title: Effects of tumor necrosis factor alpha inhibition with infliximab on lipid levels and insulin resistance in patients with inflammatory bowel disease.
abstract: BACKGROUND
  TNF-alpha is a critical mediator of inflammation with an important role in metabolic profile and insulin resistance. The regulation of these parameters by TNF-alpha in inflammatory bowel disease (IBD) is, however, poorly understood. The aim of this study was to assess the in-vivo TNF-alpha-mediated regulation of insulin resistance and of lipid levels in patients with IBD.
  
  
  METHODS
  Twenty-two patients with IBD (eight females; 19 Crohn's disease) received infliximab according to treating physician's assessment at weeks 0, 2 and 6 from baseline and subsequently every 8 weeks and were prospectively followed for 14 weeks. Fasting insulin, total cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, apolipoprotein A1 (apo-A1), apolipoprotein B100 and lipoprotein a were measured in serum at baseline and at week 14. Insulin resistance was calculated with the use of the Homeostasis Model Assessment index.
  
  
  RESULTS
  Infliximab therapy induced clinical response or remission in 19 of the 22 patients. C-reactive protein levels were significantly decreased by week 14. Body mass index was increased in all patients. No difference was observed in insulin levels, Homeostasis Model Assessment index, triglycerides, LDL cholesterol, apolipoprotein B100 and lipoprotein a. In contrast, total cholesterol, HDL cholesterol and apo-A1 levels were significantly increased from baseline.
  
  
  CONCLUSIONS
  TNF-alpha inhibition does not alter insulin resistance in IBD patients. In contrast, total cholesterol, HDL cholesterol and apo-A1 levels are significantly increased after infliximab treatment compared with baseline. The importance of these alterations needs to be clarified in future studies.
authors.affiliation: Department of Gastroenterology, University Hospital Heraklion, Heraklion, Crete, Greece. ikoutroub@med.uoc.gr
authors.forename: Ioannis E
authors.initials: IE
authors.lastname: Koutroubakis
authors.forename: Pantelis
authors.initials: P
authors.lastname: Oustamanolakis
authors.forename: Niki
authors.initials: N
authors.lastname: Malliaraki
authors.forename: Konstantinos
authors.initials: K
authors.lastname: Karmiris
authors.forename: Ioannis
authors.initials: I
authors.lastname: Chalkiadakis
authors.forename: Emmanouel
authors.initials: E
authors.lastname: Ganotakis
authors.forename: Nikolaos
authors.initials: N
authors.lastname: Karkavitsas
authors.forename: Elias A
authors.initials: EA
authors.lastname: Kouroumalis
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000494:pharmacology* / Q000627:therapeutic use; D016632:Apolipoprotein A-I / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D005765:Gastrointestinal Agents / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology; D000069285:Infliximab; D007333:Insulin Resistance / Q000502:physiology*; D050356:Lipid Metabolism / Q000187:drug effects*; D008297:Male; D011446:Prospective Studies; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D016632:Apolipoprotein A-I; D005765:Gastrointestinal Agents; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D002784:Cholesterol; D000069285:Infliximab