, e ao desconfiar do diagnóstico o paciente será beneficiado, não retardando o seu tratamento.
Autor: Referência:
Van der Vem A.; Chapman C.B.; Bowker J.H.; Review Article: Charcot Neuroarthropathy of the Foot and Ankle. JAAOS 2009;17:562-571

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Lesões ortopédicas pelo diabetes: pé de Charcot, quando devemos suspeitar? - PEBMED

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O diabetes é uma doença crônica grave, acometendo e gerando disfunções em vários órgãos, o diagnóstico é simples, mas ainda é tardio para muitos pacientes que demoram a ter assistência e acompanhamento médico adequado. A ação silenciosa da doença trará prejuízos em longo prazo de difícil solução.

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Fasting and 2-Hour Plasma Glucose

The FPG and 2-h PG may be used to diagnose diabetes (Table 2.2). The concordance between the FPG and 2-h PG tests is imperfect, as is the concordance between A1C and either glucose-based test. Numerous studies have confirmed that, compared with FPG and A1C cut points, the 2-h PG value diagnoses more people with diabetes.

A1C

The A1C test should be performed using a method that is certified by the NGSP ( www.ngsp.org) and standardized or traceable to the Diabetes Control and Complications Trial (DCCT) reference assay. Although point-of-care A1C assays may be NGSP certified, proficiency testing is not mandated for performing the test, so use of point-of-care assays for diagnostic purposes is not recommended but may be considered in the future if proficiency testing is performed and documented.

The A1C has several advantages compared with the FPG and OGTT, including greater convenience (fasting not required), greater preanalytical stability, and less day-to-day perturbations during stress and illness. However, these advantages may be offset by the lower sensitivity of A1C at the designated cut point, greater cost, limited availability of A1C testing in certain regions of the developing world, and the imperfect correlation between A1C and average glucose in certain individuals. National Health and Nutrition Examination Survey (NHANES) data indicate that an A1C cut point of ≥6.5% (48 mmol/mol) identifies one-third fewer cases of undiagnosed diabetes than a fasting glucose cut point of ≥126 mg/dL (7.0 mmol/L) ( 9).

When using A1C to diagnose diabetes, it is important to recognize that A1C is an indirect measure of average blood glucose levels and to take other factors into consideration that may impact hemoglobin glycation independently of glycemia including age, race/ethnicity, and anemia/hemoglobinopathies.

Confirming the Diagnosis

Unless there is a clear clinical diagnosis (e.g., patient in a hyperglycemic crisis or with classic symptoms of hyperglycemia and a random plasma glucose ≥200 mg/dL [11.1 mmol/L]), a second test is required for confirmation. It is recommended that the same test be repeated without delay using a new blood sample for confirmation because there will be a greater likelihood of concurrence. For example, if the A1C is 7.0% (53 mmol/mol) and a repeat result is 6.8% (51 mmol/mol), the diagnosis of diabetes is confirmed. If two different tests (such as A1C and FPG) are both above the diagnostic threshold, this also confirms the diagnosis. On the other hand, if a patient has discordant results from two different tests, then the test result that is above the diagnostic cut point should be repeated. The diagnosis is made on the basis of the confirmed test. For example, if a patient meets the diabetes criterion of the A1C (two results ≥6.5% [48 mmol/mol]) but not FPG (<126 mg/dL [7.0 mmol/L]), that person should nevertheless be considered to have diabetes.

Since all the tests have preanalytic and analytic variability, it is possible that an abnormal result (i.e., above the diagnostic threshold), when repeated, will produce a value below the diagnostic cut point. This scenario is likely for FPG and 2-h PG if the glucose samples remain at room temperature and are not centrifuged promptly. Because of the potential for preanalytic variability, it is critical that samples for plasma glucose be spun and separated immediately after they are drawn. If patients have test results near the margins of the diagnostic threshold, the health care professional should follow the patient closely and repeat the test in 3-6 months.

