Bisphosphonates and glucocorticoid-induced osteoporosis: implications for patients with respiratory diseases.

Osteoporosis is a well known consequence of glucocorti-coid treatment that can result in significant morbidity and mortality. Glucocorticoid-induced bone loss occurs early, usually within 6–12 months of starting therapy. During this time the rate of bone loss is rapid before decreasing or reaching a plateau. 1 2 4 Clinically this decrease in bone mineral density puts patients at an increased risk of fracture. 1 2 4 5 Specifically, with a decline in bone mass of one standard deviation below the mean for young adults, the risk of fracture doubles. 5 Characteristically, glucocorticoid-induced osteopenia and osteoporosis occur at a faster rate in trabecular bone; consequently, the ribs and vertebrae are common sites of fracture, although hip fractures have also been reported. 6 7 As long term treatment with oral glucocorticoids is a common practice in the management of patients with chronic respiratory diseases, strategies to decrease the burden of glucocorticoid-induced osteoporosis are needed. Glucocorticoid-induced bone loss results from a decrease in bone formation due to reduced intestinal calcium absorption, increased urinary calcium excretion, and reduced osteoblast formation and function. 1 2 4 8 The bisphosphonates, a class of drugs structurally similar to pyrophosphate, alter the bone remodelling process. By binding to hydroxyapatite these agents structurally inhibit osteoclastic activity and prevent bone resorption. 9 This significantly increases bone mineral density in the lumbar spine and femur and decreases the rate of fracture at these sites. 10–13 For this reason, bisphosphonates such as etidro-nate and alendronate have received oYcial approval for the treatment and prevention of postmenopausal osteoporosis in many countries. The bisphosphonates have also been studied in the prevention and treatment of glucocorticoid-induced osteoporosis. In this issue of Thorax Pitt et al shed further light on the use of etidronate for the treatment of glucocorticoid-induced osteoporosis. 14 Using a double blind, placebo controlled design, patients receiving oral glucocorticoids for at least six months were randomised to receive etidronate 400 mg daily or placebo for 14 days followed by 76 days of calcium and vitamin D supplementation. This three month cycle was repeated eight times over a two year period. In the primary measure of outcome a significant diVerence between etidronate and placebo was found in the mean percentage change from baseline in the lumbar spine after two years. Specifically, after six months there was a mean increase of 4.33% in the bone mineral density of the lum-bar spine for the etidronate group …