ALTERED BONE METABOLISM IN INFLAMMATORY BOWEL-DISEASE

A reduced bone mineral density has been reported in inflammatory bowel disease (IBD). Objective: To assess the mechanisms of bone disease in IBD. Methods: We studied in 90 patients (61 with Crohn's disease, 22 with ulcerative colitis, 7 with indeterminate colitis) biochemical mar kers of bone metabolism in serum and bone mineral density by periphera l quantitative computed tomography at the forearm. Results: Forty-five percent of the patients had a reduced bone density (Z score < -1). Se rum calcium was normal in most patients, vitamin D deficiency was docu mented in 17%. Osteocalcin, a serum marker of bone formation, was decr eased in 26% (1.2 +/- 0.1 ng/ml), whereas the carboxyterminal cross-li nked telopeptide of type I collagen (ICTP), a recently described serum parameter of bone breakdown, was stimulated in 38% (10.4 +/- 2.3 mu g /L). Of 33 patients with increased ICTP levels, 19 showed a decreased bone density (Z score < -1), and 2 of them never received steroids. An active status of the underlying disease in most patients with increas ed ICTP levels suggests a direct effect of the underlying IBD. In the whole series of patients with a history of active disease (n = 34), 47 % had signs of an increased bone degradation (ICTP > 5 mu g/L; mean, 1 2.9 +/- 4.7 mu g/L). Data derived from a retrospective survey of 245 p atients with IBD suggest that the prevalence of bone fractures in IBD is unexpectedly high, particularly in patients,vith a long duration of disease, frequent active phases, and high cumulative doses of cortico steroid intake. Conclusions: Several mechanisms may be involved in IBD -associated bone disease: (1) a high inflammatory activity directly in duces bone degradation via yet unknown pathways, (2) treatment with co rticosteroids may exert catabolic effects on the bone, or (3) malabsor ption and vitamin D deficiency may activate bone turnover.