GLUCOCORTICOID-INDUCED OSTEOPOROSIS - PREVENTION AND TREATMENT

Glucocorticoid excess carries the risk of inducing secondary osteoporo sis. In endogenous Gushing's syndrome, osteoporosis may be the present ing symptom of the underlying disease. Bone loss film reverse after th e condition is cured, but often active treatment of established osteop orosis is necessary. In long-term glucocorticoid treatment at therapeu tic doses, bone loss is likely and should be prevented if prevention i s ineffective, treatment is necessary. Hypercortisolism impairs calciu m homeostasis and bone metabolism in a complex, multifactorial way: Gl ucocorticoids diminish calcium absorption and increase renal calcium e xcretion: this negative calcium balance leads to secondary hyperparath yroidism and osteoclast activation. Osteoblast activity is directly im paired by glucocorticoid's, which lower activity of the gonadal hormon e axis so that hypogonadism also contributes to bone loss. Glucocortic oids lead to muscle atrophy and decreased muscle strength with negativ e consequences for bone formation. For prevention and treatment, two d ifferent strategies have been used. The pathophysiological approach su bstitutes calcium and vitamin D ill the first step; if bone loss never theless continues, bone formation is stimulated by fluorides. The alte rnative pharmaco-dynamic approach uses antire-sorptives-calcitonin or, for preference, bisphosphonates. Clinically it is mandatory to monito r all patients in whom glucocorticoids are used (e.g. organ transplant recipients) before and after the initiation of treatment to stabilize bone metabolism as early as possible. (C) 1998 by Elsevier Science In c.