Glucocorticoid-induced Osteoporosis and Its Treatment

Abstract

Osteoporosis and fractures are frequent and important consequences of glucocorticoid therapy. Many factors contribute to bone loss during glucocorticoid therapy, such as underlying disease, malnutrition, vitamin D insufficiency, hypogonadism, and low body weight. Bone loss occurs particularly in the first few months of glucocorticoid treatment and affects more cancellous than cortical bone, with reduced bone formation and increased bone resorption. The risk of fracture increases rapidly in patients with glucocorticoid therapy. The existence of a threshold is not well defined but the risk of fracture is increased in patients with higher doses of glucocorticoids. Other effects include altered production of gonadal sex hormones, inhibition of intestinal calcium absorption, and enhancement of renal excretion of calcium. Prevention of glucocorticoid-induced osteoporosis is based on general measures such as calcium and vitamin D supplementation, adequate protein intake, regular physical exercise, and specific therapies. Bisphosphonates, which are potent bone resorption inhibitors, have been shown to increase bone mineral density and to decrease fracture risk, so that they represent the first choice in the prevention of glucocorticoid-induced osteoporosis. Glucocorticoid-induced osteoporosis is a major burden to those whom it affects. It can be prevented provided efficacious preventive measures are introduced early during glucocorticoid treatment. Level V (expert opinion). See the Guidelines for Authors for a complete description of the levels of evidence.