Department of Endocrinology and Internal Medicine, Aarhus University Hospital, and Department of Clinical Medicine, Faculty of Health Sciences, Aarhus University, Tage Hansens Gade 2, 8000, Aarhus C, Denmark.
Osteoporos Int. 2013 Apr;24(4):1307-20. doi: 10.1007/s00198-012-2062-2. Epub 2012 Aug 2.
Pregnancy and lactation cause major changes in calcium homeostasis and bone metabolism. This population-based cohort study presents the physiological changes in biochemical indices of calcium homeostasis and bone metabolism during pregnancy and lactation
We describe physiological changes in calcium homeostasis, calcitropic hormones and bone metabolism during pregnancy and lactation.
We studied 153 women planning pregnancy (n=92 conceived) and 52 non-pregnant, age-matched female controls. Samples were collected prior to pregnancy, once each trimester and 2, 16 and 36 weeks postpartum. The controls were followed in parallel.
P-estradiol (E2), prolactin and 1,25-dihydroxyvitamin D (1,25(OH)2D) increased (p<0.001) during pregnancy, whereas plasma levels of parathyroid hormone (P-PTH) and calcitonin decreased (p<0.01). Insulin-like growth factor I (IGF-I) was suppressed (p<0.05) in early pregnancy but peaked in the third trimester. Postpartum, E2 was low (p<0.05); prolactin decreased according to lactation status (p<0.05). 1,25(OH)2D was normal and IGF-I was again reduced (p<0.05). P-PTH and calcitonin increased postpartum. From early pregnancy, markers of bone resorption and formation rose and fall, respectively (p<0.001). From the third trimester, bone formation markers increased in association with IGF-I changes (p<0.01). Postpartum increases in bone turnover markers were associated with lactation status (p<0.001). During lactation, plasma phosphate was increased, whereas calcium levels tended to be decreased which may stimulate PTH levels during and after prolonged lactation.
The increased calcium requirements in early pregnancy are not completely offset by increased intestinal calcium absorption caused by high 1,25(OH)2D since changes in bone markers indicated a negative bone balance. The rise in bone formation in late pregnancy may be initiated by a spike in IGF-I levels. The high bone turnover in lactating women may be related to high prolactin and PTH levels, low E2 levels and perhaps increased parathyroid hormone-related protein levels.
妊娠和哺乳期会导致钙稳态和骨代谢发生重大变化。本基于人群的队列研究展示了妊娠和哺乳期钙稳态、钙调节激素和骨代谢的生理变化。
我们描述了妊娠和哺乳期钙稳态、钙调节激素和骨代谢的生理变化。
我们研究了 153 名计划妊娠的女性（92 名成功妊娠）和 52 名未妊娠、年龄匹配的女性对照。样本在妊娠前、妊娠每三个月和产后 2、16 和 36 周采集。对照组进行了平行随访。
妊娠期间雌二醇（E2）、催乳素和 1,25-二羟维生素 D（1,25(OH)2D）增加（p<0.001），而甲状旁腺激素（P-PTH）和降钙素的血浆水平降低（p<0.01）。胰岛素样生长因子 I（IGF-I）在妊娠早期被抑制（p<0.05），但在第三个三个月达到峰值。产后，E2 水平较低（p<0.05）；催乳素根据哺乳状态而降低（p<0.05）。1,25(OH)2D 正常，IGF-I 再次降低（p<0.05）。P-PTH 和降钙素在产后增加。从妊娠早期开始，骨吸收和形成的标志物分别上升和下降（p<0.001）。从第三个三个月开始，骨形成标志物的增加与 IGF-I 的变化相关（p<0.01）。产后骨转换标志物的增加与哺乳状态相关（p<0.001）。哺乳期时，血浆磷酸盐增加，而血钙水平趋于降低，这可能会在长期哺乳期间刺激 PTH 水平。
妊娠早期增加的钙需求并未被高水平 1,25(OH)2D 引起的肠道钙吸收增加完全抵消，因为骨标志物的变化表明存在负钙平衡。妊娠晚期骨形成的增加可能是 IGF-I 水平激增引发的。哺乳期妇女的高骨转换可能与高催乳素和 PTH 水平、低雌二醇水平以及可能增加的甲状旁腺激素相关蛋白水平有关。
