Pregnancy influences the production of several endocrine hormones that control the physiologic adaptations in other organ systems.
Pregnancy produces an overall euthyroid state, despite sev-eral changes in thyroid regulation. The thyroid gland enlargesmoderately during pregnancy, but does not produce thy-romegaly or goiter. In the first trimester, human chori-onic gonadotropin (hCG), which has thyrotropin-like activity, stimulates maternal thyroxine (T4) secretion and produces a transient rise in the free T4 concentra-tion (Fig. 5.3). The decline in placental hCG produc-tion following the first trimester results in normalization of free T4 concentrations. Beginning early in pregnancy, estrogen induces hepatic synthesis of thyroxine-binding globulin (TBG), resulting in an increase in total T4 and total triiodothyronine (T3) levels. Levels of free T4 and free T3, the active hormones, are unchanged from the normal range for nonpregnant patients.
Although pregnancy does not alter the size or morphology of the adrenal gland, it does influence hormone synthesis. As with TBG,estrogen induces hepatic synthesis of cortisol-binding globulin, resulting in elevated levels of serum cortisol. The concentration of free plasma cortisol progressively increases from the first trimester until term.
Levels of corticotropin (ACTH) rise in conjunction with serum cortisol. Levels of aldosterone increase markedly due to enhanced adrenal synthesis. Maternal levels of deoxy-corticosterone increase as the result of estrogen stimu-lation of renal synthesis, rather than increased adrenal production. Maternal levels of dehydroepiandrosterone sulfate decrease due to increased hepatic uptake and conversion to estrogen.