GLUCOCORTICOID OSTEOPOROSIS - MECHANISMS AND MANAGEMENT

Glucocorticoids are potent osteopenic agents, producing negative calci um and bone balance via actions at many sites. The most significant ad verse effects of glucocorticoid drugs on the skeleton are probably a d irect inhibition of matrix synthesis by the osteoblast, reductions in calcium absorption in both the gut and the renal tubule, and the produ ction of hypogonadism, particularly in men. Reductions in bone density of 10-40% result, the loss being more marked in trabecular bone and i n patients receiving a high cumulative dose of the steroid. Fractures occur in about 30% of individuals who take these drugs for an average of 5 years. Bone loss is reversible when glucocorticoid treatment is w ithdrawn. Bone density can also be increased by sex hormone replacemen t in those with demonstrable deficiency by bisphosphonates, and possib ly by vitamin D metabolites. All patients treated with glucocorticoids for more than 6 months should be considered for bone densitometry and be offered appropriate drug treatment if values are towards the lower end of the young normal range or if there is already evidence of frac tures occurring after minimal trauma. With this approach, the signific ant morbidity associated with steroid osteoporosis might be substantia lly avoided.