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.