title: Effects of infliximab therapy on abdominal fat and metabolic profile in patients with Crohn's disease.
abstract: BACKGROUND
  Tumor necrosis factor is an adipocytokine possessing a well-established lipolytic effect. In Crohn's disease (CD) patients, infliximab therapy may thus result in visceral fat accumulation, which is associated with an increased risk of metabolic syndrome.
  
  
  METHODS
  A total of 132 CD patients were investigated. In a first prospective study, magnetic resonance imaging (MRI) quantification of subcutaneous and visceral abdominal fat was performed before and 8 weeks after initiation of infliximab induction therapy (5 mg/kg at weeks 0, 2, and 6) in 21 responding patients treated for perianal disease. In a second prospective study, fasting glycemia, glycated hemoglobin (HbA1c), HDL, LDL, and total cholesterol and triglyceride levels were assessed in 111 responding patients receiving infliximab infusions every 8 weeks, with a mean follow-up of 41 weeks.
  
  
  RESULTS
  A significant homogeneous 18% increase in total abdominal fat was observed in the 21 CD patients after infliximab induction therapy (P = 0.027), independently of body mass index evolution. Infliximab maintenance therapy was associated with a decrease in glycemia (P < 0.0001) and HbA1c (P = 0.0005) concentrations, together with an increase in both total cholesterol (P = 0.02) and HDL cholesterol (P = 0.008) concentrations. All glycemic and lipid parameters remained within the normal range throughout the study.
  
  
  CONCLUSIONS
  Infliximab induction therapy is associated with a significant increase in abdominal fat tissue in CD patients. Infliximab maintenance therapy has no deleterious effects on lipid profile and is accompanied by a decrease in glycemia and HbA1c concentrations, probably by reversing the impairment of tumor necrosis factor-induced insulin-mediated glucose uptake.
authors.affiliation: Inserm, Université Lille, CHRU Lille, Hôpital Huriez, Service des Maladies de l'Appareil Digestif et de la Nutrition, Lille, France.
authors.forename: Erika
authors.initials: E
authors.lastname: Parmentier-Decrucq
authors.forename: Alain
authors.initials: A
authors.lastname: Duhamel
authors.forename: Olivier
authors.initials: O
authors.lastname: Ernst
authors.forename: Catherine
authors.initials: C
authors.lastname: Fermont
authors.forename: Alexandre
authors.initials: A
authors.lastname: Louvet
authors.forename: Gwenola
authors.initials: G
authors.lastname: Vernier-Massouille
authors.forename: Antoine
authors.initials: A
authors.lastname: Cortot
authors.forename: Jean-Frédéric
authors.initials: JF
authors.lastname: Colombel
authors.forename: Pierre
authors.initials: P
authors.lastname: Desreumaux
authors.forename: Laurent
authors.initials: L
authors.lastname: Peyrin-Biroulet
mesh_terms: D050153:Abdominal Fat / Q000187:drug effects*; D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D001786:Blood Glucose / Q000378:metabolism; D002784:Cholesterol / Q000378:metabolism; D003113:Colonoscopy; D003424:Crohn Disease / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005500:Follow-Up Studies; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D007004:Hypoglycemic Agents / Q000378:metabolism; D000069285:Infliximab; D007328:Insulin / Q000378:metabolism; D008055:Lipids / Q000032:analysis; D008279:Magnetic Resonance Imaging; D008297:Male; D055442:Metabolome / Q000187:drug effects*; D008875:Middle Aged; D011379:Prognosis; D011446:Prospective Studies; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D055815:Young Adult
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D001786:Blood Glucose; D002784:Cholesterol; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D000069285:Infliximab; D007328:Insulin; D008055:Lipids; D014409:Tumor Necrosis Factor-alpha