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Adresati nelamuririle sau intrebarile Dvs. referitoare la subiectul abordat.

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Adresati nelamuririle sau intrebarile Dvs. referitoare la subiectul abordat.

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Folosind ca instrument ajutator imaginea de mai jos, raspundeti la urmatoarea intrebare. Unde incadram un TSH de 7 mUI/L cu fT4 normal?

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Let's start off with a clinical presentation. Ayesha is a 70-year-old woman, who was apparently healthy when she went for her routine visit to doctor. However, she complained of mild fatigue, dry skin, and difficulty in losing weight since last 2 years. The past medical and surgical history had been uneventful. There was also no reported family history of diabetes, hypertension, or ischemic heart disease. Physical examination results were normal including a non- palpable thyroid gland. ECG was normal. Fasting and postprandial blood sugar and complete blood count were within normal limits. Laboratory investigations for serum levels of TSH, free T4, total cholesterol, HDL and LDL cholesterol, triglycerides, and thyroperoxidase antibodies were carried out and the results are shown in the table. Serum TSH and free T4 tests were repeated 2 weeks after the first visit and were found to be 8.1 mIU/L and 1.4 ng/dL, respectively. Considering the mildness of symptoms, insignificant findings on physical examination, persistently high TSH levels and normal T4 level, and presence of thyroperoxidase antibodies, her doctor diagnosed her with subclinical hypothyroidism; the most likely etiology being Hashimoto's thyroiditis.

Hypothyroidism is a condition where there is a reduced production of thyroid hormone. 1 (/p1/para1) Hypothyroidism is categorized as primary and secondary on the basis of its cause. Primary hypothyroidism occurs due to the improper functioning of the thyroid gland. It may be further classified as overt and subclinical hypothyroidism on the basis of the level of severity. 2 (/p793/col2/para2) ,3 (/p1700/col2/para3) Subclinical hypothyroidism is characterized by no or minimal symptoms and moderately elevated TSH but normal free T4 levels. 3 (/p1700/col2/para3) ,4 (/p464/col2/para4) Clinical or overt hypothyroidism is characterized by apparent symptoms with elevated TSH (&gt;10 mIU/L) and lower free T4 levels. 3 (/p1700/col2/para3) ,2 (/p797/col1/para2) Primary hypothyroidism affects approximately 5% of individuals, with elderly women being the most commonly affected. 3 (/p1701/col1/para1) Secondary hypothyroidism occurs due to inadequate stimulation of thyroid gland by thyroid stimulating hormone (TSH). This could be because of either decreased TSH levels or ineffective TSH caused by congenital or acquired pituitary or hypothalamic disorders. This form of hypothyroidism is rare and occurs in less than 1% of individuals. 3 (/p1700/col2/para3) We will discuss the etiology of both the above mentioned conditions in the subsequent frames. References Hypothyroidism, Medline Plus. http://www.nlm.nih.gov/medlineplus/ency/article/000353.htm ; 2011:1-7. Accessed 01 March,2011. Roberts CGP, Ladenson PW. Hypothyroidism. Lancet . 2004;363: 793-803. Ladenson P, Kim M. Thyroid. In: Cecil RL, Goldman L, Ausiello DA, eds. Cecil medicine . 23 rd ed. Philadelphia: Saunders Elsevier; 2008:1698-1713. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. American College of Endocrinology.8, 6. 1-13.Available at: http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf . Accessed March 1, 2011.

Let's look at the etiological factors of primary hypothyroidism. Primary hypothyroidism may be caused due to either thyroid dysfunction or impaired synthesis of thyroid hormone. Absence of or defects in the thyroid gland and abnormal thyroid hormone synthesis during birth may lead to congenital hypothyroidism.(/p1701/col1/para4) Thyroid dysfunction: Iodine deficiency is the most common cause for hypothyroidism. In the United States and most of the developed countries, thyroid dysfunction is most commonly caused by a condition characterized by autoimmune-mediated destruction of thyroid gland called Hashimoto's thyroiditis. In this condition, there is alteration in the T cell-mediated immunity that leads to inflammation of the thyroid gland. This can be diagnosed by detecting antithyroid antibodies targeted against thyroid peroxidase and thyroglobulin, which act as important markers, present in the circulation.(/p1701/col1/para2) Surgical removal of thyroid gland to treat thyroid disorders and cancers of the head and neck may also lead to hypothyroidism.(/p1701/col1/para3) In addition, radioactive iodine irradiation for the treatment of hyperthyroidism, and other radiation therapy to treat head and neck cancer, are also known to cause hypothyroidism. Infiltrative disorders such as hemochromatosis, amyloidosis, systemic sclerosis, and invasive fibrous thyroiditis are also known to destroy the thyroid tissue and cause hypothyroidism.(/p1701/col1/para4) Impaired synthesis of thyroid hormone: This can be due to iodine deficiency in the diet which is still considered the primary cause of hypothyroidism in some underdeveloped countries.(/p1701/col1/para2) Treatment with drugs containing large amounts of iodine such as amiodarone, lithium, and aminoglutethimide can also lead to primary hypothyroidism.(/p1701/col1/para3) Reference Ladenson P, Kim M. Thyroid. In: Cecil RL, Goldman L, Ausiello DA, eds. Cecil medicine . 23rd ed. Philadelphia: Saunders Elsevier; 2008:1698-1713.

Secondary hypothyroidism may be caused due to the disorders of the hypothalamus or pituitary gland. Hypothalamic disorders may interfere with the secretion of thyrotropin-releasing hormone (TRH), which is responsible for the release of TSH from the pituitary gland. These disorders include tumors such as lymphoma, germinoma, or glioma (/p1700/table244-3), and infiltrative conditions such as sarcoidosis, hemochromatosis, or histocytosis. In case of pituitary gland disorders, such as pituitary adenomas and other tumors of the sella turcica, the secretion and synthesis of TSH may inhibited because of compression of the thyrotrophic cells by the overgrown tissue. Surgical removal of pituitary adenomas and radiation therapy are also known to destroy the thyrotropic tissues. Sheehan's syndrome (infarction caused by hemorrhage during labor in women) and lymphocytic hypophysis are some of the other known disorders associated with secondary hypothyroidism.(/p1701/col1/para5)(/p1700/table244-3) Let's now review the clinical manifestations of hypothyroidism. Reference Ladenson P, Kim M. Thyroid. In: Cecil RL, Goldman L, Ausiello DA, eds. Cecil medicine . 23rd ed. Philadelphia: Saunders Elsevier; 2008:1698-1713.

