Fetal skeleton mineralization requires approximately 30 g of calcium, primarily during the third trimester (Sanz-Salvador, 2015). Although this amounts to only 3 percent of the total calcium held within the maternal skeleton, the provision of calcium still challenges the mother. In most circumstances, augmented maternal calcium absorption provides the additional calcium. During pregnancy, the amount of calcium absorbed rises gradually and reaches approximately 400 mg/ d in the third trimester. Greater calcium absorption appears to be mediated by elevated maternal 1,25-dihydroxyvitamin D concentrations. This occurs despite decreased PTH levels during early pregnancy, which is the normal stimulus for active vitamin D production within the kidney. Indeed, PTH plasma concentrations decline during the irst trimester and then rise progressively throughout the remainder of pregnancy (Pitkin, 1979).
he increased production of active vitamin D is likely due to placental production of either PTH or a PTH-related protein (PTH-rP). Outside pregnancy and lactation, PTH-rP is usually detectable only in serum of women with hypercalcemia due to malignancy. During pregnancy, however, PTH-rP concentrations increase signiicantly. his protein is synthesized in both fetal tissues and maternal breasts.
he C cells that secrete calcitonin are located predominantly in the perifollicular areas of the thyroid gland. Calcitonin opposes actions of PTH and vitamin D and protects the matenal skeleton during times of calcium stress. Pregnancy and lactation cause profound maternal calcium stress, ostensibly for the sake of the fetus. Indeed, fetal calcitonin levels are at least twofold higher than maternal levels (Ohata, 2016). And although maternal levels fall during pregnancy, they generally rise postpartum (M011er, 2013).
Calcium and magnesium promote the biosynthesis and secretion of calcitonin. Various gastric hormones-gastrin, pentagastrin, glucagon, and pancreozymin-and food ingestion also increase calcitonin plasma levels.
In normal pregnancy, unlike their fetal counterparts, the maternal adrenal glands undergo little, if any, morphological change. The serum concentration of circulating cortisol rises, but much of it is bound by transcortin, the cortisol-binding globulin. The adrenal secretion rate of this principal glucocorticoid is not elevated, and probably it is lower than in the nonpregnant state. he metabolic clearance rate of cortisol, however, is diminished during pregnancy because its half-life is nearly doubled compared with that for nonpregnant women (Migeon, 1957). Administration of estrogen, including most oral contraceptives, causes changes in serum cortisol levels and transcortin similar to those of pregnancy Qung, 201i1).
During early pregnancy, the levels of circulating adrenocorticotropic hormone (A CTH) , also known as corticotropin, are dramatically reduced. As pregnancy progresses, ACTH and free cortisol levels rise equally and strikingly (Fig. 4-18). This ,50