The pregnant woman undergoes profound anatomic and physiologic changes in almost every organ system. These adaptations to the pregnant state begin just after conception and evolve through delivery, after which they almost completely revert back to the nonpregnant state over a period of weeks. The purpose of these alterations is to accommodate the needs of the maternal-fetal unit.
The normal metabolic and endocrinologic changes in pregnancy will be reviewed here. Metabolic and endocrinologic diseases complicating pregnancy are discussed separately.
Maternal endocrine adaptations to pregnancy involve the hypothalamus, pituitary, parathyroid, thyroid, adrenal glands, and ovary, and are linked to the interactions of the fetal-placental-maternal unit.
Hypothalamic hormones — The hypothalamus regulates much of the endocrine system by coordinating input from multiple areas and output via the hypothalamic-pituitary axis through cell to cell communication (paracrine signaling) and within the same cell communication (autocrine signaling). This axis directly affects the function of the thyroid gland, the adrenal gland, and the gonads and influences growth, lactation, and water balance (table 1) [1,2]. An intact hypothalamus is necessary for natural conception; however, it is not essential when assisted reproductive techniques are being employed as long as full hormone replacement therapy is administered . (See "Hypothalamic-pituitary axis".)
The hypothalamic stimulatory hormones are gonadotropin-releasing hormone (GnRH), corticotropin-releasing hormone (CRH), growth hormone-releasing hormone (GHRH), thyrotropin-releasing hormone (TRH), and prolactin-releasing factors. Somatostatin and prolactin-inhibiting factors are inhibitory hypothalamic hormones. These hormones are present at high concentrations in the portal circulation where they are biologically active, but are almost nondetectable in the systemic circulation of nonpregnant women. However, the circulating concentrations of many of these hormones rise during pregnancy due to placental production of identical or variant hormones.