In order to understand the disease better, let's now review the clinical manifestations of hypothyroidism. Hypothyroidism progresses with few or no symptoms, making it difficult to recognize the disease in the initial stages. 1 (/p1701/col2/para1) The symptoms include tiredness, dry skin, intolerance to cold, hair loss, difficulty in concentration, constipation, weight gain in spite of having poor appetite, breathlessness, hoarseness of voice, paresthesia, and hearing impairment. 1 (/p1701/col2/para1) ,2 (/p2230/col1/335-5) In women, precocious puberty, menorrhagia, amenorrhea, and galactorrhea are the common symptoms associated with hypothyroidism. 1 (/p1701/col2/para1) Depression, lack of initiative, and sociability are also noted in these patients. The range of cognitive defects are wide and may vary from mild memory loss to even seizures and coma. 1 (/p1701/col2/para1) References Ladenson P, Kim M. Thyroid. In: Cecil RL, Goldman L, Ausiello DA, eds. Cecil medicine . 23rd ed. Philadelphia: Saunders Elsevier; 2008:1698-1713. Jameson JL, Weetman AP. Disorders of the thyroid gland. In: Braunwald E, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL eds. Harrison´s Principles of Internal Medicine . 17th ed. 2008: 2224-2247.

The physical findings that hint toward hypothyroidism include cold extremities due to peripheral vasoconstriction; dry, coarse, and yellow skin; puffiness of face and extremities; brittle nails, hair loss, diffuse thinning of scalp hair, and mild hypothermia. 1 (/p1701/col2/para2) ,2 (/p2231/col1/para4) Cardiovascular signs include bradycardia, diastolic hypertension, and distant heart sounds. 1 (/p1701/col2/para2) Neurological examination may reveal slowing of tendon reflexes associated with a delay in the terminal relaxation phase. 1 (/p1701/col2/para2) Peripheral edema and the effusions of the serous cavities are also common signs seen in hypothyroid patients. 1 (/p1701/col2/para2), 2 (/p2231/col1/para6) The thyroid gland may be normal in size or it can be enlarged. In some cases, the gland may be atrophied to an extent that it would be difficult to detect it on palpation. On examination, the texture of the gland may vary from being soft and smooth to firm and irregular. 1 (/p1701/col2/para3) In children with hypothyroidism, delayed growth in spite of weight gain may be seen associated with delayed onset of puberty and pseudo hypertrophy of the muscles. 1 (/p1701/col2/para2) References Ladenson P, Kim M. Thyroid. In: Cecil RL, Goldman L, Ausiello DA, eds. Cecil medicine . 23rd ed. Philadelphia: Saunders Elsevier; 2008:1698-1713. Jameson JL, Weetman AP. Disorders of the thyroid gland. In: Braunwald E, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL eds. Harrison´s Principles of Internal Medicine . 17th ed. 2008: 2224-2247.

The most important test recommended to arrive at a diagnosis of primary hypothyroidism is the measurement of TSH levels.(/p464/col1/para1) Other recommended tests include estimation of free T 3 and T 4 hormone levels and test for thyroid antibodies such as antithyroid peroxidase and antithyroglobulin autoantibodies.(/p464/col1/para2) Thyroid scan, ultrasonography, or sometimes both may be required in case of doubtful structural thyroid defects.(/p464/col1/para2) The principal defining criteria for patients with overt and subclinical hypothyroidism are the laboratory test values of free T 3 and T 4 estimates and TSH levels. In patients with overt hypothyroidism, free T 3 andT 4 levels are reduced accompanied by an increase in TSH levels. In patients with subclinical hypothyroidism, levels of free T 3 and T 4 hormone are normal, whereas TSH levels are moderately higher.(/p464/col1/para4) Reference AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. American College of Endocrinology.8, 6. 1-13.Available at: http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf . Accessed March 1, 2011.

After having discussed about the diagnosis of hypothyroidism, let us now have an overview of the management of the disease. The treatment goal for the management of hypothyroidism is to mimic normal, physiological levels of thyroid hormone and alleviate signs, symptoms, and biochemical abnormalities. The treatment must be adapted to the needs of the individual patient.(/p464/col1/para5) The treatment of choice for most patients with hypothyroidism is thyroid hormone replacement therapy using levothyroxine (LT4).(/p464/col1/para5) There is no definite treatment of choice for subclinical hypothyroidism. However, treatment with LT4 is advised for patients whose TSH levels are above 10 mIU/mL. Based on the AACE, 2006 guidelines, LT4 treatment is also recommended in patients with TSH between 5 and 10 mIU/mL when they have associated goiter or in the presence of antithyroid antibodies.(/p465/col1/para3) Desiccated thyroid hormone or a combination of T 3 and T 4 hormones is not recommended by the AACE guidelines because of the insufficient evidence available for their use in the management of hypothyroidism.(/p464/col1/para6;/col2/para3) Reference AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. American College of Endocrinology.8, 6. 1-13.Available at: http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf . Accessed March 1, 2011.

Going back to the Ayesha's case, recall that she was diagnosed with subclinical hypothyroidism. In the next few slides, we will be discussing subclinical hyperthyroidism , its treatment options, and also see how Ayesha was treated and how she responded to her treatment. The main diagnostic criteria that define subclinical hyperthyroidism are slightly elevated levels of serum TSH and levels of FT 4 and T 3 within the reference range.(/p464/col2/para4) It affects 1% to 10% of adults and with higher prevalence seen in women. The chief cause of subclinical hyperthyroidism is autoimmune thyroiditis, also called as Hashimoto's disease.(/p464/col1/para1) The main predisposing factors include advancing age and people with higher iodine consumption.(/p464/col2/para4) Though subclinical hyperthyroidism represents early thyroid failure, it is commonly asymptomatic.(/p464/col2/para4) Reference AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. American College of Endocrinology.8, 6. 1-13.Available at: http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf . Accessed March 1, 2011.

