title: [Improvement of bone metabolism after infliximab therapy in Crohn's disease].
abstract: 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.
  
  
  OBJECTIVE
  The authors evaluated the effect of infliximab on bone metabolism in patients with Crohn's disease.
  
  
  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 administration of each infliximab infusion. 54 patients were studied with inactive Crohn's disease (Crohn's disease activity index < 150) as a control.
  
  
  RESULTS
  There were significant differences 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 treatment, but there were no notable differences at the day 42.
  
  
  CONCLUSIONS
  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 diseases.
authors.affiliation: Semmelweis Egyetem, Altalános Orvostudományi Kar, II. Belgyógyászati Klinika, Budapest.
authors.forename: Pál
authors.initials: P
authors.lastname: Miheller
authors.forename: Györgyi
authors.initials: G
authors.lastname: Muzes
authors.forename: Tamás
authors.initials: T
authors.lastname: Zágoni
authors.forename: Miklós
authors.initials: M
authors.lastname: Tóth
authors.forename: Károly
authors.initials: K
authors.lastname: Rácz
authors.forename: Zsolt
authors.initials: Z
authors.lastname: Tulassay
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D001862:Bone Resorption / Q000175:diagnosis / Q000378:metabolism / Q000517:prevention & control*; D001842:Bone and Bones / Q000187:drug effects* / Q000378:metabolism*; D003094:Collagen / Q000097:blood; D003424:Crohn Disease / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism*; D005260:Female; D005765:Gastrointestinal Agents / Q000627:therapeutic use*; D006801:Humans; D000069285:Infliximab; D008297:Male; D015675:Osteocalcin / Q000097:blood; D010024:Osteoporosis / Q000097:blood / Q000209:etiology / Q000517:prevention & control; D010446:Peptide Fragments / Q000097:blood; D016896:Treatment Outcome
chemical_list: D000911:Antibodies, Monoclonal; D015415:Biomarkers; D005765:Gastrointestinal Agents; D010446:Peptide Fragments; C110762:glutamyl-lysyl-alanyl-histidyl-aspartyl-glycyl-glycyl-arginine; D015675:Osteocalcin; D003094:Collagen; D000069285:Infliximab