Supplement Article |
OP28. GLUCOCORTICOID-INDUCED OSTEOPOROSIS
Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge, UK
Glucocorticoid therapy is widely used in the treatment of a variety of medical disorders. In the UK, approximately 1% of the population takes oral glucocorticoids and this figure rises to 2.5% in older people. Osteoporosis is a recognised complication of glucocorticoid use but surveys indicate that only a minority of glucocorticoid-treated patients receive appropriate advice about preventive measures.
Epidemiological studies have demonstrated that fracture risk is increased at all doses of oral glucocorticoids; fracture risk increases sharply during the first few months of therapy and declines when treatment is stopped. Similarly, bone loss is most rapid in the early stages of therapy, affecting both cortical and cancellous bone. The pathogenesis of glucocorticoid-induced bone loss is multifactorial and includes direct effects on osteoblast and osteoclast generation and activity, hypogonadism and reduced intestinal calcium absorption. Increased bone resorption and turnover predominate in the early stages, whilst long-term glucocorticoid use is associated mainly with reduced bone turnover and formation.
Measurement of BMD using dual energy X-ray absorptiometry is currently recommended for the assessment of fracture risk in most individuals treated with glucocorticoids. Other secondary causes of osteoporosis should be excluded in individuals with a previous fragility fracture. General measures to reduce bone loss include reduction of the dose of glucocorticoids to a minimum, consideration of alternative formulations or routes of administration, and prescription of alternative immunosuppressive agents. Good nutrition, adequate dietary calcium intake and appropriate physical activity should be encouraged and tobacco use and alcohol abuse avoided.
Clinical trials have demonstrated the efficacy of bisphosphonates in the prevention of glucocorticoid-induced bone loss and these drugs are now widely approved for this indication. Primary prevention should be advised in patients with a high short-term fracture probability; these include men and women aged 65 years or older and individuals with a previous history of fragility fracture. In such cases intervention with a bisphosphonate should be commenced at the time of starting glucocorticoids, without the need for bone densitometry. In other patients taking glucocorticoids, the decision to treat should be based on bone mineral density assessment of the hip and/or spine. Age should also be taken into consideration, since fracture probability in premenopausal women and younger men is low.