The flowchart in this slide depicts the treatment algorithm for subclinical hyperthyroidism as suggested by American Medical Association. When the laboratory results show higher TSH levels with normal T4 levels, the test is repeated twice after an interval of 6 weeks. If the laboratory values show that the levels of TSH is greater than 10 mIU per mL, then testing for antithyroid antibodies is recommended. When the result for antithyroid antibodies is positive, therapy with LT4 is initiated. When the laboratory results show absence of antithyroid antibodies, therapy is initiated even if the patient is asymptomatic. If the TSH values are between 4.5 to 10 and is accompanied by low FT4 Rule out hypopituitarism before starting levothyroxine because starting levothyropxine treatment can precipitate adrenal crisis in case patient has adrenal insufficency also. If the TSH values are between 5 and 10 mIU/mL, testing for antithyroid antibodies is recommended. If the result for antithyroid antibodies is positive, treatment is initiated. If the result for antithyroid antibodies is negative, the patient is put on observation and retested every 6 months. 1 (/p240/figure1) Treatment is also initiated in women who are attempting for pregnancy, in order to avoid obstetric and fetal complications due to reduced TSH. 2 (/p234/col1/para1) References Col NF, Surks MI, Daniels GH. Subclinical thyroid disease: clinical applications. JAMA . 2004; 291:239-243. Surks MI, Ortiz E, Daniels DH, Sawin CT, Col NF, Cobin RH, et al. Subclinical thyroid disease. Scientific review and guidelines for diagnosis and management. Scientific review and clinical applications. JAMA . 2004;291:228-238.

The recommended initial dosage of LT4 is 25 to 50 mcg/day. 1 (/p465/col1/para3) The initial dose of LT4 should be reduced in elderly patients and in patients with coronary artery disease. 2 (/p21/col2/para4) The serum TSH levels should be monitored every 6 to 8 weeks after initiation of LT4 therapy and the dosage should be adjusted accordingly. 1 (/p465/col1/para3) The target TSH level in subclinical hyperthyroidism should be between 0.3 and 3.0 µ IU/mL. 1 (/p465/col1/para3) After achieving stable TSH levels through therapy, annual follow-up is recommended. 1 (/p465/col1/para3) Progression to overt hypothyroidism is seen in 3% to 20% of patients.(/p465/col1/para1) In patients with goiter and antithyroid antibodies (or both), the risk of progression is comparatively higher. 1 (/p465/col1/para1) The associated risks of subclinical hyperthyroidism include, progression to overt hypothyroidism, cardiovascular effects, hyperlipidemia, and neuropsychiatric effects. 1 (/p465/col1/para2) References AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. American College of Endocrinology.8, 6. 1-13.Available at: http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf . Accessed March 1, 2011. Shah SN, Joshi SR. Indian Thyroid Guidelines 2011. JAPI. 2011;59(Suppl):1-68.

Let's now come back to the case we started with. To recapitulate, Ayesha was diagnosed with subclinical hypothyroidism due to Hashimoto's thyroiditis; thereafter, she was put on LT4 therapy based on the following findings: Increased TSH Positive antithyroid antibodies Dyslipidemia Dosage administered was 30 mcg/day. She was asked to visit again for follow-up after 8 weeks.

Now let 's discuss in detail about LT4, its indications, dosing, and drug interactions. Levothyroxine, or LT4, is a synthetic form of T4 and is similar to the naturally produced hormone in the thyroid gland of humans.(/p1/para1) It is mainly indicated for hypothyroidism and pituitary TSH suppression. All categories of hypothyroidism, including congenital, acquired, primary, secondary, and subclinical can be treated with LT4.(/p3/para1) LT4 can be used to treat and prevent various euthyroid goiters such as thyroid nodules, subacute or chronic lymphocytic thyroiditis (Hashimoto's thyroiditis) and those caused by pituitary TSH suppression. It is also indicated in the treatment of thyroid cancer as an adjunct to surgery and iodine irradiation therapy.(/p3/para2) Reference Synthroid Prescribing Information. Abbott Laboratories, North Chicago, USA. Revised March 2008.

It is important to know some important, unique facts of LT4, which would help us in our practice. LT4 is a molecule with a narrow therapeutic index with very less difference between the therapeutic and toxic doses.(/p464/col2/para2). A very less change in dose administered may change an euthyroid patient into hypo or hyperthyroid state. Hence, careful dose titration of LT4 is required in case of absorption variability or drug interactions. This would prevent the consequences of over- or under-treatment.(/p464/col2/para2) AACE recommends the use of high-quality brand of LT4, since the bioequivalence of LT4 is not the same as therapeutic equivalence. The bioequivalence is also based on total T4 levels and not on the TSH levels. Also the commercially available LT4 products are compared against another brand (innovator brand) and not against LT4 standard. This leads to the possibility of minor changes in dose administered to the patient, if the brands of LT4 are changed during the course of the treatment. In order to avoid this, AACE recommends that the patients should receive the same brand of LT4 throughout the treatment duration.(/p464/col1/para6) REFERENCE: AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. American College of Endocrinology.8, 6. 1-13.Available at: http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf . Accessed March 1, 2011.

Let's see in detail the dosing and monitoring requirements during the treatment with LT4. The mean daily dose of LT4 recommended for hormone replacement therapy is 1.6 mcg/kg of body weight. However, the dosage may vary among patients, tailored to their individual needs.(/p464/col1/para6) The patient can start with an initial daily dose ranging from 12.5 mcg to a full replacement therapy. Further, based on patient factors, such as age, weight, and cardiac status, and disease factors, such as severity and duration of hypothyroidism, the dose of full replacement therapy may vary.(/p464/col1/para6;/col2/para1) Patients are advised to reassess their hormone levels after at least 6 weeks following therapy initiation, a dose change, or a change in the brand of LT4.(/p464/col2/para1) Once normal levels of TSH is achieved, follow-up after 6 months and thereafter annually is recommended.(/p464/col2/para1) Absorption of LT4 is affected in malabsorptive states and dose adjustments are required in case of absorption variability and drug interactions.(/p464/col2/para2) If the dose titration is not appropriate, then the cost of treatment may increase due to additional follow-up visits and laboratory tests.(/p464/col2/para2) Reference AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. American College of Endocrinology.8, 6. 1-13.Available at: http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf . Accessed March 1, 2011.

