Division of Endocrinology, University of Pittsburgh School of Medicine, NW 810, UPMC Montefiore, 3459 5th Avenue, Pittsburgh, Pennsylvania 15213, USA.
J Clin Endocrinol Metab. 2010 Apr;95(4):1767-76. doi: 10.1210/jc.2009-1518. Epub 2010 Feb 11.
Mothers who exclusively breastfeed lose up to 10% of their bone mass. This is primarily mediated by PTHrP, in combination with low estrogen levels. The mechanisms underlying this marked bone loss are unknown. Uncoupling of bone turnover, which is seen in other prototypical states of bone loss, would seem the likely explanation. However, the most current markers of bone turnover have not been studied in human lactation.
The purpose of this study was to assess bone formation in lactating humans using the most current bone turnover markers.
We conducted a prospective cohort study with repeated measures of bone metabolism in a volunteer sample of 49 women, recruited into three study groups: lactating, bottle feeding, and healthy controls. The postpartum women were studied at 6-8 and 12-14 wk postpartum, whereas the controls were studied at the follicular phase of their menstrual cycles.
Biochemical markers of bone turnover were assessed.
Mean serum C-telopeptide of type I collagen, a sensitive marker of bone resorption, was approximately 2-fold higher in lactating women as compared with bottle-feeding and healthy controls (P = 0.037 and P < 0.001, respectively). Surprisingly, amino-terminal telopeptides of procollagen 1, the most current marker of bone formation, bone-specific alkaline phosphatase, and osteocalcin were all significantly higher in the lactating group as compared with controls (P < 0.001, P = 0.002, and P < 0.001, respectively).
In contrast to prototypical states of rapid bone loss (myeloma, cancer, and immobilization) in which markers of bone turnover display marked uncoupling, lactational bone loss, as assessed in this small exploratory study, is distinct, showing comparably rapid bone loss in the face of apparent osteoclast-osteoblast coupling.
纯母乳喂养的母亲会损失高达 10%的骨量。这主要是由甲状旁腺激素相关肽(PTHrP)介导的,同时还伴随着雌激素水平降低。导致这种明显骨丢失的机制尚不清楚。在其他典型的骨丢失状态中观察到的骨转换解偶联似乎是合理的解释。然而,在人类哺乳期尚未研究最当前的骨转换标志物。
本研究旨在使用最当前的骨转换标志物评估哺乳期人类的骨形成。
我们对 49 名志愿者进行了一项前瞻性队列研究,对其进行了重复的骨代谢测量,这些志愿者被招募到三个研究组中:哺乳期、奶瓶喂养和健康对照组。产后女性在产后 6-8 周和 12-14 周进行研究,而对照组则在其月经周期的卵泡期进行研究。
评估了骨转换的生化标志物。
与奶瓶喂养和健康对照组相比,哺乳期妇女的血清 I 型胶原 C 端肽(一种敏感的骨吸收标志物)平均高出约 2 倍(P = 0.037 和 P < 0.001)。令人惊讶的是,与对照组相比,前胶原 1 氨基末端肽、最当前的骨形成标志物、骨碱性磷酸酶和骨钙素均显著升高(P < 0.001、P = 0.002 和 P < 0.001)。
与典型的快速骨丢失状态(骨髓瘤、癌症和固定)相反,在这些状态中,骨转换标志物显示出明显的解偶联,在这项小型探索性研究中评估的哺乳期骨丢失不同,在面对明显的破骨细胞-成骨细胞偶联时,显示出相当快速的骨丢失。