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INTRODUCTION: Maternal and fetal thyroid function are intimately related, and drug that affect the maternal thyroid also affect the fetal gland. Thyroid autoantibodies have been associated with increased rates of early pregnancy wastage and uncontrolled thyrotoxicosis. Thyroid autoantibodies and untreated hypothyroidism both are associated with adverse pregnancy outcome. Finally, evidence suggest that the severity of some autoimmune thyroid disorder may ameliorate during pregnancy, only to be exacerbated during postpartum period [1] . Serum TSH levels decline in early pregnancy because of the massive quantity of HCG secreted by placental trophoblast. Because TSH does not cross the placenta, it has no direct fetal effects, during the first 12 weeks of gestation, when HCG serum level are maximal, thyroid hormone secretion is stimulated. The resulting increased serum free thyroxin level acts to suppress hypothalamic thyrotropin releasing hormone (TRH) and in turn limit pituitary TSH secretion. Throughout pregnancy, maternal thyroxin is transferred to the fetus. Maternal thyroxin is important for normal fetal brain development, especially before the onset of fetal thyroid gland function. Maternal source account for 30% of thyroxin in fetal serum at term. Thyroid disorders in pregnancy are associated with poor pregnancy outcome. Both hypothyroidism and hyperthyroidism can lead to adverse obstetric outcome. The prevalence of hypothyroidism reported in India is 12 %, whereas hyperthyroidism is seen in 1.25% in pregnant women [2] . The most common cause of hypothyroidism in pregnancy is Hashimoto thyroiditis. Clinical identification of hypothyroidism is especially difficult during pregnancy because many of the signs or symptoms are also common to pregnancy itself. Thyroid analyte testing should be performed on symptomatic women or those with a history of thyroid disease. Pregnancy is associated with an increased thyroxine demand; this is believed to be related to increased estrogen production. Pregnancy Outcome with Overt Hypothyroidism are–preeclampsia, placental abruption, preterm birth, still birth, cardiac dysfunction and birth weight. The clinical practice guidelines from the endocrine society, the American Thyroid Association, American Association Introduction Page | 4 of Clinical Endocrinologists and American College of Obstetricians and Gynecologists (2017) now uniformly recommend screening only those at increased risk during pregnancy [3] . ATA revised their recommendations in 2017. They recommended that the first trimester upper normal limit cut off should be obtained by deducting ‘0.5 mIU/L’ from pre pregnancy TSH value. But if it is not known then ‘4.0 mIU/L’ should be taken as upper limit of normal cutoff [5] ,This cut off should be maintained at 0.1 - 2.5 miu/ml in the first trimester and at 0.2 -3.0 miu/ml in the second trimester and 0.3 - 3miu/ml in the third trimester as well as endocrinology society guidelines, (2012) [4]. Thyroid disorders in pregnancy are important causes of adverse pregnancy outcome. So, it is very pertinent that thyroid function is maintained in normal range during pregnancy. Serum thyroid –stimulating hormone (TSH) value is the best indicator for assessing and monitoring thyroid function. |
