Kovacs Christopher S.
Faculty of Medicine – Endocrinology, Health Sciences Centre, Memorial University of Newfoundland, 300 Prince Philip Drive, St. John’s, Newfoundland, A1B 3V6, Canada
Pregnancy and lactation require women to provide calcium to the fetus and neonate in amounts that may exceed their normal daily intake. Specific adaptations are invoked within each time period to meet the fetal, neonatal, and maternal calcium requirements. During pregnancy, intestinal calcium and phosphate absorption more than double, and this appears to be the main adaptation to meet the fetal demand for mineral. During lactation, intestinal calcium absorption is normal. Instead, the maternal skeleton is resorbed through the processes of osteoclast-mediated bone resorption and osteocytic osteolysis, in order to provide most of the calcium content of breast milk. In women this lactational loss of bone mass and strength is not suppressed by higher dietary intakes of calcium. After weaning, the skeleton appears to be restored to its prior bone density and strength, together with concomitant increases in bone volumes and cross-sectional diameters that may offset any effect of failure to completely restore the trabecular microarchitecture. These maternal adaptations during pregnancy and lactation also influence the presentation, diagnosis, and management of disorders of calcium, phosphorus, and bone metabolism such as primary hyperparathyroidism, hypoparathyroidism, vitamin D deficiency, and phosphate disorders. Pregnancy and lactation can also cause pseudohyperparathyroidism, a form of hypercalcemia that is mediated by parathyroid hormone-related protein, produced in the breasts or placenta during pregnancy, and by the breasts alone during lactation. Although rarely women may experience fragility fractures during pregnancy or lactation, for most women parity and lactation do not affect the long-term risks of low bone density, osteoporosis, or fracture. For complete coverage of all related areas of Endocrinology, please visit our on-line FREE web-text, WWW.ENDOTEXT.ORG.
怀孕和哺乳期要求女性为胎儿和新生儿提供的钙量可能超过其正常每日摄入量。在每个时间段都会产生特定的适应性变化，以满足胎儿、新生儿和母体对钙的需求。怀孕期间，肠道对钙和磷的吸收增加一倍多，这似乎是满足胎儿对矿物质需求的主要适应性变化。哺乳期，肠道对钙的吸收正常。相反，母体骨骼通过破骨细胞介导的骨吸收和骨细胞溶骨过程被吸收，以提供母乳中的大部分钙含量。在女性中，这种哺乳期骨量和骨强度的损失不会因更高的钙饮食摄入量而受到抑制。断奶后，骨骼似乎恢复到之前的骨密度和骨强度，同时骨体积和横截面直径增加，这可能抵消未能完全恢复小梁微结构的任何影响。怀孕和哺乳期的这些母体适应性变化也会影响钙、磷和骨代谢紊乱（如原发性甲状旁腺功能亢进、甲状旁腺功能减退、维生素D缺乏和磷紊乱）的表现、诊断和管理。怀孕和哺乳期还可能导致假性甲状旁腺功能亢进，这是一种高钙血症，由孕期乳房或胎盘产生的甲状旁腺激素相关蛋白介导，哺乳期仅由乳房产生。虽然很少有女性在怀孕或哺乳期会发生脆性骨折，但对大多数女性来说，生育和哺乳并不影响低骨密度、骨质疏松症或骨折的长期风险。欲全面涵盖内分泌学的所有相关领域，请访问我们的在线免费网络文本，网址为WWW.ENDOTEXT.ORG。
