Glucocorticoid-induced osteoporosis: pathogenesis, diagnosis, and management

被引:32
作者
McIlwain, HH [1 ]
机构
[1] Tampa Med Grp Res, Tampa, FL 33614 USA
关键词
osteoporosis; glucocorticoid-induced osteoporosis; fracture risk; bone mineral; density management;
D O I
10.1016/S0091-7435(02)00019-1
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 [公共卫生与预防医学]; 120402 [社会医学与卫生事业管理];
摘要
Glucocorticoid-induced bone loss is dose- and duration-related, develops rapidly (within months of therapy), and leads to an increased risk of fractures. Moreover, less than one in four patients prescribed oral glucocorticoids receive any treatment to prevent or treat osteoporosis. The American College of Rheumatology recommends bisphosphonate therapy to prevent bone loss in most patients beginning long-term glucocorticoid therapy (prednisone equivalent of greater than or equal to5 mg/day for at least 3 months), and in men and postmenopausal women receiving long-term glucocorticoids who have an abnormal bone mineral density (T score below -1). Patients with glucocorticoid-induced osteoporosis are at particularly high risk for fractures, and should be treated aggressively to reduce fracture risk. Risedronate is approved in the United States for both prevention and treatment of glucocorticoid-induced osteoporosis and alendronate is approved for treatment. Both drugs increase bone mass in patients with established glucocorticoid-induced osteoporosis. Risedronate has been shown to significantly reduce the incidence of fractures after I year of treatment. Prevention or treatment of glucocorticoid-induced bone loss is recommended for patients at risk. (C) 2003 American Health Foundation and Elsevier Science (USA). All rights reserved.
引用
收藏
页码:243 / 249
页数:7
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