Abstract
In 1932, Harvey Cushing wrote: ‘The greatly compressed bodies of the vertebrae ... were so soft they could easily be cut with a knife’. Today, steroid-induced osteoporosis is still of major clinical relevance. Glucocorticosteroids induce a biphasic bone loss with a rapid initial phase of ;10–15% during the first few months and a slower phase of ;2–5% annually. As shown in Figure 1, steroids do not only reduce the lifespan and promote the apoptosis of osteoblasts and osteoclasts but also decrease the recruitment of osteoblasts and osteoclasts from progenitor cells [1]. Apoptosis and changes in the expression of bone growth factors contribute to a decline in bone formation and the occurrence of osteonecrosis. Steroid therapy affects particularly the axial skeleton and the proximal femur. The earliest changes of steroidinduced bone loss can be detected in the lumbar spine (preferably lateral position). During long-term ()3 month) use of steroids ()7.5 mg prednisone) bone loss occurs in ;50% of patients, osteoporotic Correspondence and offprint requests to: Peter M. Jehle, MD, Klinik fur Innere Medizin, Evangelisches Krankenhaus der PaulGerhardt-Stiftung, Akademisches Lehrkrankenhaus der MartinLuther-Universitat Halle-Wittenberg, Postfach 10 02 52, D-06872 Lutherstadt Wittenberg, Germany. Email: p.jehle@pgstiftung.de Nephrol Dial Transplant (2003) 18: 861–864 DOI: 10.1093/ndt/gfg067
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