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Increased Body Mass Index Is Associated with Earlier Time to Loss of Response to Infliximab in Patients with Inflammatory Bowel Disease

Harper, Jason W. MD*; Sinanan, Mika N. MD; Zisman, Timothy L. MD, MPH*

Inflammatory Bowel Diseases:
doi: 10.1097/MIB.0b013e31829cf401
Original Clinical Articles

Background: Obesity is an emerging problem in the care of inflammatory bowel disease (IBD) patients and has been associated with a diminished response to adalimumab. Whether obesity influences the response to infliximab (IFX) is not known.

Methods: A retrospective cohort of 124 subjects with IBD initiating IFX, naive to biologic therapy, was identified. Subjects were stratified according to their weight and body mass index (BMI). The primary outcome was the first occurrence of an IBD flare defined as dose escalation of IFX, corticosteroid use, discontinuation of IFX, hospitalization, or surgery. Multivariable logistic regression was performed considering body mass and BMI as categorical and continuous variables.

Results: Obese (BMI > 30 kg/m2) patients with Crohn’s disease were more likely to have an IBD flare than nonobese patients (adjusted hazard ratio [HR]: 3.03, P < 0.001); overweight (BMI > 25 kg/m2) patients with ulcerative colitis trended toward a similar observation (HR: 9.68, P = 0.06). When considered as continuous variables, increasing mass and BMI were associated with earlier IBD flare in both Crohn’s disease (adjusted HR: 1.06 per unit increase in BMI [P = 0.02] and 1.02 per kg increase in body mass [P = 0.02]) and ulcerative colitis (adjusted HR: 1.3 per unit increase in BMI [P = 0.01] and 1.11 per kg increase in body mass [P = 0.004]).

Conclusions: Increased body weight is associated with an earlier time to loss of response to IFX in Crohn’s disease and ulcerative colitis, a novel finding given that IFX is the only antitumor necrosis factor agent whose dosing reflects increased body weight.

In Brief

Article first published online 16 July 2013

Author Information

*Division of Gastroenterology, Department of Medicine, University of Washington Medical Center, Seattle, Washington; and

Department of Surgery; University of Washington Medical Center, Seattle, Washington.

Reprints: Timothy L. Zisman, MD, MPH, Division of Gastroenterology, Department of Medicine, University of Washington Medical Center, Division of Gastroenterology, 1959 NE Pacific Street, Box 356424, Seattle, WA 98195 (e-mail:

Guarantor: Dr. Jason W. Harper; specific author contributions: Jason W. Harper: study concept and design, data acquisition, analysis and interpretation of data, drafting of the manuscript; Mika N. Sinanan: critical revision of the manuscript for important intellectual content; Timothy L. Zisman: study supervision, study concept and design, critical revision of the manuscript for important intellectual content, approval of final draft submitted.

The authors have no conflicts of interest to disclose.

Received April 27, 2013

Accepted May 21, 2013

© Crohn's & Colitis Foundation of America, Inc.

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