Background: Osteoporosis has received increasing attention as a potential complication of Crohn's disease. Among cytokines tumor necrosis factor-alpha plays a pivotal role in the pathogenesis of inflammatory bowel diseases by inducing a wide variety of inflammatory responses, including bone resorption. Only few data are present about the effect of infliximab on bone metabolism. Aims: The authors evaluated the effect of infliximab on bone metabolism in patients with Crohn's disease. Patients and methods: Twenty seven patients (17 females, 10 males, mean age 32.58 yrs) with refractory fistulizing Crohn's disease were treated with a series of three infusions of 5 mg infliximab per kg at weeks 0, 2, and 6. Biochemical markers of bone formation (osteocalcin) and bone resorption (beta-CrossLaps) were measured before administrate of each infliximab infusion. 54 patients were studied with inactive Crohn's disease (Crohns's disease activity index < 150) as a control. Results: There were significant difference in beta-CrossLaps concentrations (ng/ml) between the day 0 and 14 (0.57 ± 0.32 vs. 0.46 ± 0.29, p < 0.01) and the day 0 and 42 (0.57 ± 0.32 vs. 0.45 ± 0.26, p < 0.05). The osteocalcin levels significantly increased from day 0 to day 42 (21.31 ± 12.14 vs. 25.64 ± 16.97, p < 0.05). The serum beta-CrossLaps and osteocalcin levels were 0.47 ± 0.24, 27.2 ± 8.44 in the control group respectively. These results differed from the serum levels of active patients before the tratment, but teher were no any notable difference at the day 42. Conclusion: Infliximab therapy in Crohn's disease patients displayed a rapid influence on bone metabolism by enhancing bone formation and decreasing bone resorption. In addition to its mucosal effect affecting the bone homeostasis, indicate a further rationale usage of tumor necrosis factor-alpha blockade in the therapy of inflammatory bowel diseaese.
|Translated title of the contribution||Improvement of bone metabolism after infliximab therapy in Crohn's disease|
|Number of pages||4|
|Publication status||Published - Dec 1 2005|
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