Description

In 1997 and 2003, the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus ( 17, 18) recognized a group of individuals whose glucose levels did not meet the criteria for diabetes but were too high to be considered normal. "Prediabetes" is the term used for individuals with IFG and/or IGT and/or A1C 5.7-6.4% (39-47 mmol/mol). Prediabetes should not be viewed as a clinical entity in its own right but rather as an increased risk for diabetes (Table 2.3) and cardiovascular disease (CVD). Prediabetes is associated with obesity (especially abdominal or visceral obesity), dyslipidemia with high triglycerides and/or low HDL cholesterol, and hypertension.

Diagnosis

The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus ( 17, 18) defined IFG as FPG levels between 100 and 125 mg/dL (between 5.6 and 6.9 mmol/L) and IGT as 2-h PG after 75-g OGTT levels between 140 and 199 mg/dL (between 7.8 and 11.0 mmol/L). It should be noted that the World Health Organization (WHO) and numerous other diabetes organizations define the IFG cutoff at 110 mg/dL (6.1 mmol/L).

As with the glucose measures, several prospective studies that used A1C to predict the progression to diabetes as defined by A1C criteria demonstrated a strong, continuous association between A1C and subsequent diabetes. In a systematic review of 44,203 individuals from 16 cohort studies with a follow-up interval averaging 5.6 years (range 2.8-12 years), those with A1C between 5.5 and 6.0% (between 37 and 42 mmol/mol) had a substantially increased risk of diabetes (5-year incidence from 9 to 25%). An A1C range of 6.0-6.5% (42-48 mmol/mol) had a 5-year risk of developing diabetes between 25 and 50% and a relative risk 20 times higher compared with A1C of 5.0% (31 mmol/mol) ( 19). In a community-based study of African American and non-Hispanic white adults without diabetes, baseline A1C was a stronger predictor of subsequent diabetes and cardiovascular events than fasting glucose ( 20). Other analyses suggest that A1C of 5.7% (39 mmol/mol) or higher is associated with a diabetes risk similar to that of the high-risk participants in the Diabetes Prevention Program (DPP) ( 21), and A1C at baseline was a strong predictor of the development of glucose-defined diabetes during the DPP and its follow-up ( 22).

Hence, it is reasonable to consider an A1C range of 5.7-6.4% (39-47 mmol/mol) as identifying individuals with prediabetes. Similar to those with IFG and/or IGT, individuals with A1C of 5.7-6.4% (39-47 mmol/mol) should be informed of their increased risk for diabetes and CVD and counseled about effective strategies to lower their risks (see Section 5 "Prevention or Delay of Type 2 Diabetes"). Similar to glucose measurements, the continuum of risk is curvilinear, so as A1C rises, the diabetes risk rises disproportionately ( 19). Aggressive interventions and vigilant follow-up should be pursued for those considered at very high risk (e.g., those with A1C >6.0% [42 mmol/mol]).

Table 2.4 summarizes the categories of prediabetes and Table 2.3 the criteria for prediabetes testing. The ADA diabetes risk test is an additional option for screening (Fig. 2.1). For recommendations regarding risk factors and screening for prediabetes, see pp. S17-S18 ("Screening and Testing for Type 2 Diabetes and Prediabetes in Asymptomatic Adults" and "Screening and Testing for Type 2 Diabetes and Prediabetes in Children and Adolescents").

Diagnosis

In a patient with classic symptoms, measurement of blood glucose is sufficient to diagnose diabetes (symptoms of hyperglycemia or hyperglycemic crisis plus a random plasma glucose ≥200 mg/dL [11.1 mmol/L]). In these cases, knowing the blood glucose level is critical because, in addition to confirming that symptoms are due to diabetes, it will inform management decisions. Some providers may also want to know the A1C to determine how long a patient has had hyperglycemia.

