Glucocorticoid-induced osteoporosis

被引:28
|
作者
Tamura, Y [1 ]
Okinaga, H
Takami, H
机构
[1] Teikyo Univ, Sch Med, Dept Internal Med, Itabashi Ku, Tokyo 1738605, Japan
[2] Univ Tokyo, Sch Med, Dept Internal Med, Div Nephrol & Endocrinol,Bunkyo Ku, Tokyo 1138655, Japan
[3] Teikyo Univ, Sch Med, Dept Surg, Itabashi Ku, Tokyo 1738605, Japan
关键词
glucocorticoids; osteoporosis; fracture;
D O I
10.1016/j.biopha.2004.08.018
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Glucocorticoids are important drugs in the treatment of variety diseases, but long-term period use can lead to various adverse effects, including osteoporosis. Glucocorticoid-induced osteoporosis is mainly caused by inhibition of osteoblastic bone formation, which results not only in decreased bone mineral density, but reduction of bone strength by trabecular thinning in bone microstructures. The evidence suggests that daily oral glucocorticoid doses higher than 5 mg prednisolone or equivalent increase the risk of fracture within 3-6 months after the start of therapy. High-dose inhaled glucocorticoids may also increase fracture risk. The diagnostic procedures are similar to those for primary osteoporosis, but the diagnostic threshold for bone mineral density needs to be higher than that for primary osteoporosis. Treatment with vitamin D, calcitonin, sex hormone replacement, and bisphosphonates has been shown to be effective, and bisphosphonates have been demonstrated to be the most valuable drugs for glucocorticoid-induced osteoporosis. There are several lines of evidence indicating that they are effective in preventing and treating low bone mineral density and in reducing fracture risk. (C) 2004 Elsevier SAS. All rights reserved.
引用
收藏
页码:500 / 504
页数:5
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