Thyroid hormone is highly protein bound and hence the drugs that compete for binding affect the amount of free T4 hormone in the blood. The dose of LT4 when coadministered with such drugs must be altered in order to exert optimum effect. 1 (/p1722/col2/para2) Also, there are a few drugs that alter the production, absorption, and metabolism of thyroxine. Hence, the dose of LT4 should be increased when administered with such drugs. Drugs that reduce thyroxine production include lithium, iodine-containing drugs, and amiodarone. Drugs that reduce thyroxine absorption include sucralfate, ferrous sulfate, cholestyramine, colestipol, aluminum-containing antacids, and calcium supplements. Drugs that increase thyroxine metabolism include rifampin, phenobarbital, carbamazepine, warfarin, and oral hypoglycemic agents. Dose of LT4 should be decreased when administered with drugs that displace thyroxine from binding proteins, such as furosemide, mefenamic acid, and salicylates. 1 (/p1723/col1/table4) ,2 (/p464/col2/para2) References Hueston WJ, Treatment of hypothyroidism. Am Fam Physician. 2001;64:1717-24. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. American College of Endocrinology.8, 6. 1-13.Available at: http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf . Accessed March 1, 2011.

Coming back to Ayesha's case, let's see how she had responded to treatment. To recapitulate, Ayesha was diagnosed with subclinical hypothyroidism due to Hashimoto's thyroiditis; thereafter, she was put on LT4 therapy. Dosage administered was 30 mcg/day. She was asked to revisit for follow-up after 8 weeks of commencing the treatment. Serum TSH measurement was repeated. Her TSH levels had fallen to 1.2 mIU/mL, but remained within the normal range of 1 to 1.5 mIU/mL on consecutive visits. She was asked to stay on the treatment and follow up after 1 year. After 1 year of treatment, she had lost weight and was asymptomatic. On investigation, her serum cholesterol and low-density lipoprotein (LDL) cholesterol levels were 190 and 100 mg/dL, respectively.

Now we shall see another clinical case. This case is about a pregnant woman and the baby that she delivers subsequently. Shobha, a 32-week pregnant, 30-year-old woman presents premature labor. She complains of inappropriate weight gain for gestational age and cold intolerance during past few months. In past, she was diagnosed with hypothyroidism at the age of 20. She was put on LT4 therapy. The last dose modification was 2 years back after which she continued to take the same dose.

On physical examination, Shobha weighed 100 kg. Her pulse rate were 68 per minute. Systemic blood pressure was 140/90 mm Hg in right arm in supine position. Her face was puffy. Skin was cold and dry. Slow relaxation was seen when deep tendon reflexes such as bicep reflex, supinator reflex, knee jerk, and ankle jerk were elicited. Considering her symptoms and past history, thyroid function tests were performed. Serum TSH and free T4 levels were 11 mIU/L and 1.2 pmol/L, respectively. Can hyperlink this slide to slide #27 which gives reference values for all three trimesters. Further, on fetal monitoring, fetal distress was diagnosed. Considering gestational age, fetal maturity, and the amount of dilation and effacement of the cervix, fetal distress labor was allowed to continue. She delivered a preterm and low birth weight male child. To get an insight on Shobha's condition, let's see some details about maternal hypothyroidism.

Maternal hypothyroidism is one of the common hormonal disorders encountered during pregnancy. 1 (/p215/col2/para2) The prevalence of overt hypothyroidism in pregnancy is 1.3 per 1000 females and that of subclinical hypothyroidism is 23 per 1000. 1 (/p215/col2/para2) The most common cause of maternal hypothyroidism is endemic iodine deficiency. 2 (/p8/para2) Hypothyroidism in women may result in increased incidence of infertility, miscarriage rates, and risk for obstetric and fetal complications. 1 (/p215/col2/para2) The obstetric complications include anemia, preeclampsia, cardiac dysfunction, placental abruption, and postpartum hemorrhage. 1 (/p215/col2/para2) The fetal complications include premature birth, low-birth weight, fetal distress in labor, fetal death, perinatal death, and congenital hypothyroidism. 1 (/p215/col2/para2) Studies have shown that even mild, untreated maternal hypothyroidism may impair the cognitive function of the offspring. This can be prevented by administering thyroid hormone replacement therapy during pregnancy. 3 (/p464/col1/para4) References Sahu MT, et al. Overt and subclinical thyroid dysfunction among Indian pregnant women and its effect on maternal and fetal outcome. Arch Gynaecol Obstet . 2010;218:215-220. Lazaras JH. Thyroid function in pregnancy. Br Med Bull . 2010;1-12. AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. American College of Endocrinology.8, 6. 1-13.Available at: http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf . Accessed March 1, 2011.

The flowchart on this slide is a schematic representation of thyroid regulation during pregnancy. The mechanism of regulation of thyroid hormone synthesis slightly differs during gestation under the influence of various gestation-related physiological changes in women. Many of the processes here are interlinked. Influence of placenta on thyroid physiology starts during the first trimester of pregnancy with elevated human chorionic gonadotropin (hCG) production. As already discussed in detail, since hCG can act as a functional agonist of TSH on TSH receptor, it stimulated TSH receptor mediated thyroid hormone production in the thyroid gland leading to increased thyroid hormone in circulation. Apart from these, placental production of type 3 deiodinase leads to elevated peripheral degradation of thyroid hormones, which again stimulated the thyroid for the production of thyroid hormones. In addition to these factors, increased placental transport of T4 also reduces maternal T4 in circulation, stimulating maternal thyroid gland to produce more and more thyroid hormones. Gestational period is also characterized by increase in estrogen production. Estrogen stimulates increased hepatic production of thyroxin-binding globulin (TBG) as well as increase in the half life of serum TBG. This results in increased serum concentration of TBG, which leads to decreased free thyroid hormone in circulation. This stimulates hypothalamic pituitary axis to produce TSH, which in turn stimulates thyroid for further production of thyroid hormone. This overall increase in thyroid hormone reduces serum TSH. Increased stimulation of thyroid gland can result in thyroid hypertrophy/goiter mainly in iodine-deficient area or in case of iodine deficiency in the pregnant woman. 1 (p1847/col1/para2,3;/col2/para1) 2 (/p173/para3)(/p174/para1,2). This calls for a need to establish gestational reference range for thyroid hormones. References Galofre JC, Davies TF. Autoimmune thyroid disease in pregnancy: a review. J Womens Health (Larchmt). 2009;18(11):1847-1856. Fitzpatrick DL, Russel MA. Diagnosis and management of thyroid disease in pregnancy. Obstet Gynecol Clin N Am. 37 (2010) 173-193.

