Corticosteroid osteoporosis - ScienceDirect

Best Practice & Research Clinical Rheumatology

Volume 15, Issue 3, July 2001, Pages 401-413

Best Practice & Research Clinical Rheumatology

https://doi.org/10.1053/berh.2001.0157 Get rights and content

Abstract

Corticosteroids are widely used and effective agents for the control of many inflammatory diseases, but corticosteroid osteoporosis is a common problem associated with their long term high dose use. Prevention of corticosteroid osteoporosis is preferable to treatment of established corticosteroid bone loss.

Several large double-blind controlled clinical trials in patients with corticosteroid osteoporosis have recently been published that provide new insights into its treatment. Based upon available evidence, the rank order of choice for prophylaxis would be a bisphosphonate followed by a vitamin D metabolite or an oestrogen type medication. Calcium alone appears to be unable to prevent rapid bone loss in patients starting corticosteroids, especially with prednisolone doses at 10 mg a day or greater . If an active vitamin D metabolite is used, calcium supplementation should be avoided unless dietary calcium intake is low. Hormone replacement therapy should be considered if hypogonadism is present. Since vertebral fracture is a common and important complication of high dose corticosteroid therapy, these findings suggest that rapid bone loss and hence fractures, can be prevented by prophylactic treatment. Although the follow-up data is limited, it is likely that such therapy needs to be continued beyond 12 months whilst patients continue significant doses of corticosteroid therapy.

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Though the underlying disease itself may be associated with an increased incidence of fractures, the chronic use of GCs further enhances this increased risk by a factor of 2 (Da Silva et al., 2006). There is strong support for the concept that patients under GC tend to suffer fractures at a higher bone mineral density than controls, suggesting that these medications deteriorate bone resistance beyond densitometry-based expectations (Sambrook and Lane, 2001). GC-induced osteoporosis seems, on the other hand, reversible after stopping the medication and several drugs and other interventions have been shown to prevent GC-induced osteoporosis and associated fractures.
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This chapter focuses on the primary prevention of rapid early bone loss after transplantation. There are a number of agents that are effective in the prevention of post-transplantation bone loss of various organs. Further clinical trials are necessary to establish the comparative efficacy of different agents, but some form of primary prophylaxis for osteoporosis should be considered in patients undergoing organ transplantation. Bisphosphonates are the most effective agents for the prevention and treatment of posttransplantation osteoporosis. Prophylaxis should involve a bisphosphonate with active vitamin D metabolites as second line or adjunctive therapy. A potential reduction in immunosuppressive requirements with active vitamin D metabolites is an additional consideration, but hypercalcemia and hypercalciuria also become relatively common. Testosterone replacement should be reserved for men with true hypogonadism post-transplant. Patients who are receiving anti-osteoporosis therapy prior to transplantation can theoretically experience less bone loss after transplantation, but whether drug therapy for osteoporosis before transplantation reduces bone loss and fracture risk after transplantation is currently unclear.

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