GLUCOCORTICOID OSTEOPOROSIS

Glucocorticoids act on calcium metabolism at many levels to produce os teoporosis, the major pathogenic effect probably being an inhibition o f bone formation. In men, this is likely to be contributed to by a dos e-related reduction in circulating testosterone concentrations. Bone d ensity is reduced 10-20% at the commonly assessed sites, but deficits of twice this magnitude are found in trabecular bone. Dose and duratio n of steroid treatment influence the degree of osteopenia, but biochem ical indexes of calcium metabolism are not predictive. In managing a s teroid-treated patient, bone densitometry is usually helpful. Those wi th low densities should optimize their calcium intake, and those with sex hormone deficiency should receive appropriate replacement therapy. If bone loss is severe or continues despite these measures, the addit ion of bisphosphonate, calcitonin, fluoride, or a vitamin D metabolite may be appropriate, according to local availability. Thiazide diureti cs can be combined with all these regimens. If thiazide diuretics are combined with vitamin D or its metabolites, careful monitoring of seru m calcium should be undertaken. Bone density should be monitored annua lly until it is stable.