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• W2900541686 abstract "See “Rome Foundation Working Team report on post-infection irritable bowel syndrome,” by Barbara G, Grover M, Bercik P, et al, on page 46. See “Rome Foundation Working Team report on post-infection irritable bowel syndrome,” by Barbara G, Grover M, Bercik P, et al, on page 46. Ask any patient with irritable bowel syndrome (IBS) when their condition began and most will struggle to answer but the occasional patient will cite a specific date, saying “I was fine until….” Such patients, who have a sudden onset of their IBS after an episode of infectious gastroenteritis, seem to be rather different from the others, or are they? As the current review1Barbara G. Grover M. Bercik P. et al.Rome Foundation Working Team report on post-infection irritable bowel syndrome.Gastroenterology. 2019; 156: 46-58Abstract Full Text Full Text PDF Scopus (109) Google Scholar shows, this area of research been very active, and the implications are both clinical, mechanistic, and therapeutic. Clinically, it is important to recognize this condition to provide the patients with a rational explanation for symptoms and to reassure them that the prognosis is relatively benign with recovery rates of around one-quarter by 1 year2Card T. Enck P. Barbara G. et al.Post-infectious IBS: defining its clinical features and prognosis using an internet-based survey.United European Gastroenterol J. 2018; (2050640618779923)Crossref Scopus (28) Google Scholar and one-half by 6–8 years.3Neal K.R. Barker L. Spiller R.C. Prognosis in post-infective irritable bowel syndrome: a six year follow up study.Gut. 2002; 51: 410-413Crossref PubMed Scopus (223) Google Scholar, 4Marshall J.K. Thabane M. Garg A.X. et al.Eight year prognosis of postinfectious irritable bowel syndrome following waterborne bacterial dysentery.Gut. 2010; 59: 605-611Crossref PubMed Scopus (168) Google Scholar Mechanistically, it offers important opportunities to understand the causation of IBS and has stimulated a wealth of research focused on features associated with infection including impaired barrier function, immune activation, and altered microbiota.5Martinez C. Rodino-Janeiro B.K. Lobo B. et al.miR-16 and miR-125b are involved in barrier function dysregulation through the modulation of claudin-2 and cingulin expression in the jejunum in IBS with diarrhoea.Gut. 2017; 66: 1537-1538Crossref PubMed Scopus (83) Google Scholar, 6Camilleri M. Carlson P. Valentin N. et al.Pilot study of small bowel mucosal gene expression in patients with irritable bowel syndrome with diarrhea.Am J Physiol Gastrointest Liver Physiol. 2016; 311: G365-G376Crossref PubMed Scopus (21) Google Scholar, 7Jalanka-Tuovinen J. Salojarvi J. Salonen A. et al.Faecal microbiota composition and host-microbe cross-talk following gastroenteritis and in postinfectious irritable bowel syndrome.Gut. 2014; 63: 1737-1745Crossref PubMed Scopus (218) Google Scholar The therapeutic implications are discussed elsewhere in this commentary. The authors report that the incidence of postinfectious (PI)-IBS is highly variable worldwide. We should perhaps not be surprised, because the infecting pathogens have evolved different strategies to overcome host defences.8Simren M. Barbara G. Flint H.J. et al.Intestinal microbiota in functional bowel disorders: a Rome foundation report.Gut. 2013; 62: 159-176Crossref PubMed Scopus (651) Google Scholar Some, like Vibrio cholera, secrete a toxin that binds to a specific receptor, ganglioside GM1, causing chloride secretion from enterocytes greatly amplified by serotonin (5-HT) released from enteroendocrine cells. This causes profuse intestinal secretion and diarrhea without much inflammation; in contrast, Shigella flexneri causes extensive immune activation and ulceration followed by increases in substance P and 5-HT–positive nerve fibers along with mast cells, particularly those surrounded by enteric nerves, changes that are more prominent in patients who develop PI-IBS.9Wang L.H. Fang X.C. Pan G.Z. Bacillary dysentery as a causative factor of irritable bowel syndrome and its pathogenesis.Gut. 2004; 53: 1096-1101Crossref PubMed Scopus (342) Google Scholar Campylobacter jejuni, one of the commonest causes of PI-IBS in Europe, also causes a striking increase in gut permeability with associated increase in the proportion of enteroendocrine cells, which stain for 5-HT along with evidence of long lasting immune activation.10Spiller R.C. Jenkins D. Thornley J.P. et al.Increased rectal mucosal enteroendocrine cells, T lymphocytes, and increased gut permeability following acute Campylobacter enteritis and in post-dysenteric