Immune-Mediated Diabetes

This form, previously called "insulin-dependent diabetes" or "juvenile-onset diabetes," accounts for 5-10% of diabetes and is due to cellular-mediated autoimmune destruction of the pancreatic β-cells. Autoimmune markers include islet cell autoantibodies and autoantibodies to GAD (GAD65), insulin, the tyrosine phosphatases IA-2 and IA-2β, and ZnT8. Type 1 diabetes is defined by the presence of one or more of these autoimmune markers. The disease has strong HLA associations, with linkage to the DQA and DQB genes. These HLA-DR/DQ alleles can be either predisposing or protective.

The rate of β-cell destruction is quite variable, being rapid in some individuals (mainly infants and children) and slow in others (mainly adults). Children and adolescents may present with ketoacidosis as the first manifestation of the disease. Others have modest fasting hyperglycemia that can rapidly change to severe hyperglycemia and/or ketoacidosis with infection or other stress. Adults may retain sufficient β-cell function to prevent ketoacidosis for many years; such individuals eventually become dependent on insulin for survival and are at risk for ketoacidosis. At this latter stage of the disease, there is little or no insulin secretion, as manifested by low or undetectable levels of plasma C-peptide. Immune-mediated diabetes commonly occurs in childhood and adolescence, but it can occur at any age, even in the 8th and 9th decades of life.

Autoimmune destruction of β-cells has multiple genetic predispositions and is also related to environmental factors that are still poorly defined. Although patients are not typically obese when they present with type 1 diabetes, obesity should not preclude the diagnosis. Patients with type 1 diabetes are also prone to other autoimmune disorders such as Hashimoto thyroiditis, Graves disease, Addison disease, celiac disease, vitiligo, autoimmune hepatitis, myasthenia gravis, and pernicious anemia (see Section 3 "Comprehensive Medical Evaluation and Assessment of Comorbidities").

Idiopathic Type 1 Diabetes

Some forms of type 1 diabetes have no known etiologies. These patients have permanent insulinopenia and are prone to ketoacidosis, but have no evidence of β-cell autoimmunity. Although only a minority of patients with type 1 diabetes fall into this category, of those who do, most are of African or Asian ancestry. Individuals with this form of diabetes suffer from episodic ketoacidosis and exhibit varying degrees of insulin deficiency between episodes. This form of diabetes is strongly inherited and is not HLA associated. An absolute requirement for insulin replacement therapy in affected patients may be intermittent.

Testing for Type 1 Diabetes Risk

The incidence and prevalence of type 1 diabetes is increasing ( 23). Patients with type 1 diabetes often present with acute symptoms of diabetes and markedly elevated blood glucose levels, and approximately one-third are diagnosed with life-threatening ketoacidosis ( 3). Several studies indicate that measuring islet autoantibodies in relatives of those with type 1 diabetes may identify individuals who are at risk for developing type 1 diabetes ( 5). Such testing, coupled with education about diabetes symptoms and close follow-up, may enable earlier identification of type 1 diabetes onset. A study reported the risk of progression to type 1 diabetes from the time of seroconversion to autoantibody positivity in three pediatric cohorts from Finland, Germany, and the U.S. Of the 585 children who developed more than two autoantibodies, nearly 70% developed type 1 diabetes within 10 years and 84% within 15 years ( 24). These findings are highly significant because, while the German group was recruited from offspring of parents with type 1 diabetes, the Finnish and American groups were recruited from the general population. Remarkably, the findings in all three groups were the same, suggesting that the same sequence of events led to clinical disease in both "sporadic" and familial cases of type 1 diabetes. Indeed, the risk of type 1 diabetes increases as the number of relevant autoantibodies detected increases ( 25- 27).

Although there is currently a lack of accepted screening programs, one should consider referring relatives of those with type 1 diabetes for antibody testing for risk assessment in the setting of a clinical research study ( http://www.diabetestrialnet.org). Widespread clinical testing of asymptomatic low-risk individuals is not currently recommended due to lack of approved therapeutic interventions. Individuals who test positive will be counseled about the risk of developing diabetes, diabetes symptoms, and DKA prevention. Numerous clinical studies are being conducted to test various methods of preventing type 1 diabetes in those with evidence of autoimmunity ( www.clinicaltrials.gov).

