Management of Glucocorticoid-Induced Osteoporosis

Osteoporosis affects at least 25 million Americans, caus-ing approximately 1.5 million fractures with a cost of more than $13.8 billion per year.1 This disease of low bone mass and skeletal fragility is more common among wom-en, but is not uncommon in men. Osteoporosis in men is often attributed to secondary causes, the most common be-ing glucocorticoid therapy.2 The pathogenesis of glucocorticoid-induced osteoporo-sis is incompletely understood, but is undoubtedly multi-factorial.3-6 Specifically, corticosteroid treatment decreases osteoblast recruitment, reduces formation of osteoid by os-teoblasts, and increases osteoclastic bone resorption. Addi-tionally, absorption of dietary calcium is decreased and for-mation of gonadal steroids may be impaired.3-6 As such, it is not surprising that glucocorticoid therapy causes bone loss (trabecular more than cortical), which is greatest in the first six to 12 months, and is both dose- and duration-dependent.2-9 For example, lumbar spine bone mineral density (BMD) may be reduced by up to 8 % with-in 20 weeks following initiation of prednisone therapy.10 This loss leads to fractures in 30–50 % of patients who have used oral glucocorticoids for five years.3,7,8 One sur-vey11 of approximately 66 000 patients followed in general practices (48 % men, median age 69 y) showed that ap-proximately 0.5 % were taking long-term oral glucocorti-coids. Usage was 1.4 % for those ‡ 55 years of age. Given the adverse skeletal effects and the frequency of utilization, it is appropriate that glucocorticoid-induced osteoporosis has received increased attention.3-4,6,10-20 Pre-vention and management guidelines for glucocorticoid-in-duced osteoporosis were published by the American Col