Prince Richard L, Devine Amanda, Dhaliwal Satvinder S, Dick Ian M
School of Medicine and Pharmacology, University of Western Australia, Australia.
Arch Intern Med. 2006 Apr 24;166(8):869-75. doi: 10.1001/archinte.166.8.869.
Increased dietary calcium intake has been proposed as a population-based public health intervention to prevent osteoporotic fractures. We have examined whether calcium supplementation decreases clinical fracture risk in elderly women and its mechanism of action.
Five-year, double-blind, placebo-controlled study of 1460 women recruited from the population and older than 70 years (mean age, 75 years) who were randomized to receive calcium carbonate, 600 mg twice per day, or identical placebo. The primary end points included clinical incident osteoporotic fractures, vertebral deformity, and adverse events ascertained in 5 years. Bone structure was also measured using dual x-ray absorptiometry of the hip and whole body, quantitative ultrasonography of the heel, and peripheral quantitative computed tomography of the distal radius.
Among our patients, 16.1% sustained 1 or more clinical osteoporotic fractures. In the intention-to-treat analysis, calcium supplementation did not significantly reduce fracture risk (hazard ratio, 0.87; 95% confidence interval, 0.67-1.12). However, 830 patients (56.8%) who took 80% or more of their tablets (calcium or placebo) per year had reduced fracture incidence in the calcium compared with the placebo groups (10.2% vs 15.4%; hazard ratio, 0.66; 95% confidence interval, 0.45-0.97). Calcium-treated patients had improved quantitative ultrasonography findings of the heel, femoral neck and whole-body dual x-ray absorptiometry data, and bone strength compared with placebo-treated patients. Of the 92 000 adverse events recorded, constipation was the only event increased by the treatment (calcium group, 13.4%; placebo group, 9.1%).
Supplementation with calcium carbonate tablets supplying 1200 mg/d is ineffective as a public health intervention in preventing clinical fractures in the ambulatory elderly population owing to poor long-term compliance, but it is effective in those patients who are compliant.
增加膳食钙摄入量已被提议作为一项基于人群的公共卫生干预措施，以预防骨质疏松性骨折。我们研究了补钙是否能降低老年女性的临床骨折风险及其作用机制。
对从人群中招募的1460名70岁以上（平均年龄75岁）的女性进行了为期5年的双盲、安慰剂对照研究，她们被随机分配接受每天两次、每次600毫克的碳酸钙或相同的安慰剂。主要终点包括5年内确定的临床骨质疏松性骨折、椎体畸形和不良事件。还使用髋部和全身双能X线吸收法、足跟定量超声检查和桡骨远端外周定量计算机断层扫描测量了骨结构。
在我们的患者中，16.1%发生了1次或更多次临床骨质疏松性骨折。在意向性分析中，补钙并未显著降低骨折风险（风险比，0.87；95%置信区间，0.67-1.12）。然而，每年服用80%或更多片剂（钙或安慰剂）的830名患者（56.8%）中，与安慰剂组相比，钙组的骨折发生率降低（10.2%对15.4%；风险比，0.66；95%置信区间，0.45-0.97）。与安慰剂治疗的患者相比，钙治疗的患者足跟定量超声检查结果、股骨颈和全身双能X线吸收法数据以及骨强度均有所改善。在记录的92000例不良事件中，便秘是唯一因治疗而增加的事件（钙组，13.4%；安慰剂组，9.1%）。
由于长期依从性差，每天补充1200毫克碳酸钙片剂作为公共卫生干预措施对预防非卧床老年人群的临床骨折无效，但对依从性好的患者有效。