Description

Type 2 diabetes, previously referred to as "noninsulin-dependent diabetes" or "adult-onset diabetes," accounts for 90-95% of all diabetes. This form encompasses individuals who have relative (rather than absolute) insulin deficiency and have peripheral insulin resistance. At least initially, and often throughout their lifetime, these individuals may not need insulin treatment to survive.

There are various causes of type 2 diabetes. Although the specific etiologies are not known, autoimmune destruction of β-cells does not occur, and patients do not have any of the other known causes of diabetes. Most, but not all, patients with type 2 diabetes are overweight or obese. Excess weight itself causes some degree of insulin resistance. Patients who are not obese or overweight by traditional weight criteria may have an increased percentage of body fat distributed predominantly in the abdominal region.

Ketoacidosis seldom occurs spontaneously in type 2 diabetes; when seen, it usually arises in association with the stress of another illness such as infection. Type 2 diabetes frequently goes undiagnosed for many years because hyperglycemia develops gradually and, at earlier stages, is often not severe enough for the patient to notice the classic diabetes symptoms. Nevertheless, even undiagnosed patients are at increased risk of developing macrovascular and microvascular complications.

Whereas patients with type 2 diabetes may have insulin levels that appear normal or elevated, the higher blood glucose levels in these patients would be expected to result in even higher insulin values had their β-cell function been normal. Thus, insulin secretion is defective in these patients and insufficient to compensate for insulin resistance. Insulin resistance may improve with weight reduction and/or pharmacological treatment of hyperglycemia but is seldom restored to normal.

The risk of developing type 2 diabetes increases with age, obesity, and lack of physical activity. It occurs more frequently in women with prior GDM, in those with hypertension or dyslipidemia, and in certain racial/ethnic subgroups (African American, American Indian, Hispanic/Latino, and Asian American). It is often associated with a strong genetic predisposition, more so than type 1 diabetes. However, the genetics of type 2 diabetes is poorly understood. In adults without traditional risk factors for type 2 diabetes and/or younger age, consider antibody testing for type 1 diabetes (i.e., GAD).

Screening and Testing for Type 2 Diabetes and Prediabetes in Asymptomatic Adults

Screening for prediabetes and type 2 diabetes through an informal assessment of risk factors (Table 2.3) or with an assessment tool, such as the ADA risk test (Fig. 2.1), is recommended to guide providers on whether performing a diagnostic test (Table 2.2) is appropriate. Prediabetes and type 2 diabetes meet criteria for conditions in which early detection is appropriate. Both conditions are common and impose significant clinical and public health burdens. There is often a long presymptomatic phase before the diagnosis of type 2 diabetes. Simple tests to detect preclinical disease are readily available. The duration of glycemic burden is a strong predictor of adverse outcomes. There are effective interventions that prevent progression from prediabetes to diabetes (see Section 5 "Prevention or Delay of Type 2 Diabetes") and reduce the risk of diabetes complications (see Section 9 "Cardiovascular Disease and Risk Management" and Section 10 "Microvascular Complications and Foot Care").

Approximately one-quarter of people with diabetes in the U.S. and nearly half of Asian and Hispanic Americans with diabetes are undiagnosed ( 28). Although screening of asymptomatic individuals to identify those with prediabetes or diabetes might seem reasonable, rigorous clinical trials to prove the effectiveness of such screening have not been conducted and are unlikely to occur.

A large European randomized controlled trial compared the impact of screening for diabetes and intensive multifactorial intervention with that of screening and routine care ( 29). General practice patients between the ages of 40 and 69 years were screened for diabetes and randomly assigned by practice to intensive treatment of multiple risk factors or routine diabetes care. After 5.3 years of follow-up, CVD risk factors were modestly but significantly improved with intensive treatment compared with routine care, but the incidence of first CVD events or mortality was not significantly different between the groups ( 29). The excellent care provided to patients in the routine care group and the lack of an unscreened control arm limited the authors' ability to determine whether screening and early treatment improved outcomes compared with no screening and later treatment after clinical diagnoses. Computer simulation modeling studies suggest that major benefits are likely to accrue from the early diagnosis and treatment of hyperglycemia and cardiovascular risk factors in type 2 diabetes ( 30); moreover, screening, beginning at age 30 or 45 years and independent of risk factors, may be cost-effective (<$11,000 per quality-adjusted life-year gained) ( 31).

