[Osteoporosis in pregnancy and lactation]

Abstract

Normal pregnancy and lactation lead to a combination of adaptive metabolic responses, the end result of which is to assure adequate delivery of mineral to the fetus while affording protection to the maternal skeleton. Elevated circulating levels of 1.25-OH vitamin D lead to increased efficiency of maternal intestinal calcium absorption and possibly lead to hypersecretion of calcitonin. Although serum concentrations of parathyroid hormone do not change during pregnancy, increased levels of a related hormone, PTH-related peptide, seem to contribute to a state of maternal functional hyperparathyroidism and maintain the fetal-maternal calcium gradient necessary to provide calcium to the fetus. Bone turnover increases during lactation and diminishes urinary calcium loss mobilizing mineral for the milk. Elevated levels of ionized calcium and phosphorus possibly correlate with increased bone resorption and decreased urinary excretion of these minerals. Bone mass is not normally lost during pregnancy but may decrease with sustained lactation for as long as six months. If lactation ceases before nine months, however, bone mass usually is restored. However, several rare forms of osteoporosis have been associated with pregnancy and lactation.