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年龄相关性骨质疏松性骨折的发病机制:膳食钙缺乏的影响。

The pathogenesis of age-related osteoporotic fracture: effects of dietary calcium deprivation.

作者信息

Prince R L, Dick I M, Lemmon J, Randell D

机构信息

Department of Medicine, University of Western Australia, Perth, Australia.

出版信息

J Clin Endocrinol Metab. 1997 Jan;82(1):260-4. doi: 10.1210/jcem.82.1.3694.

Abstract

The pathogenesis of osteoporotic fracture after the menopause is uncertain. We studied the effects of a 4-day low calcium diet on 17 subjects with vertebral osteoporotic fracture and 17 age-matched controls with a bone density within the young normal range and without fracture. At baseline, the osteoporotic patients were well matched to normal subjects in terms of calcium intake and absorption and renal function, but had higher bone turnover and relative secondary hyperparathyroidism. After the low calcium diet, the rise in calcitriol was deficient in the osteoporotic subjects. These data are consistent with the suggested pathogenesis of type II or age-related osteoporosis and show that in these subjects with osteoporotic fracture there was a primary defect in calcitriol production that resulted in secondary hyperparathyroidism. This defect may be the cause of the high bone turnover and may play an important role in the development of bone loss in these subjects.

摘要

绝经后骨质疏松性骨折的发病机制尚不清楚。我们研究了为期4天的低钙饮食对17名椎体骨质疏松性骨折患者和17名年龄匹配、骨密度在年轻正常范围内且无骨折的对照者的影响。在基线时,骨质疏松患者在钙摄入、吸收及肾功能方面与正常受试者匹配良好,但骨转换率较高且存在相对继发性甲状旁腺功能亢进。低钙饮食后,骨质疏松受试者中骨化三醇的升高不足。这些数据与II型或年龄相关性骨质疏松的发病机制假说一致,并表明在这些骨质疏松性骨折患者中存在骨化三醇生成的原发性缺陷,导致继发性甲状旁腺功能亢进。这一缺陷可能是骨转换率高的原因,并且可能在这些患者骨质流失的发展过程中起重要作用。

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