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Thyroid diseases are among the most common endocrine disorders encountered during pregnancy. They are challenging both because of pregnancy-related changes in thyroid physiology that make diagnosis of thyroid disorders difficult and because of the limited number of medications used to treat mother and fetus. Screening for subclinical thyroid disorders remains a highly debated topic.


Thyroid Function during Normal Pregnancy


The thyroid, a gland that functions to provide thermal and metabolic regulation, develops from the third week in gestation from the primitive pharynx. The gland then migrates to the neck and starts to produce thyroid hormone by 10–12 weeks' gestation.


Maternal thyroid physiology is altered during normal pregnancy. There is glandular hyperplasia with thyroid enlargement. Thyroid volume is increased on ultrasound examination, but the echostructure is unchanged. The normal increase in the renal glomerular filtration rate causes an increase in urinary iodide clearance, necessitating increased intake of dietary iodine in order to make and maintain thyroid hormone concentrations. Both total thyroxine (T4) and triiodothyronine (T3) levels increase because the level of their carrier, thyroxine-binding globulin (TBG), becomes elevated. Estrogen causes increased TBG synthesis with decreased TBG clearance. Because of the similar subunits of chorionic gonadotropin and thyrotropin (thyroid-stimulating hormone [TSH]), crossover between these 2 peptides can lead to an increase in free thyroxine (fT4) in the first trimester. The TSH level is lowest and fT4 level highest when human chorionic gonadotropin (hCG) levels peak. Elevated fT4 causes suppression of TSH, which, in turn, causes barely detectable levels of maternal thyrotropin-releasing hormone (TRH). Overall, the demand for T4 increases by an estimated 1–3% above daily nonpregnant needs. The increased demand starts very early, reaching a plateau at 16–20 weeks. These normal physiologic changes make diagnosis of thyroid disease during pregnancy difficult.


Studies from animal models have helped to elucidate the role of maternal T4 in the fetus. T3 is made by conversion of maternal T4. It has been demonstrated that if maternal T4 is low, fetal T3 levels in the brain will be low even in the presence of normal maternal and fetal serum T3, suggesting that both T3 and T4 in the fetal brain are maternal T4 dependent. Further evidence of a maternal source of T3 in the fetal brain is that by midgestation, fetal concentration of T3 is 34% of adult levels. This is much higher than would be expected considering the low circulating fetal serum levels. It is during midgestation that initial growth velocity of the fetal brain occurs, and animal data suggest that the thyroid hormone necessary for this development is primarily maternally derived. Toward the end of the first trimester, the fetal hypothalamic–pituitary–thyroid axis becomes active. By 14 weeks' gestation, fetal production of T4 is detectable. Normal thyroid hormones levels in the fetus and newborn ...

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