Additional considerations regarding testing for type 2 diabetes and prediabetes in asymptomatic patients include the following.

Screening and Testing for Type 2 Diabetes and Prediabetes in Children and Adolescents

In the last decade, the incidence and prevalence of type 2 diabetes in adolescents has increased dramatically, especially in racial and ethnic minority populations ( 23). Recent studies question the validity of A1C in the pediatric population, especially among certain ethnicities, and suggest OGTT or FPG as more suitable diagnostic tests ( 42). However, many of these studies do not recognize that diabetes diagnostic criteria are based on long-term health outcomes, and validations are not currently available in the pediatric population ( 43). The ADA acknowledges the limited data supporting A1C for diagnosing type 2 diabetes in children and adolescents. Although A1C is not recommended for diagnosis of diabetes in children with cystic fibrosis or symptoms suggestive of acute onset of type 1 diabetes and only A1C assays without interference are appropriate for children with hemoglobinopathies, the ADA continues to recommend A1C for diagnosis of type 2 diabetes in this cohort ( 44, 45). The modified recommendations of the ADA consensus report "Type 2 Diabetes in Children and Adolescents" are summarized in Table 2.5 ( 46).

Definition

For many years, GDM was defined as any degree of glucose intolerance that was first recognized during pregnancy ( 17), regardless of whether the condition may have predated the pregnancy or persisted after the pregnancy. This definition facilitated a uniform strategy for detection and classification of GDM, but it was limited by imprecision.

The ongoing epidemic of obesity and diabetes has led to more type 2 diabetes in women of childbearing age, with an increase in the number of pregnant women with undiagnosed type 2 diabetes ( 47). Because of the number of pregnant women with undiagnosed type 2 diabetes, it is reasonable to test women with risk factors for type 2 diabetes (Table 2.3) at their initial prenatal visit, using standard diagnostic criteria (Table 2.2). Women diagnosed with diabetes in the first trimester should be classified as having preexisting pregestational diabetes (type 2 diabetes or, very rarely, type 1 diabetes). GDM is diabetes that is first diagnosed in the second or third trimester of pregnancy that is not clearly either preexisting type 1 or type 2 diabetes (see Section 13 "Management of Diabetes in Pregnancy"). The International Association of the Diabetes and Pregnancy Study Groups (IADPSG) GDM diagnostic criteria for the 75-g OGTT were not derived from data in the first half of pregnancy, so the diagnosis of GDM in early pregnancy by either FPG or OGTT values is not evidence based ( 48).

Diagnosis

GDM carries risks for the mother and neonate. Not all adverse outcomes are of equal clinical importance. The Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study ( 49), a large-scale multinational cohort study completed by more than 23,000 pregnant women, demonstrated that risk of adverse maternal, fetal, and neonatal outcomes continuously increased as a function of maternal glycemia at 24-28 weeks, even within ranges previously considered normal for pregnancy. For most complications, there was no threshold for risk. These results have led to careful reconsideration of the diagnostic criteria for GDM. GDM diagnosis (Table 2.6) can be accomplished with either of two strategies:

1. "One-step" 75-g OGTT or

2. "Two-step" approach with a 50-g (nonfasting) screen followed by a 100-g OGTT for those who screen positive

Different diagnostic criteria will identify different degrees of maternal hyperglycemia and maternal/fetal risk, leading some experts to debate, and disagree on, optimal strategies for the diagnosis of GDM.