Normally T 3 and T 4 occur in two forms: bound with TBG and unbound or free (active) form. 1 (/p2226/col2/para3) Thyroid hormone levels vary in pregnancy based on the trimester. The upper graph (A) depicts the levels of HCG and TSH against weeks of gestation. Lower graph (B), (C) depicts TBG, total T 4 , free T 3 , and free T 4 levels with respect to the gestational week. There is a rise in total T 3 and total T 4 levels during the first trimester of pregnancy, which reaches a plateau by mid-gestation until delivery. Similarly, FT 3 and FT 4 levels also increase during the first trimester, which decrease to reach a plateau in second and third trimesters of pregnancy. In a normal pregnancy, there is increase in estrogen and progesterone levels as weeks of pregnancy progress. Level of TSH shows an inverse relationship with hCG concentration and, hence, during the first trimester of pregnancy, levels of TSH decrease with increase in hCG concentrations. An increase in circulating TBG is also reported during the first trimester of pregnancy, which reaches a plateau during midgestation. Half life of TBG is reported to increase as a result of altered glycosylation by estrogen during gestation. 2 (/p2/para2)(/p3/fig1)(/p4/fig1) ,3 (/p1847/col1/para2)(/p1848/fig 2) This calls for a need to establish gestational reference range for thyroid hormones, which is discussed in the next slide. References Jameson JL, Weetman AP. Disorders of the thyroid gland. In: Kasper DL, Fauci AS, Longo DL, Braunwald E, Hauser SL, Jameson JL, eds. Harrison&apos;s Principles of Internal Medicine . 17th ed. New York: McGraw-Hill Medical; 2008:2224-2247. Lazarus JH. Thyroid function in pregnancy. Br Med Bull. 2010;1-12. Galofre JC, Davies TF. Autoimmune thyroid disease in pregnancy: a review. J Womens Health (Larchmt). 2009;18(11):1847-1856.

The table here details the referral values for thyroid function tests in pregnant Indian women as reported by Marwaha (2008). 1 (/p604/table2) 2 (/p1-6) Reference 1. Marwaha RK, Chopra S, Gopalakrishnan S, et al. Establishment of reference range for thyroid hormones in normal pregnant Indian women. BJOG. 2008;115(5):602-606. 2. SI Units for Clinical Data. University of North Carolina. Available at: http://www.unc.edu/~rowlett/units/scales/clinical_data.html. Accessed March 22, 2011.

Since thyroid disorders are common during pregnancy, the AACE recommends that thyroid hormone tests should be routinely performed before pregnancy or during the screening performed in the first semester. The obstetric and fetal complications due to hypothyroidism can be avoided by thyroid hormone replacement therapy. LT4 is found to be safe during pregnancy and it can be administered for both overt and subclinical hypothyroidism. (/p465/col1/para4) The serum TSH levels should be monitored every 6 weeks during pregnancy and based on the results, appropriate dose adjustments for LT4 should be made to meet the requirements.(/p465/col2/para1) In pregnant patients with moderate to severe hypothyroidism, the dosage of LT4 should be increased appropriately.(/p465/col2/para1) Reference AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. American College of Endocrinology.8, 6. 1-13.Available at: http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf . Accessed March 1, 2011.

Let's now review some of the important aspects of thyroxine treatment during pregnancy During preconception phase, the dose of LT4 should be optimized in patients with preexisting hypothyroidism in order to avoid infertility issues. Once the pregnancy is confirmed, the dose of LT4 should be increased by 30% to 50% of the preconception dose. The TSH levels are checked early in first trimester and should be aimed at less than 2.5 mIU/L. During the later stages of pregnancy, the TSH levels should be less than 3 mIU/L. After delivery, the dose of LT4 should be reduced to preconception dose. After 6 weeks of delivery, the thyroid function should be reassessed. Post-ablative and post-surgical hypothyroidism require higher doses of LT4.(/p9/table3) Reference Lazaras JH. Thyroid function in pregnancy. Br Med Bull . 2010;1-12.

Now that we have discussed maternal hypothyroidism and its complications, let's return to Shoba's case. The baby delivered by Shobha was apparently normal. Findings on neonatal examination are within normal limits, except for low birth weight. Neonatal screening for congenital hypothyroidism was carried out on the third day using cord blood . TSH and serum free T4 were 38 mIU/L and 0.5 ng/dL, respectively. Considering the laboratory test results, he was diagnosed with congenital hypothyroidism. In the next few slides we will have an overview of congenital hypothyroidism and it's diagnosis and management.

Congenital hypothyroidism occurs due to the agenesis or dysgenesis of thyroid gland and defect in the biosynthesis of the thyroid hormones. The prevalence rate of congenital hypothyroidism is 1 in 4000 of new born infants in regions of sufficient daily intake of iodine. Incidence in female infants is twice more that of males. The major cause for congenital hypothyroidism is endemic iodine deficiency. Other causes in neonates include genetic mutation and hemangiomas.(/p794/col2/para2) Most of the affected infants do not show obvious clinical manifestations, hence the practice of routine screening for thyroid function is recommended for all the newborn infants.(/p797/col1/para4) Congenital hypothyroidism when left untreated results in a syndrome known as Cretinism. Do not delay diagnosis of congenital hypothyroidism until physical manifestations are seen which is characterized by mental retardation, deafness, short stature, and facial deformities.(/p794/col1/para1) Reference Roberts CGP, Ladenson PW. Hypothyroidism. Lancet . 2004;363:793-803.

In infants, congenital hypothyroidism is present with hypothermia, poor feeding, bradycardia, jaundice, enlarged posterior fontanel, and umbilical hernia. In children and adolescents with congenital hypothyroidism, the clinical manifestations include growth failure with delayed bone maturation, delay in the eruption of permanent teeth, pseudo hypertrophy of muscles, enlargement of pituitary gland, galactorrhoea, and delayed or precocious puberty.(/p797/col1/para4) Reference Roberts CGP, Ladenson PW. Hypothyroidism. Lancet . 2004;363:793-803.

The flowchart in this slide represents the diagnostic algorithm for evaluating congenital hypothyroidism. If the screening results of the newborn show increased values for TSH or if the values for initial T 4 is less than 10% of the normal range, then measurement of serum TSH and free T 4 is recommended. The above tests are also recommended when there is a clinical suspicion of hypothyroidism. If the TSH levels recorded are greater than 9 mIU/L or if the free T 4 values are lesser than 0.6 ng/dL, diagnosis of primary congenital hypothyroidism is confirmed. In order to determine the etiology of the disease, additional optional tests such as radionuclide uptake and scan, ultrasonography, tests for serum thyroglobulin, maternal antithyroid antibodies, and urinary iodine are recommended. If the TSH levels recorded are reduced or normal, and less than 9 mIU/L, and if the free T 4 values are less than 0.6 ng/dL, secondary hypothyroidism is suspected. Additional tests to confirm the diagnosis include gene analysis, evaluation for other pituitary hormone deficiencies, MRI of brain, and eye check-up for optic nerve hypoplasia.(/p10/figure4) Reference Rastogi, LaFranchi. Congenital hypothyroidism. Orphanet J Rare Diseases. 2010,5:17;1-22.

