Glucocorticoid osteoporosis.

Glucocorticoids act on calcium metabolism at many levels to produce osteoporosis, the major pathogenic effect probably being an inhibition of bone formation. In men, this is likely to be contributed to by a dose-related reduction in circulating testosterone concentrations. Bone density is reduced 10-20% at the commonly assessed sites, but deficits of twice this magnitude are found in trabecular bone. Dose and duration of steroid treatment influence the degree of osteopenia, but biochemical indexes of calcium metabolism are not predictive. In managing a steroid-treated patient, bone densitometry is usually helpful. Those with 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 addition of bisphosphonate, calcitonin, fluoride, or a vitamin D metabolite may be appropriate, according to local availability. Thiazide diuretics can be combined with all these regimens. If thiazide diuretics are combined with vitamin D or its metabolites, careful monitoring of serum calcium should be undertaken. Bone density should be monitored annually until it is stable.