Neonatal Diabetes

Diabetes occurring under 6 months of age is termed "neonatal" or "congenital" diabetes, and about 80-85% of cases can be found to have an underlying monogenic cause ( 69). Neonatal diabetes occurs much less often after 6 months of age, whereas autoimmune type 1 diabetes rarely occurs before 6 months of age. Neonatal diabetes can either be transient or permanent. Transient diabetes is most often due to overexpression of genes on chromosome 6q24, is recurrent in about half of cases, and may be treatable with medications other than insulin. Permanent neonatal diabetes is most commonly due to autosomal dominant mutations in the genes encoding the Kir6.2 subunit ( KCNJ11) and SUR1 subunit ( ABCC8) of the β-cell K atp channel. Correct diagnosis has critical implications because most patients with K atp -related neonatal diabetes will exhibit improved glycemic control when treated with high-dose oral sulfonylureas instead of insulin. Insulin gene ( INS) mutations are the second most common cause of permanent neonatal diabetes, and, while treatment presently is intensive insulin management, there are important genetic considerations as most of the mutations that cause diabetes are dominantly inherited.

Maturity-Onset Diabetes of the Young

MODY is frequently characterized by onset of hyperglycemia at an early age (classically before age 25 years, although diagnosis may occur at older ages). MODY is characterized by impaired insulin secretion with minimal or no defects in insulin action (in the absence of coexistent obesity). It is inherited in an autosomal dominant pattern with abnormalities in at least 13 genes on different chromosomes identified to date. The most commonly reported forms are GCK-MODY (MODY2), HNF1A-MODY (MODY3), and HNF4A-MODY (MODY1).

Clinically, patients with GCK-MODY exhibit mild, stable, fasting hyperglycemia and do not require antihyperglycemic therapy except sometimes during pregnancy. Patients with HNF1A- or HNF4A-MODY usually respond well to low doses of sulfonylureas, which are considered first-line therapy. Mutations or deletions in HNF1B are associated with renal cysts and uterine malformations (renal cysts and diabetes [RCAD] syndrome). Other extremely rare forms of MODY have been reported to involve other transcription factor genes including PDX1 ( IPF1) and NEUROD1.

Diagnosis

A diagnosis of one of the three most common forms of MODY including GCK-MODY, HNF1A-MODY, and HNF4A-MODY allows for more cost-effective therapy (no therapy for GCK-MODY; sulfonylureas as first-line therapy for HNF1A-MODY and HNF4A-MODY). Additionally, diagnosis can lead to identification of other affected family members.

A diagnosis of MODY should be considered in individuals who have atypical diabetes and multiple family members with diabetes not characteristic of type 1 or type 2 diabetes, although admittedly "atypical diabetes" is becoming increasingly difficult to precisely define in the absence of a definitive set of tests for either type of diabetes. In most cases, the presence of autoantibodies for type 1 diabetes precludes further testing for monogenic diabetes, but the presence of autoantibodies in patients with monogenic diabetes has been reported ( 70). Individuals in whom monogenic diabetes is suspected should be referred to a specialist for further evaluation if available, and consultation is available from several centers. Readily available commercial genetic testing following the criteria listed below now enables a cost-effective ( 71), often cost-saving, genetic diagnosis that is increasingly supported by health insurance. It is critical to correctly diagnose one of the monogenic forms of diabetes because these patients may be incorrectly diagnosed with type 1 or type 2 diabetes, leading to suboptimal, even potentially harmful, treatment regimens and delays in diagnosing other family members ( 72). The information is especially critical for GCK-MODY mutations where multiple studies have shown that no complications ensue in the absence of glucose-lowering therapy ( 73). Genetic counseling is recommended to ensure that affected individuals understand the patterns of inheritance and the importance of a correct diagnosis.

The diagnosis of monogenic diabetes should be considered in children and adults diagnosed with diabetes in early adulthood with the following findings:

○ Diabetes diagnosed within the first 6 months of life (with occasional cases presenting later, mostly INS and ABCC8 mutations) ( 69, 74)

○ Diabetes without typical features of type 1 or type 2 diabetes (negative diabetes-associated autoantibodies; nonobese, lacking other metabolic features, especially with strong family history of diabetes)

○ Stable, mild fasting hyperglycemia (100-150 mg/dL [5.5-8.5 mmol/L]), stable A1C between 5.6 and 7.6% (between 38 and 60 mmol/mol), especially if nonobese

View Abstract

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2. Classification and Diagnosis of Diabetes

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Diabetes can be classified into the following general categories: 1. Type 1 diabetes (due to autoimmune β-cell destruction, usually leading to absolute insulin deficiency) 2. Type 2 diabetes (due to a progressive loss of β-cell insulin secretion frequently on the background of insulin resistance) 3.

