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Chronic Glucocorticoid Therapy-Induced Osteoporosis in Patients With Obstructive Lung Disease*

Marc F. Goldstein, MD, FCCP; Joseph J. Fallon, Jr, MD; Ronald Harning, PhD
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*From the Asthma Center (Dr. Goldstein), Philadelphia, PA; the Pavilions of Voorhees (Dr. Fallon), Voorhees, NJ; and Merck Research Laboratories (Dr. Harning), Rahway, NJ.

Correspondence to: Ronald Harning, PhD, Merck Research Laboratories, PO Box 2000, RY 32–541, Rahway, NJ 07065-0900; e-mail: ronald_harning@merck.com



Chest. 1999;116(6):1733-1749. doi:10.1378/chest.116.6.1733
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Long-term glucocorticoid (GC) therapy has been instrumental in decreasing morbidity and mortality in a variety of chronic inflammatory diseases, including persistent asthma. Long-term GC therapy is also widely prescribed for COPD. One of the important and often unrecognized side effects of chronic GC therapy is secondary osteoporosis. The risk of GC-induced bone loss is roughly correlated with daily dose, duration, and total cumulative lifetime dose of GC treatment. Oral prednisone increases the risk of bone loss and fracture. High doses of inhaled GCs may also increase the risk of osteopenia/osteoporosis, but the risk appears to be less than that associated with oral GCs. Hormone replacement therapy, oral and parenteral bisphosphonates, supplemental calcium and vitamin D, calcitonin, and fluoride compounds have been used, experimentally, in the management of GC-induced bone loss. Asthma and COPD specialists are key prescribers of oral and inhaled steroids and are likely to encounter patients with significant bone loss. Despite known risk factors and the availability of reliable diagnostic tools to recognize bone loss, the opportunity to slow, reverse, and treat bone loss is often missed. We present a review of the current literature regarding the incidence, treatment, and prevention of osteopenia/osteoporosis secondary to chronic GC therapy in adult asthma and COPD patients. Guidelines are presented regarding the identification of patients at risk for developing GC-induced secondary bone loss, and therapeutic alternatives are discussed.

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