Lets now see how Shobha's child was doing in the initial phase. Shobha's child was referred to a paediatric endocrinologist. Thyroid ultrasonography showed a normal thyroid gland. Maternal antithyroid antibodies were absent. The baby was started on LT4 at an initial daily dose of 50 mcg. The serum T4 normalized in 3 days. TSH normalized by end of 2 weeks. Shobha was asked to follow-up along with her new born on a monthly basis.

The goal of therapy in the management of congenital hypothyroidism is to normalize TSH values, and maintain T4 and free T4 hormone levels in the upper half of the reference range. Permanence of congenital hypothyroidism can be assessed by the presence of ectopic or absence of thyroid gland in the thyroid scan. If the initial TSH values are less than 50 mIU/L, with no rise in TSH values after newborn period, off therapy is tried at 3 years. If TSH increases during the off-therapy period, the condition may be considered as permanent congenital hypothyroidism. During the phase of initial work-up, detailed history and physical examination of the child is recorded. This is followed by referring the patient to pediatric endocrinologist. The serum TSH and FT4 values are reassessed, followed by thyroid ultrasonography and/or thyroid scan to confirm the diagnosis of congenital hypothyroidism. Congenital hypothyroidism can be managed by administering oral, once daily, LT4 at a dose of 10 to 15 mcg/day. T4 and TSH levels are monitored 2 to 4 weeks after initiation of the treatment. During the first 6 months, monitoring hormone levels every 1 to 2 months, and between 6 months and 3 years of age, monitoring hormone levels every 3 to 4 months is recommended. From 3 years of age to end of growth period, monitoring every 6 to 12 months is recommended.(/p2297/col1/table1) Reference Rose SR, Brown RS. Update of newborn screening and therapy for congenital hypothyroidism. Pediatric s. 2006;117(6):2290-2303.

Now, let's discuss the major comorbid conditions associated with hypothyroidism. The major comorbid conditions include autoimmune disorders, infertility, depression, and hyperlipidemia. 1 (/p465/col2/para3,4)2(/p27/col1/para1) The autoimmune diseases that occur concurrently with hypothyroidism are diabetes mellitus, vitiligo, rheumatoid arthritis, Addison's disease, and pernicious anemia. Autoimmune diseases are associated with autoimmune thyroiditis. 1 (/p463/col2/para4) References AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. American College of Endocrinology.8, 6. 1-13.Available at: http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf . Accessed March 1, 2011. Duntas LH, Biondi B. New insights into subclinical hypothyroidism and cardiovascular risk. Semin Thromb Hemost . 2011;37(1):27-34.

Let's now have a look at the effect of the above-mentioned comorbid conditions on hypothyroidism. Diabetes mellitus Hashimoto's thyroiditis may be associated with 10% patients of type 1 diabetes mellitus. Approximately one-fourth of female patients with type 1 diabetes mellitus develop postpartum thyroiditis. The AACE recommends that patients with diabetes mellitus should be examined for goiter development and should assess TSH levels regularly in the presence of a goiter or other autoimmune disorders.(/p465/col2/para2) Infertility In some patients, it is found that infertility and menstrual irregularities have underlying thyroid disorder. Chronic thyroiditis can be confirmed by physical examination and laboratory evaluation. Treatment with LT4 replacement therapy restores normal menstrual cycle and fertility.(/p465/col2/para3) Reference AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. American College of Endocrinology.8, 6. 1-13.Available at: http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf . Accessed March 1, 2011.

Depression According to the AACE recommendations, in every patient with depression, diagnosis of overt or subclinical hypothyroidism should be considered. Periodic evaluation for thyroid function should be performed in patients receiving lithium therapy, because lithium is known to induce goiter and hypothyroidism. LT4 replacement therapy is used in the management of depression associated with hypothyroidism. It is indicated occasionally in combination with antidepressants in euthyroid patients with depression.(/p465/col2/para5) Reference AACE medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. American College of Endocrinology.8, 6. 1-13.Available at: http://www.aace.com/pub/pdf/guidelines/hypo_hyper.pdf . Accessed March 1, 2011.

When overt hypothyroidism coexists with dyslipidemia, the blood levels of total and LDL cholesterols are increased.(/p30/col2/para4) The mechanisms associated with dyslipidemia include impaired production of total cholesterol and decreased expression of LDL receptor. Severe cardiovascular disease and premature atherosclerosis, left untreated, can lead to the development of pericardial effusion, congestive heart failure, and coronary artery disease.(/p28/col2/para3) Reference Duntas LH, Biondi B. New insights into subclinical hypothyroidism and cardiovascular risk. Semin Thromb Hemost . 2011;37(1):27-34.

In middle-aged patients with subclinical hyperthyroidism , impaired diastolic function and reduced left ventricular systolic function at rest and during physical exertion are noted.(/p29/col1/para1) Studies reveal that subclinical hyperthyroidism is also associated with atherosclerosis and myocardial infarction.(/p29/col1/para4) Meta-analysis of high-quality studies reveal that total and cardiovascular-related mortality was noted only in patients who had subclinical hyperthyroidism and were less than 65 years of age.(/p29/col2/para4) Subclinical hyperthyroidism is associated with proatherogenic mechanisms leading to low-grade inflammation and this may also suggest cardiovascular disease.(/p30/col2/para4) Subclinical hyperthyroidism is known to be linked to a hypercoagulable state, but the degree of impact is yet to be studied.(/p32/col1/para1) LT4 therapy for subclinical hyperthyroidism reverses cardiovascular alterations, reduces risk factors, improves dyslipidaemia, and minimizes neurobehavioral changes.(/p31/col1/para1) Reference Duntas LH, Biondi B. New insights into subclinical hypothyroidism and cardiovascular risk. Semin Thromb Hemost . 2011;37(1):27-34.

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Let's start off with a clinical presentation. Ayesha is a 70-year-old woman, who was apparently healthy when she went for her routine visit to doctor. However, she complained of mild fatigue, dry skin, and difficulty in losing weight since last 2 years. The past medical and surgical history had been uneventful.

