title: Treatment with tumour necrosis factor inhibitor oxpentifylline does not improve corticosteroid dependent chronic active Crohn's disease.
abstract: BACKGROUND
  In Crohn's disease, inflammation is presumably sustained by an increased production of proinflammatory cytokines, in particular tumour necrosis factor alpha (TNF alpha) and interleukin 1 beta (IL 1 beta). TNF alpha can induce a host of cellular effector events resulting in perpetuation of the inflammatory process. In vivo studies with anti-TNF alpha antibody treatment have led to impressive clinical results.
  
  
  OBJECTIVE
  To investigate whether treatment with the TNF alpha inhibitor oxpentifylline results in clinical improvement in corticosteroid dependent chronic active Crohn's disease.
  
  
  METHODS
  Sixteen Crohn's disease patients received oxpentifylline 400 mg four times a day in a four week open label study.
  
  
  RESULTS
  Blockade of TNF alpha production in 16 patients with corticosteroid dependent Crohn's disease did not improve the clinical disease activity (CDAI mean (SEM) 188.75 (5.65) versus 185.13 (10.87) or the endoscopic degree of inflammation (CDEIS 14.9 (2.87) versus 14.8 (2.27) or laboratory parameters.
  
  
  CONCLUSIONS
  In this study, use of the TNF alpha inhibitor oxpentifylline does not improve inflammation in Crohn's disease. This finding suggests that there may be more key mediators than only TNF alpha in the inflammatory process in Crohn's disease.
authors.affiliation: Charité University Hospital, 4th Department of Medicine/Mucosal, Berlin, Germany.
authors.forename: J
authors.initials: J
authors.lastname: Bauditz
authors.forename: J
authors.initials: J
authors.lastname: Haemling
authors.forename: M
authors.initials: M
authors.lastname: Ortner
authors.forename: H
authors.initials: H
authors.lastname: Lochs
authors.forename: A
authors.initials: A
authors.lastname: Raedler
authors.forename: S
authors.initials: S
authors.lastname: Schreiber
mesh_terms: D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D002478:Cells, Cultured; D002908:Chronic Disease; D003424:Crohn Disease / Q000188:drug therapy* / Q000276:immunology; D004359:Drug Therapy, Combination; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000187:drug effects / Q000276:immunology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D010431:Pentoxifylline / Q000627:therapeutic use*; D010726:Phosphodiesterase Inhibitors / Q000627:therapeutic use*; D011239:Prednisolone / Q000627:therapeutic use*; D017211:Treatment Failure; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D008070:Lipopolysaccharides; D010726:Phosphodiesterase Inhibitors; D014409:Tumor Necrosis Factor-alpha; D011239:Prednisolone; D010431:Pentoxifylline