There are no endocrine disorders that are unique to pregnancy. However, endocrinopathies seem particularly closely related to pregnancy due to their proclivity for hormone secretion. Indeed, some hormones are secreted in prodigious quantities. This is probably 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.
Taken in aggregate, these are common in young women and thus frequently managed in pregnancy. There is an intimate relationship between maternal and fetal thyroid function, and drugs that affect the maternal thyroid also affect the fetal gland. Moreover, thyroid autoantibodies have been associated with increased early pregnancy wastage, and uncontrolled thyrotoxicosis and untreated hypothyroidism are both associated with adverse pregnancy outcomes. Finally, there is evidence that autoimmune thyroid disorder severity may be ameliorated during pregnancy, only to be exacerbated postpartum.
Thyroid Physiology and Pregnancy
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 (Prolactin), and normal 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. 4-17, Iodine Status). Second, thyrotropin, also called thyroid-stimulating hormone (TSH), currently plays a central role in screening and diagnosis of many thyroid disorders. Serum TSH levels in early pregnancy decline because of weak TSH-receptor stimulation from 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 hCG serum levels are maximal, thyroid hormone secretion is stimulated. The resulting increased serum free thyroxine 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, beginning at midpregnancy, TRH becomes detectable in fetal serum, but levels are static and do not increase with advancing gestation.
Gestational age-specific values for serum thyroid-stimulating hormone (TSH) levels (black lines) and free thyroxine (T4) levels (blue lines). Data were derived from 17,298 women tested during pregnancy. For each color, the dark solid lines represent the 50th percentile, whereas the upper and lower light lines represent the 2.5th and ...
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