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Identificati 2 aspecte caracteristice ale bolii autoimune in urmatoarea imagine ecografica:

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Identificati 2 aspecte caracteristice ale bolii autoimune in urmatoarea imagine ecografica:

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Enumerati principalele complicatii ale hipotiroidismului netratat in sarcina asupra fatului/nou-nascutului.

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Enumerati principalele complicatii ale hipotiroidismului netratat in sarcina asupra fatului/nou-nascutului.

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Exemple de imagini ecografice reprezentative bolii autoimune tiroidiene:

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Exemple de imagini ecografice reprezentative bolii autoimune tiroidiene:

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Cum se modifica valorile normale ale TSH-ului pe parcursul sarcinii?

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Pregnancy and Autoimmune Thyroid Disease

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Dr. Emilia Gudovan, Medic primar endocrinolog

Centrul Medical ProVita - Diagnostic și tratament
Rezumat:
Tiroida prin hormonii secretați influențează întreaga existență a unui organism, intervenind în balanța energetică ce asigură funcționarea normală a tuturor organelor, vitalitatea, energia fizică şi mentală. În timpul sarcinii se produc modificări hormonale profunde şi creșterea necesităților metabolice ale fătului modifică funcţia tiroidei maternale.

Cuvinte-cheie: tiroidă, sarcină, făt
Abstract:
Hormones secreted by the thyroid affect the whole existence of the body, interfering in the energy balance that ensures normal functioning of all organs, vitality, physical and mental energy. During pregnancy, deep hormonal changes occur and the increasing metabolic needs of the fetus and change maternal thyroid functions.

Keywords: thyroid, pregnancy, fetus

Estrogenii cresc thyroid binding globulin (TBG) de 2-3 ori la câteva săptămâni după concepţie. Astfel crește cu 50% concentraţia tiroxinei totale TT4 şi a triiodotironinei - TT3 , acestea fiind legate de TBG. FT3 şi FT4 sunt în limite normale. O valoare uşor scăzută a FT4 în trimestrul al doilea şi/sau al treilea de sarcină poate fi normală sau poate reprezenta hipotiroidism, astfel că trebuie interpetat în contextul valorilor TT4 şi a TSH. Valoarea TSH-ului poate fi afectată de hCG (human chorionic gonadotropin), 95% poate fi mai mic de 0,03 mU/L în primul şi al doilea trimestru şi 0,13 mU/L în trimestrul al treilea de sarcină. Limita maximă a TSH-ului în trimestrul I de sarcină este mai mică de 3,0 mU/L şi mai mică de 3,5 mU/L în trimestrul al doilea şi al treilea de sarcină.
Modificări hormonale tiroidiene în timpul sarcinii
În timpul sarcinii volumul plasmatic maternal creşte cu 30-40% necesitând o expansiune a pool-ului hormonal tiroidian.

Deiodinaza placentară tip 3 (D3) creşte metabolizarea T4 matern în rT3 (reverse T3).

T4 maternal traversează placenta spre fetus.

HCG scade nivelul hormonilor liberi.
Factori ce scad capacitatea maternă de a creşte producţia de hormoni tiroidieni
Femei cu rezerve limitate de hormoni tiroidieni prin afecţiuni tiroidiene ca ablaţia parţială a glandei tiroide pentru macronodul tiroidian sau ablaţia totală pentru cancer tiroidian.

Tiroidite autoimune cu hipotiroidism determinat de distrugerea foliculilor tiroidieni de procesul autoimun.

Hipotiroidism post radioterapie cu I131 pentru hipertiroidism.

Aport inadecvat de iod, mai ales în zonele guşogene, necesarul de iod fiind mai mare în sarcină cu 40-50%. În sarcină, necesarul de iod creşte ca rezultat al pierderii de iod prin urină, secundar creşterii cu 50-100% a ratei filtratului gromerular (GFR); creşterea necesarului matern de iod şi a faptului că iodul nu ajunge la făt pentru sinteza de hormoni tiroidieni.

În timpul sarcinii, volumul glandei tiroide creşte, mai ales la femeile din zone cu deficit de iod. OMS recomandă administrarea de iod - 250 μg/zi - în timpul sarcinii şi a lactaţiei şi 150 μg/zi la femeile ce nu sunt gravide. Dacă aportul de iod este insuficient scade sinteza de hormoni tiroidieni, creşte secreţia de TSH, care stimulează creşterea în volum a tiroidei - guşa, fără a creşte însă şi sinteza de hormoni tiroidieni. În cazul unui deficit sever de iod, hiopotiridismul se manifestă atât la mamă cât şi la făt, uneori poate apăre cretinismul endemic.

Anticorpii antitiroidieni TSI, TRAB pot trece prin placentă la făt la 18-20 de săptămâni de sarcină şi pot determina hipertiroidism neonatal copiilor mamelor cu boală Graves. Se recomandă monotorizarea TSI şi TRAB şi urmărirea fătului dacă valoarea lor este mai mare de 2,5-3 ori.

Pot traversa placenta anticorpii antitiroglobulină (ATG) şi antiperoxidază tiroidiană (ATPO) care nu au influenţe asupra fătului, decât în rare cazuri putând determina hipotiroidism neonatal.

Hormonii tiroidieni fetali apar după dezvoltarea tiroidei fetale la aproximativ 12-14 săptămâni de sarcină, când axul hipotalamic-hipofiză-tiroidian devine funcţional. Până la 16 săptămâni de sarcină este funcţională numai tiroxina - T4 - eliberată transplacentar. Hormonii tiroidieni sunt necesari pentru dezvoltarea creierului fetal.

Hormonii tiroidieni şi deiodaza tip 2 (D2) au fost evidenţiaţi în cortexul cerebral fetal în săptămânile 5-7 de sarcină.

În creierul fetal T4 matern se converteşte în T3 ce influenţează proliferarea neuronilor şi astrocitelor şi migrarea lor în prima parte a sarcinii. Hormonii tiroidieni au un rol crucial în dezvoltarea creierului fetal.

Din trimestrul al doilea de sarcină, axa hipotalamo-hipofizo-tiroidiană a fătului este independentă de mamă cu excepţia aportului de iod maternal adecvat.

Medicamentele cu efect antitiroidian ca PTU, Metimasole, Carbimasole sau nivele crescute de TSI și TRAB pot afecta fătul și da gușă. În săptămânile 35-37 de sarcină, nivelul hormonilor tiroidienei şi TBG crește în platou. În timpul travaliului şi a perioadei neonatale creşte T4 şi capacitatea de conversie hepatică a T4 în T3.