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Condições dermatológicas associadas ao DM2

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Condições dermatológicas associadas ao DM2

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Dermatologic Conditions Associated With T2DM

Acrochordons

Acrochordons, often referred to as skin tags, are pedunculated outgrowths of normal skin on a narrow stalk, commonly located on the neck, axillae, eyelids, and groin. They consist of hyperplastic soft dermis and epidermis and are usually skin colored or brownish (Fig. 1A). Acrochordons are relatively common and can be found in approximately 25% to 46% of the adult population, and their number and prevalence increase with advancing age and pregnancy. The link between acrochordons and the metabolic syndrome (obesity, dyslipidemia, hypertension, insulin resistance, and elevated C-reactive protein levels) has been well established.

The diagnosis of acrochordons is based on the clinical appearance and location of the lesions. In rare cases they may look suspicious for malignancy and should be sent for histological testing. The presence of acrochordons should be an indicator for the evaluation of possible DM by the PCP, if not previously diagnosed. These lesions often are asymptomatic and do not need to be removed unless desired by the patient for cosmetic reasons or in cases that involve irritation. The treatment of acrochordons consists of excision and can be performed with forceps, fine-grade scissors, cryosurgery with liquid nitrogen, or electrodesiccation.

Acanthosis Nigricans

Acanthosis nigricans (AN) is the most widely recognized cutaneous manifestation of DM. AN is present in up to 74% of obese adults and can be predictive of hyperinsulinemia; one study found that patients with AN demonstrated higher fasting plasma insulin levels than their nonacanthotic counterparts. It is postulated that in hyperinsulinemic states, excess insulin binds to insulin-like growth factor-1 receptors on keratinocytes and fibroblasts, stimulating hyperproliferation and leading to the development of AN. The presence of AN also is an independent prognostic indicator for the development of T2DM. AN is particularly common in African Americans and the incidence is equal between men and women. Insulin resistance is not the only underlying etiology for AN because it also can be associated with cancer as a result of tumor cell expression of the peptides that enhance the cellular proliferation. AN also has been described in other endocrine disorders (eg, polycystic ovary syndrome, Cushing syndrome, thyroid disease, acromegaly) and with the use of certain drugs (eg, insulin, oral contraceptives, nicotinic acid, corticosteroids, diethylstilbestrol, heroin, fusidic acid, methyltestosterone).

AN is a dermatosis characterized by velvety, papillomatous, brownish-black, hyperkeratotic plaques, located typically on the intertriginous surfaces and neck (Fig. 1B). Diagnosis is largely clinical, with histopathology needed only for the confirmation of unclear cases. The primary treatment consists of managing the underlying cause. Significant weight loss effectively resolves most forms of AN. Topical or systemic retinoids and topical keratinolytics (eg, tretinoin and ammonium lactate creams) can be used to manage cutaneous disease.

Eruptive Xanthomatosis

Eruptive xanthomatosis (EX) is a dermatosis characterized by the sudden appearance of yellow papules with an erythematous base on the buttocks, shoulders, and extensor surfaces of the extremities (Fig. 2). The sudden appearance of these lesions can be worrisome to patients and may prompt a visit to their PCP for further evaluation. EX is associated with the markedly elevated serum triglyceride levels that occur with hyperlipidemia syndromes (eg, Fredrickson-Levy types I, IV, and V) or with poorly controlled T2DM, hypothyroidism, obesity, pancreatitis, nephrotic syndrome, cholestatic liver disease, dysglobulinemia, and as an adverse effect of certain medications (eg, estrogens, corticosteroids, systemic retinoid agents). EX can be the first sign of DM.

