Corticosteroid Induced Osteoporosis

Journal/Book: Z Rheumatol 1998; 57 Suppl. 1: 2 (H 7). 1998;

Abstract: Department of Rheumatology Royal North Shore Hospital University of Sydney Bone loss leading to osteoporotic fractures at sites such as the spine and ribs is a well recognised complication of prolonged corticosteroid therapy. Corticosteroids exert inhibitory effects on osteoblasts and bone formation directly. Corticosteroid effects on bone also include increased bone resorption due to decreased calcium absorption and increased urinary calcium loss leading to secondary hyperparathyroidism. Bone loss appears to be rapid initially with rates approaching 4 - 10 % per/yr but not all patients on corticosteroids lose bone and some corticosteroid bone loss is reversible. The question of a 'safe' dose (ie a dose that does not cause bone loss) is controversial. Some authors have found that doses of 7.5 mg or less are relatively safe although it may be that for the majority of patients cumulative dose is more important. Alternate day therapy does not appear to offer any advantages. As ex-users have normal bone density use of low doses for between 6 - 12 months is unlikely to lead to clinical sequelae in the majority of subjects. Controlled trials have demonstrated beneficial effects of bisphosphonates and D-hormones (active vitamin D metabolites such as calcitriol and 1-( hydroxyvitamin D or alfacalcidol) in prevention and treatment of corticosteroid bone loss. The role of calcitonin and deflazacort is less clear. Hormone replacement therapy is probably appropriate in postmenopausal women and males with markedly reduced serum testosterone levels. In clinical practice it would seem reasonable to reassure patients on low dose steroids for under 12 months. In those commencing long term therapy an adequate calcium intake oestrogen replacement (in postmenopausal women) and on the basis of published studies prophylactic therapy with D-hormones or bisphosphonates to reduce vertebral bone loss should be considered. le

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