REDUCED BONE-DENSITY IN PATIENTS WITH INFLAMMATORY BOWEL-DISEASE

Background-Reduced bone mineral density in patients with inflammatory bowel disease is thought to be due to disturbances in calcium homeosta sis or the effects of corticosteroid treatment. Aims-To assess the pre valence and mechanism of reduced bone mineral density ire 79 patients with inflammatory bowel disease (44 with Crohn's disease, 35 with ulce rative colitis) who did not have significant risk factors for low bone densities. Methods-Dual x ray absorptiometry was used to measure bone mineral density and serum and urinary markers of osteoblast (alkaline phosphatase, procollagen 1 carboxy terminal peptide and osteocalcin) and osteoclast (pyridinoline, deoxypyridinoline, and type 1 collagen c arboxy terminal peptide) activities to assess bone turnover. Results-T here was a high pre valence of low bone mineral density (prevalence of T scores <-1.0 from 51%-77%; T scores <-2.5 (osteoporosis) from 17%-2 8%) with hips being more often affected than vertebrae (p<0.001). Redu ced bone mineral density did not relate to concurrent or past corticos teroid intake, or type, site, or severity of disease. Whereas calcium homeostasis was normal, bone markers showed increased bone resorption without a compensatory increase in hone formation. Conclusions-The gre ater prevalence of reduced hip bone mineral density, as opposed to ver tebral, mineral density and the pattern of a selective increase in hon e resorption contrasts with that found in other known causes of metabo lic bone disease.