Article Text

Download PDFPDF
Alendronate increased bone mineral density but did not reduce new fractures in glucocorticoid induced osteoporosis
  1. J E COMPSTON
  1. Department of Medicine
  2. Box 157, Level 5
  3. Addenbrooke’s Hospital
  4. Hills Road
  5. Cambridge CB2 2QQ, UK

Statistics from Altmetric.com

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

Osteoporosis is a common complication of glucocorticoid therapy and causes significant morbidity. Nevertheless, it remains relatively neglected and many patients on long term glucocorticoid therapy receive no prophylaxis against bone loss. However, recent evidence from randomised controlled trials, including that by Saaget al, suggests that bisphosphonates are effective in the prevention and treatment of glucocorticoid induced osteoporosis.1 ,2 These agents, which inhibit bone resorption, are already widely used in the prevention and treatment of postmenopausal osteoporosis.

In the largest study by Saag et al the effects of alendronate were investigated in patients taking a median dose of around 10 mg of prednisolone daily at baseline. After 48 weeks, significant treatment benefits were demonstrated on bone mineral density (BMD) in the spine and proximal femur and, although the study was not powered to demonstrate a reduction in fracture, the overall incidence of vertebral fractures was lower in treated patients. These results are similar to those reported by Adachi and colleagues1 in a randomised controlled study of …

View Full Text

Footnotes

  • Sources of funding: Merck & Company and the General Clinical Research Centers Programs; National Center for Research Resources; National Institutes of Health.

  • For correspondence: Dr K G Saag, Clinical Immunology and Rheumatology, University of Alabama at Birmingham, 813–6 Amity South, MEB 625, Birmingham, AL 35294, USA. Fax +1 205 975 6859.