irritable bowel syndrome.Gut. 2000; 47: 804-811Crossref PubMed Scopus (1001) Google Scholar The nature of the pathogen influences the risk for developing PI-IBS, the hazard ratio being 4.3 for E coli, 2.9 for C jejuni, 2.5 for Salmonella spp, and just 2.2 for viral gastroenteritis.11Donnachie E. Schneider A. Mehring M. et al.Incidence of irritable bowel syndrome and chronic fatigue following GI infection: a population-level study using routinely collected claims data.Gut. 2018; 67: 1078-1086Crossref PubMed Scopus (38) Google Scholar This finding is in keeping with the lesser mucosal damage12Troeger H. Loddenkemper C. Schneider T. et al.Structural and functional changes of the duodenum in human norovirus infection.Gut. 2009; 58: 1070-1077Crossref PubMed Scopus (118) Google Scholar and typically more rapid recovery after viral enteritis.13Marshall J.K. Thabane M. Borgaonkar M.R. et al.Postinfectious irritable bowel syndrome after a food-borne outbreak of acute gastroenteritis attributed to a viral pathogen.Clin Gastroenterol Hepatol. 2007; 5: 457-460Abstract Full Text Full Text PDF PubMed Scopus (191) Google Scholar Within a single species such as C jejuni, it can be seen that the expression of a cytotoxin increases the risk of developing persistent bowel dysfunction.14Thornley J.P. Jenkins D. Neal K. et al.Relationship of Campylobacter toxigenicity in vitro to the development of postinfectious irritable bowel syndrome.J Infect Dis. 2001; 184: 606-609Crossref PubMed Scopus (133) Google Scholar Giardiasis differs from the above, being a protozoan that affects predominantly the upper small bowel,15Hanevik K. Hausken T. Morken M.H. et al.Persisting symptoms and duodenal inflammation related to Giardia duodenalis infection.J Infect. 2007; 55: 524-530Abstract Full Text Full Text PDF PubMed Scopus (100) Google Scholar whereas C jejuni cause ileal and colonic ulceration. Although C jejuni increases 5-HT containing enteroendocrine cells, Giardia decreases them but causes an increase in cholecystokinin-containing cells.16Dizdar V. Spiller R. Singh G. et al.Relative importance of abnormalities of CCK and 5-HT (serotonin) in Giardia-induced post-infectious irritable bowel syndrome and functional dyspepsia.Aliment Pharmacol Ther. 2010; 31: 883-891PubMed Google Scholar Although both types of infection are associated with PI-IBS, Giardia is associated with a much higher rate of PI functional dyspepsia, being 25.9% after 3 years17Wensaas K.A. Langeland N. Hanevik K. et al.Irritable bowel syndrome and chronic fatigue 3 years after acute giardiasis: historic cohort study.Gut. 2011; PubMed Google Scholar compared with just 13% 1 year after Salmonellosis.18Mearin F. Perez-Oliveras M. Perello A. et al.Dyspepsia and irritable bowel syndrome after a Salmonella gastroenteritis outbreak: one-year follow-up cohort study.Gastroenterology. 2005; 129: 98-104Abstract Full Text Full Text PDF PubMed Scopus (353) Google Scholar This finding may relate to the higher postprandial cholecystokinin levels, which correlate with dyspepsia scores.16Dizdar V. Spiller R. Singh G. et al.Relative importance of abnormalities of CCK and 5-HT (serotonin) in Giardia-induced post-infectious irritable bowel syndrome and functional dyspepsia.Aliment Pharmacol Ther. 2010; 31: 883-891PubMed Google Scholar Host immune status is important with older age protecting against PI-IBS19Neal K.R. Hebden J. Spiller R. Prevalence of gastrointestinal symptoms six months after bacterial gastroenteritis and risk factors for development of the irritable bowel syndrome: postal survey of patients.BMJ. 1997; 314: 779-782Crossref PubMed Scopus (526) Google Scholar and also infection,20Wouters M.M. Van W.S. Nguyen A. et al.Psychological comorbidity increases the risk for postinfectious IBS partly by enhanced susceptibility to develop infectious gastroenteritis.Gut. 2016; 65: 1279-1288Crossref PubMed Scopus (52) Google Scholar possibly reflecting greater immunity or less hygienic conditions in the young, which a recent survey suggested increases the risk of PI-IBS.2Card T. Enck P. Barbara G. et al.Post-infectious IBS: defining its clinical features and prognosis using an internet-based survey.United European Gastroenterol J. 2018; (2050640618779923)Crossref Scopus (28) Google Scholar Given this marked variability in initial insult and host response, it is perhaps not surprising that PI-IBS is as heterogeneous, both in its symptoms and underlying mechanisms, as other sorts of IBS. Indeed perhaps the greatest discovery of the last decade has been that PI-IBS is remarkably similar to other sorts of IBS, both in the importance of a psychological predisposition,11Donnachie E. