Effects of infliximab therapy on abdominal fat and metabolic profile in patients with Crohn's disease

Erika Parmentier-Decrucq, Alain Duhamel, Olivier Ernst, Catherine Fermont, Alexandre Louvet, Gwenola Vernier-Massouille, Antoine Cortot, Jean Frédéric Colombel, Pierre Desreumaux, Laurent Peyrin-Biroulet

Research output: Contribution to journalArticlepeer-review

63 Scopus citations

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.

Original languageEnglish
Pages (from-to)1476-1484
Number of pages9
JournalInflammatory Bowel Diseases
Volume15
Issue number10
DOIs
StatePublished - 2009
Externally publishedYes

Keywords

  • Abdominal fat
  • Cholesterol
  • Crohn's disease
  • Infliximab
  • Lipid

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