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Overview of thyroid disease in pregnancy

INTRODUCTION

The evaluation and treatment of pregnant women with thyroid disease parallel that of nonpregnant women and men, but present some unique problems. An overview of thyroid physiology and disease during pregnancy is presented here. Some of the disorders reviewed below are discussed separately in individual topic reviews. (See "Hypothyroidism during pregnancy: Clinical manifestations, diagnosis, and treatment" and "Hyperthyroidism during pregnancy: Clinical manifestations, diagnosis, and causes" and "Hyperthyroidism during pregnancy: Treatment".)

THYROID ADAPTATION DURING NORMAL PREGNANCY

The diagnosis of thyroid disease during pregnancy requires an understanding of the changes in thyroid physiology and thyroid function tests that accompany normal pregnancy.

Thyroid physiology — To meet the increased metabolic needs during a normal pregnancy, there are changes in thyroid physiology that are reflected in altered thyroid function tests [1]. The major changes in thyroid function during pregnancy are an increase in serum thyroxine-binding globulin (TBG) concentrations and stimulation of the thyrotropin (TSH) receptor by human chorionic gonadotropin (hCG).

Thyroxine binding globulin — During pregnancy, serum TBG concentrations rise almost two-fold because estrogen increases TBG production and TBG sialylation, which results in decreased clearance of TBG [2]. To maintain adequate free thyroid hormone concentrations during this period, thyroxine (T4) and triiodothyronine (T3) production by the thyroid gland must increase. Total T4 and T3 concentrations rise during the first half of pregnancy, plateauing at approximately 20 weeks of gestation, at which time a new steady state is reached and the overall production rate of thyroid hormones returns to prepregnancy rates. Thus, TBG excess leads to an increase in both serum total T4 and T3 concentrations. (See "Euthyroid hyperthyroxinemia and hypothyroxinemia".)

hCG and thyroid function — hCG is one of a family of glycoprotein hormones, including TSH, with a common alpha-subunit and a unique beta-subunit. However, there is considerable homology between the beta-subunits of hCG and TSH. As a result, hCG has weak thyroid-stimulating activity [3]. In a human thyroid cell-culture assay, as an example, 1 microU of hCG was equivalent to 0.0013 microU of TSH [4].

                               

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Literature review current through: Nov 2014. | This topic last updated: Jun 19, 2014.
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