The diagnosis of EX can be made clinically and confirmed with a biopsy of the lesions. Fasting lipid levels should be obtained once the diagnosis is made because patients with EX are at a higher risk of early coronary artery disease and pancreatitis caused by hypertriglyceridemia. The treatment of EX involves management of the underlying condition, and the PCP should aim to lower triglyceride levels with dietary modifications and systemic medications. EX lesions resolve usually within 6 to 8 weeks with appropriate treatment.

Scleredema Diabeticorum

Scleredema diabeticorum (SD) is a rare chronic connective tissue disorder that is associated primarily with T2DM. The condition is seen in 2.5% to 14% of patients with DM and is most common in obese middle-aged men with T2DM. SD is characterized by thick, indurated, and sometimes erythematous skin on the upper back, neck, and shoulders. The skin with SD may have a peau d'orange appearance. Pathogenesis of SD is believed to be linked to increased stimulation of insulin and nonenzymatic glycosylation of collagen, which leads to increased collagen cross-linking, rendering the collagen fibers resistant to degradation by collagenase and leading to increased amounts of collagen overall.

Patients with SD often are asymptomatic, but pain and decreased mobility (especially of the neck and back) may be present in severe cases. The diagnosis of SD usually is made based on clinical appearance. A definitive diagnosis requires a full-thickness excisional biopsy along with histologic examination of the dermis. Treatments for SD have shown limited benefit. Psoralen + ultraviolet A (PUVA) light seems to be the most effective treatment, but others that have demonstrated therapeutic efficacy include potent topical and intralesional steroids (eg, triamcinolone, betamethasone), penicillamine, intralesional insulin, low-dose methotrexate, prostaglandin E1, and pentoxifylline. Combination therapy with PUVA and physical therapy may help improve mobility in patients with severe SD. Although strict glycemic control has not shown consistent therapeutic benefit for SD, it is proposed to be an effective preventive measure.

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Acrochordons Acrochordons, often referred to as skin tags, are pedunculated outgrowths of normal skin on a narrow stalk, commonly located on the neck, axillae, eyelids, and groin. They consist of hyperplastic soft dermis and epidermis and are usually skin colored or brownish (Fig. 1A).

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Revisão dos guidelines de diabetes

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2016 in Review: Key Guidelines in Diabetes and Endocrinology You Need to Know

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Stay current on new important guidelines and recommendations.

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Standards of Medical Care in Diabetes | American Diabetes Association

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The ADA strives to improve and update the Standards of Medical Care in Diabetes to ensure that clinicians, health plans, and policy makers can continue to rely on them as the most authoritative and current guidelines for diabetes care. Readers who wish to comment on the 2018 Standards of Medical Care in Diabetes are encouraged to do so.

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Diabético VIII Semana Estadual de Saúde Vascular

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Campanha de Prevenção do Pé Diabético VIII Semana Estadual de Saúde Vascular 07 a 14 de novembro

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Guia de bolso para exame do pé diabético

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Retinopatia diabética

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Community Eye Health Journal " The diabetes epidemic and its implications for eye health

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Diabetes is a complex disease requiring the involvement of many health professionals, and patients have many different appointments to keep and tests to undergo. With so much going on, raising awareness of diabetic retinopathy (DR) can be difficult.

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Diabetic foot ulcers, as shown in the images below, occur as a result of various factors, such as mechanical changes in conformation of the bony architecture of the foot, peripheral neuropathy, and atherosclerotic peripheral arterial disease, all of which occur with higher frequency and intensity in the diabetic population.{file40038}{file400...

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TÉCNICA PARA LA APLICACIÓN DE LA INSULINA

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A aplicação da insulina é uma parte fundamental no tratamento da pessoa com Diabetes que necessita desta medicação. Nesse vídeo você irá aprender a técnica adequada para a aplicação da insulina.

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Dr. Walter Minicucci dá todas as dicas de como adquirir, armazenar e aplicar diversos tipos de insulina