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Enteropathogenic Viruses: Triggers for Exacerbation in IBD? A Prospective Cohort Study Using Real-time Quantitative Polymerase Chain Reaction

Masclee, Gwen M.C. MD*,†; Penders, John PhD†,‡; Pierik, Marieke MD, PhD*,‡; Wolffs, Petra PhD†,‡; Jonkers, Daisy PhD*,‡

doi: 10.1002/ibd.22976
Original Basic Science Articles

Background: While the role of bacteria as an etiological factor triggering relapse in inflammatory bowel disease (IBD) has been studied extensively, little is known of the role of enteric viruses. We aimed to prospectively study the prevalence and risk factors for common enteropathogenic viruses in IBD patients in relation to disease activity.

Methods: IBD patients visiting the outpatient clinic of the Maastricht University Medical Center were included in a prospective cohort with a follow-up of 1 year. Every 3 months and during relapses, fecal samples, demographic, and clinical data were collected and disease activity was scored. A fecal sample from patients at baseline (Crohn’s disease [CD] n = 170, ulcerative colitis [UC] n = 116) and an additional sample from a subgroup with changing disease activity during follow-up (CD n = 57, UC n = 31) were analyzed for the presence of rotavirus, norovirus GI and GII, human astrovirus, and adenovirus using quantitative polymerase chain reaction (qPCR).

Results: Overall viral pathogen detection, defined by the detection of at least one of the studied viruses, at baseline was 5.2% and differed neither between CD (6.5%) or UC patients (3.4%) (P = 0.20), nor between active disease (4.7%) and remission (5.5%) (P = 0.79). Within the subgroup of patients with changing disease activity no association was found between overall viral pathogen detection and disease activity (P = 0.39). Using multivariate logistic regression, age, gender, disease subtype, disease activity, medication, and season of sampling were not associated with overall viral pathogen detection.

Conclusions: Enteropathogenic viruses are not frequently observed in a consecutive cohort of IBD patients and are not a common trigger for active disease in daily clinical practice.

Article first published online 16 April 2012

*Division of Gastroenterology and Hepatology, Department of Internal Medicine, Maastricht University Medical Center+, Maastricht, The Netherlands

Department of Medical Microbiology, Maastricht University Medical Center+, Maastricht, The Netherlands

School for Nutrition, Toxicology and Metabolism (NUTRIM), Maastricht University Medical Center+, Maastricht, The Netherlands.

Reprints: Gwen M.C. Masclee, Erasmus University Medical Center, Dept. of Medical Informatics, Postbus 2040, 3000 CA Rotterdam, The Netherlands (e-mail: g.masclee@erasmusmc.nl).

Received March 09, 2012

Accepted March 14, 2012

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