title: Endocrine regulation of calcium homeostasis during pregnancy.
abstract: The principal maternal physiologic adjustment with respect to calcium metabolism is increasing PTH secretion, which maintains the serum ionic calcium level within its characteristically narrow physiologic limits in the face of an expanding extracellular fluid volume, increased urinary excretion, and calcium transfer to the fetus. Additionally, PTH promotes increased renal synthesis of 1,25-(OH)2D3, which acts in concert with PTH to meet the calcium demands of gestation. Whether or not calcitonin secretion increases as well is not clear; if so, this effect may be important in protecting the maternal skeleton. The primary characteristic of perinatal calcium metabolism is the active placental transport of calcium ions from mother to fetus, making the fetus relatively hypercalcemic. Since none of the calcitropic hormones cross the placenta, hypercalcemia apparently suppresses either secretion or activity of PTH by the fetus and stimulates fetal calcitonin release, creating an environment (high calcium, low PTH, high calcitonin) favorable to skeletal growth. With birth, the transplacental calcium source terminates abruptly and the serum calcium level declines for 24 to 48 hours, after which it stabilizes and then rises slightly. Neonatal calcium homeostasis probably reflects multiple influences, including the respective calcitropic hormones and other involved ions such as magnesium and phosphate. The physiologic mechanisms regulating calcium homeostasis during pregnancy and the perinatal period generally operate very effectively. Thus, aberrations leading to clinically evident disease states are relatively infrequent. Maternal hyperparathyroidism causes several complications, notably hypocalcemic tetany in the newborn, and maternal hypoparathyroidism may be associated with perinatal hyperparathyroidism. Diabetic pregnancy leads to altered calcium metabolism in mother, fetus, and newborn; the primary feature may be chronic hypomagnesemia, which leads to hypoparathyroidism to mother and fetus. There is some suggestion of an etiologic role for calcium in hypertensive disorders, and, in any event, magnesium sulfate therapy influences calcium homeostasis. Finally, leg cramps in the pregnant woman may reflect alterations in calcium metabolism.
mesh_terms: D000818:Animals; D002112:Calcifediol / Q000097:blood; D002116:Calcitonin / Q000502:physiology; D002118:Calcium / Q000378:metabolism / Q000502:physiology*; D005260:Female; D005333:Fetus / Q000502:physiology; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000188:drug therapy; D006996:Hypocalcemia / Q000209:etiology; D007231:Infant, Newborn; D008274:Magnesium / Q000097:blood; D008278:Magnesium Sulfate / Q000627:therapeutic use; D009120:Muscle Cramp / Q000209:etiology; D010279:Parathyroid Diseases; D010281:Parathyroid Hormone / Q000502:physiology; D010920:Placenta / Q000502:physiology; D011247:Pregnancy; D011248:Pregnancy Complications; D011249:Pregnancy Complications, Cardiovascular / Q000188:drug therapy; D011254:Pregnancy in Diabetics; D014807:Vitamin D / Q000502:physiology
chemical_list: D010281:Parathyroid Hormone; D014807:Vitamin D; D008278:Magnesium Sulfate; D002116:Calcitonin; D008274:Magnesium; D002112:Calcifediol; D002118:Calcium