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In a small number of cases the thyroid gland increases markedly in size, though we are ignorant as to its significance.
—J. Whitridge Williams (1903)
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In 1903, little was known of many endocrine disorders. Still, endocrinopathies seem particularly closely related to pregnancy because of its gestational proclivity for prodigious hormone secretion. This is best illustrated by placental lactogen in diabetes, the most common endocrinopathy encountered in pregnancy (Chap. 57, Types of Diabetes). Pregnancy is also interrelated with some endocrinopathies that are at least partially due to autoimmune dysregulation. Clinical manifestations of this result from complex interplay among genetic, environmental, and endogenous factors that activate the immune system against targeted cells within endocrine organs. An extraordinary example of these interactions comes from studies that implicate maternal organ engraftment by fetal cells that were transferred during pregnancy. These cells later provoke antibody production, tissue destruction, and autoimmune endocrinopathies.
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Taken in aggregate, disorders of the thyroid gland are common in young women and thus frequently encountered in pregnancy. Maternal and fetal thyroid function are intimately related, and drugs that affect the maternal thyroid also affect the fetal gland. Moreover, thyroid autoantibodies have been associated with increased rates of early pregnancy wastage. Also, uncontrolled thyrotoxicosis and untreated hypothyroidism are both associated with adverse pregnancy outcomes. Finally, evidence suggests that the severity of some autoimmune thyroid disorders may be ameliorated during pregnancy, only to be exacerbated postpartum.
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Thyroid Physiology and Pregnancy
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Maternal thyroid changes are substantial, and normally altered gland structure and function are sometimes confused with thyroid abnormalities. These alterations are discussed in detail in Chapter 4 (Thyroid Gland), and normal serum hormone level values are found in the Appendix (Serum and Blood Constituents). First, maternal serum concentrations of thyroid binding globulin are increased concomitantly with total or bound thyroid hormone levels (Fig. 4-16). Second, thyrotropin, also called thyroid-stimulating hormone (TSH), currently plays a central role in screening and diagnosis of many thyroid disorders. Notably, TSH receptors are cross stimulated, albeit weakly, by massive quantities of human chorionic gonadotropin (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 maternal hCG serum levels are maximal, thyroid hormone secretion is stimulated. The resulting greater serum free thyroxine (T4) levels act to suppress hypothalamic thyrotropin-releasing hormone (TRH) and in turn limit pituitary TSH secretion (Fig. 58-1). Accordingly, TRH is undetectable in maternal serum. Conversely, in fetal serum, beginning at midpregnancy, TRH becomes detectable, but levels are static and do not increase.
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