Preventing glucocorticoid-induced osteoporosis.

Abstract

Glucocorticoids are a potent cause of osteoporosis and thus a potential source of substantial morbidity in patients who are already significantly disabled by their underlying condition. These agents interact with calcium metabolism at many levels; in particular they reduce the osteoblast's synthesis of the principal proteins of bone matrix. They also reduce circulating sex hormone concentrations, particularly in men and postmenopausal women. Glucocorticoids cause rapid bone loss within weeks of their introduction, but this loss continues even after many years of chronic use. About one third of patients will develop fractures, those with low initial bone densities (e.g., postmenopausal women) being at higher risk. Fracture risk can be assessed from a patient's age, body weight, duration of steroid use, average dose of glucocorticoid, past history of fracture and bone density. In those at high risk of fracture, bone density can be increased by use of sex hormone replacement (in men or women who have a demonstrable deficiency) or a bisphosphonate (e.g., etidronate, alendronate, risedronate). Calcitriol, calcitonin and fluoride may have roles as adjunctive therapies but documentation of their efficacy is less satisfactory. It is incumbent on all physicians supervising long-term glucocorticoid therapy to ensure that a skeletal assessment is carried out and that osteoporosis prophylaxis is instituted, where appropriate.