TY - JOUR
T1 - Effects of infliximab therapy on abdominal fat and metabolic profile in patients with Crohn's disease
AU - Parmentier-Decrucq, Erika
AU - Duhamel, Alain
AU - Ernst, Olivier
AU - Fermont, Catherine
AU - Louvet, Alexandre
AU - Vernier-Massouille, Gwenola
AU - Cortot, Antoine
AU - Colombel, Jean Frédéric
AU - Desreumaux, Pierre
AU - Peyrin-Biroulet, Laurent
PY - 2009
Y1 - 2009
N2 - 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.
AB - 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.
KW - Abdominal fat
KW - Cholesterol
KW - Crohn's disease
KW - Infliximab
KW - Lipid
UR - http://www.scopus.com/inward/record.url?scp=70350604310&partnerID=8YFLogxK
U2 - 10.1002/ibd.20931
DO - 10.1002/ibd.20931
M3 - Article
C2 - 19291781
AN - SCOPUS:70350604310
SN - 1078-0998
VL - 15
SP - 1476
EP - 1484
JO - Inflammatory Bowel Diseases
JF - Inflammatory Bowel Diseases
IS - 10
ER -