Tireotoxicoza gestaţională tranzitorie cauzată de hCG care se leagă de receptorul TSH, stimulând sinteza de hormoni tiroidieni. Aceasta se observă la femeile cu hiperemesis gravidorum, la sarcinile gemelare, şi mai ales în sarcina molară. hCG are valori crescute peste 75000 UI/Ml. Pentru precizarea diagnosticului este necesar examenul ecografic fetal. Hipertiroidismul poate apare la circa 0,2 % din femeile gravide, boala Graves fiind în 85 % din cazuri.

Bolile tiroidiene autoimune se manifestă mai frecvent în primul trimestru de sarcină sau postpartum, deoarece sarcina are o acţiune de supresie imună şi până în al II-lea trimestru de sarcină nivelul AC antitiroidieni scade semnificativ.

În timpul sarcinii pot apare manifestări ce mimează hipertiroidismul, cum sunt intoleranţa la căldură, tahicardia, vasodilataţie periferică, scădere ponderală.

Diagnosticul este susținut de nivelul scăzut al TSH, crescut al FT4. Examenul ecografic tiroidian evidentiază guşă cu structură hipodensă, şi/sau hipoechogenă, cu circualţie crescută la examenul Color Flow Doppler. Iar ecografia fetală exclude mola hidatiformă.

Boala Graves reprezintă un risc crescut pentru mamă, tratamentul inadecvat putând duce la preeclampsie, tulburări de ritm cardiac - tahicardie, fibrilaţie atrială, scădere ponderală, insuficienţă cardiacă, rareori la criză tireotoxică. Tratamentul inadecvat al hipertiroidiei materne determină tulburări fetale, ca tulburări de creştere, naştere prematură, greutate mică la naştere sau supresia axului hipotalamo-hipofizo-tiroidian cu hipotiroidism central temporar la noul-născut. Toate gravidele cu boala Graves sau cu istoric de boală Graves trebuie testate penru TSI şi TRAB până în săptămâna a 22-a de sarcină. Dacă valorile TSI şi TRAB sunt crescute, se examinează ecografic fătul la 20 de săptămâni, examinarea se repetă la 4-6 săptămâni.
Tratament
Tratamentul hipertiroidismului la făt se face cu PTU - Propil thiouracil în doză suficient de mare pentru a trece în circualţia fetală. Anticorpii simulatorii de TSH -TSI rămân cu valori crescute după naştere şi stimulează tiroida neonatală, care produce hormoni tiroidieni în exces. Hipertiroidismul neonatal se manifestă cu iritabilitate, hiperkinezie, diaree, tahicardie, icter, tulburări de alimentaţie, guşă, mai rar exoftalmie, insuficienţă cardiacă, trombocitopenie, sindrom de hipervâscozitate, craniostenosis. Dacă boala nu este diagnosticată şi tratată, rata de mortalitate este de 30%. Tratatemntul cu ATS este indicat cel puțin 12 săptămâni, până când titrul de AC-TSI scade. Hipertiroidismul subclinic din perioada de sarcină, TSH-ul fiind supresat în mod normal, la unele gravide nu trebuie tratat.

Tiroidita postpartum apare la circa 5% din femeile aparent sănătoase şi la 25% la femeile cu diabet zaharat tip I, astfel că se recomandă screening cu determinarea ATPO şi ecografie tiroidiană. 19% din femeile cu tiroidită postpartum au hipertiroidism prin citoliză tiroidiană, 49% au hipotiroidism, iar 32% au hipertiroidism urmat de hipotiroidism post citoliză tiroidiană. Se recomandă urmăriea TSH, ATPO la 6-12 săptămâni şi 6 luni postpartum.

Femeile cu hipertiroidism vor fi tratate cu levothyroxină 6-12 luni până la un an postpartum. 70-80% dintre paciente revin la eutiroidism în 12 luni postpartum. Este necesară monitorizarea anuală a funcţiei tiroidiene, studiile arătând că 23% dintre femei sunt cu hipotiroidism 2-4 ani; 50% dintre femei fac hipotiroidism circa 7-9 ani postpartum. Cele cu titruri mari de ATPO fac hipotiroidism sever şi permanent. 70% dintre femeile care au devenit hipotiroidiene în primul an postpartum prezintă un risc de 70% de a face tiroidită postpartum la următoarea sarcină.

Bolile tiroidiene autoimune se întâlnesc la 5-10% dintre femeile sănătoase, hipotiroidismul subclinic fiind asimptomatic poate rămâne nediagnosticat. Bolile tiroidiene autoimune se pot asocia cu alte boli autoimune şi cu sindromul ovarelor polichistice, cu impact asupra fertilităţii crescând riscul de avorturi spontante sau infertilitate.

Screeningul pentru ATPO, FT4, TSH şi ecografic tiroidian pentru evidenţierea hipoechogenităţii tiroidiene caracteristică în tiroidita autoimună este obligatoriu la femeile cu infertilitate, precum şi la gravide trimestrial şi postpartum pentru diagnosticarea şi tratarea hipotiroidismului.

Sarcina contribuie la incidenţa mai crescută a patologiei nodulare tiroidiene, prevalenţa nodulilor tiroidieni fiind de 3,56%. Cancerul tiroidian are o prevalenţă de 4,4% la gravide procent apropiat de cel din populaţia generală.

Cunoscând repercusiunile hipotiroidismului matern asupra evoluţiei sarcinii şi a dezvoltării neuropsihice a fătului, depistarea din timp a hipotiroidismului şi tratarea lui sunt obligatorii în protocolul de monitorizare a gravidelor.

„Orice întârziere în diagnosticul şi tratamentul hipotiroidismului matern, chiar şi a formei subclinice poate costa inteligenţe urmaşilor" (Glinoer, 2000).

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Patologia tiroidiană în sarcină - Revista Galenus

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Dr. Emilia Gudovan, Medic primar endocrinolog Centrul Medical ProVita - Diagnostic și tratament Rezumat: Tiroida prin hormonii secretați influențează întreaga existență a unui organism, intervenind în balanța energetică ce asigură funcționarea normală a tuturor organelor, vitalitatea, energia fizică şi mentală. În timpul sarcinii se produc modificări hormonale profunde şi creșterea necesităților metabolice ale fătului modifică funcţia tiroidei maternale.