Preventing glucocorticoid-induced osteoporosis

Journal/Book: Z Rheumatol 1999; 58: 305-306. 1999;

Abstract: Ian R. Reid; Department of Medicine University of Auckland 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 including type I collagen and osteocalcin. Osteoblast production of insulin-like growth factors is also reduced and their bioactivity is diminished by glucocorticoid effects on concentrations of their binding proteins. Glucocorticoids probably cause malabsorption of calcium (and possibly phosphate) in the gut and the renal tubule and they 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. Up to one third of patients will develop fractures after glucocorticoid use over a five year period those with lower initial bone densities (e.g. postmenopausal women) being at highest risk. Fracture risk can be assessed to some extent from a patient's age body weight the duration of steroid use and the average dose of glucocorticoid but in most cases bone density measurement at a trabecular-rich site (e.g. the spine) is necessary. Bone density T-scores 1 to 2 units lower than those in control subjects are generally found in patients taking steroids. Treatment is usually offered to those whose bone density is more than 1-2 standard deviations below the young normal mean value. ln an individual beginning steroid therapy it can be predicted that their bone density will drop a further 1-2 standard deviations below its current level in the first year of treatment and this should be factored into the decision-making process. ... le

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