Endocrine Abstracts (2003) 6 S19


J Compston

Department of Medicine, University of Cambridge School of Clinical Medicine, Cambridge UK.

The association between inflammatory bowel disease (IBD) and osteoporosis has been known for many decades but has only recently received appropriate recognition. This has largely resulted from the increasing awareness of the high morbidity and mortality attributable to osteoporosis in the general population and the application of advances in its detection to populations with gastrointestinal disease Recent population-based studies in individuals with inflammatory bowel disease have indicated a small increase in relative risk of fracture. Many of the risk factors for osteoporosis that have been identified in the general population are common in individuals with gastrointestinal diseases, for example glucocorticoid therapy, low body mass index, vitamin D deficiency and hypogonadism. In addition, interactions between immune cells, cytokines and osteoclastogenesis may be important in bone loss associated with IBD and alterations in leptin production may also play a role.

Assessment of fracture probability should include bone densitometry in older individuals and those with other strong risk factors such as hypogonadism or glucocorticoid therapy. Control of the underlying gastrointestinal disease, where possible, is of prime importance and risk factors such as hypogonadism and vitamin D deficiency should be treated. Body mass index is a major determinant of bone mineral density and appropriate nutritional support is an important aspect of management.

Data on the effects of pharmacological interventions on bone loss in patients with gastrointestinal disorders are sparse and fracture reduction has not been an end-point in any study. There is limited evidence for the efficacy of bisphosphonates but identification of effective treatment strategies remains an important priority for the future.

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