Corticosteroid-induced osteoporosis

Abstract

Since Harvey Cushing first noted the coexistence of excess cortisol and loss of skeletal mass over 50 years ago, it has been accepted that supraphysiologic doses of corticosteroids cause clinically significant bone loss. Currently, high-dose oral corticosteroids are used to treat people with a variety of medical conditions, including: rheumatic diseases, such as rheumatoid arthritis, polymyalgia rheumatica, systemic lupus erythematosus and vasculitis; inflammatory lung diseases, like asthma; gastrointestinal diseases, such as inflammatory bowel disease and chronic liver disease; skin diseases, in particular pemphigus, and more recently those who have undergone transplantation. Clinically significant bone loss occurs in the vast majority of patients exposed to corticosteroids, and fractures at the spine and hip have been reported with corticosteroid use. Between 30 and 50 percent of patients taking long-term corticosteroids will experience fractures. Today, fractures due to corticosteroid-induced osteoporosis may be prevented. A number of well-designed randomized controlled trials have been conducted that demonstrate preservation and, in some instances, actual increases in bone mass with the use of appropriate drug treatment. Some have even demonstrated reductions in fracture risk. As a result, it is extremely important for clinicians to appreciate the very high risk for vertebral fracture, particularly in postmenopausal women on corticosteroids.