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Practice Guideline
. 2019 Jan;156(1):46-58.e7.
doi: 10.1053/j.gastro.2018.07.011. Epub 2018 Nov 28.

Rome Foundation Working Team Report on Post-Infection Irritable Bowel Syndrome

Affiliations
Practice Guideline

Rome Foundation Working Team Report on Post-Infection Irritable Bowel Syndrome

Giovanni Barbara et al. Gastroenterology. 2019 Jan.

Abstract

Background & aims: The existence of postinfection irritable bowel syndrome (PI-IBS) has been substantiated by epidemiology studies conducted in diverse geographic and clinical settings. However, the available evidence has not been well summarized, and there is little guidance for diagnosis and treatment of PI-IBS. The ROME Foundation has produced a working team report to summarize the available evidence on the pathophysiology of PI-IBS and provide guidance for diagnosis and treatment, based on findings reported in the literature and clinical experience.

Methods: The working team conducted an evidence-based review of publication databases for articles describing the clinical features (diagnosis), pathophysiology (intestinal sensorimotor function, microbiota, immune dysregulation, barrier dysfunction, enteroendocrine pathways, and genetics), and animal models of PI-IBS. We used a Delphi-based consensus system to create guidelines for management of PI-IBS and a developed treatment algorithm based on published findings and experiences of team members.

Results: PI-IBS develops in about 10% of patients with infectious enteritis. Risk factors include female sex, younger age, psychological distress during or before acute gastroenteritis, and severity of the acute episode. The pathogenesis of PI-PBS appears to involve changes in the intestinal microbiome as well as epithelial, serotonergic, and immune system factors. However, these mechanisms are incompletely understood. There are no evidence-based, effective pharmacologic strategies for treatment of PI-IBS. We provide a consensus-based treatment algorithm, based on clinical presentation and potential disease mechanisms.

Conclusions: Based on a systematic review of the literature and team experience, we summarize the clinical features, pathophysiology (from animal models and human studies), and progression of PI-IBS. Based on these findings, we present an algorithm for diagnosis and treatment of PI-IBS based on team consensus. We also propose areas for future investigation.

Keywords: Barrier Function; Campylobacter; Gastrointestinal Infection; Microbiome; Serotonin.

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Conflict of interest statement

Conflicts of interest: The authors disclose the following competing interests: GB has been a consultant or served on the advisory board or received speaker’s bureau fees and/or research support from Danone, Yakult, Ironwood, Malesci, Nestlè, Noos, Synergy, Alfa Wassermann, Almirall and Shire; MG has served on the advisory board or received research support from Takeda, DongA, Ironwood and Napo; PB has been consultant and/or served on advisory board or received research support from Nestle, Allergan, Lupin Pharma, IM Health Science and Innovate Biopharma; MC acts as consultant for Allergan and Kiowa Kirin and has been speaker for Shire and Menarini; UCG has no conflicts to disclose; LÖ has served on the advisory board of Genetic Analyses and received research support from Danone and AstraZeneca. MRS has no conflicts to disclose.

Figures

Figure 1.
Figure 1.
Rome IV diagnostic algorithm for post-infection irritable bowel syndrome
Figure 2.
Figure 2.
Geographic distribution of post-infection irritable bowel syndrome prevalence by pathogen type
Figure 3.
Figure 3.
Schematic representation of putative pathophysiology underlying post-infection irritable bowel syndrome.
Figure 4.
Figure 4.
Putative role of infection associated shifts in microbial community post-infection IBS. A host with Clostridiales predominant microbiota type is likely to remain in eubiosis state following infection, whereas, presence of Bacteroidetes predominant community may predispose to development of long-term dysbiosis upon infection. Dysbiosis can then result in shifts in bile acid composition, cytokine and immune milieu which can affect epithelial and neuromuscular function and further perpetuate dysbiosis.
Figure 5.
Figure 5.
Summary of animal models for post-infection irritable bowel syndrome. Various pathogen types have ascertained unique or overlapping mechanisms associated with irritable bowel syndrome. The proximity to the center reflects the strength of association.
Figure 6.
Figure 6.
An expert-consensus based proposed treatment algorithm for PI-IBS

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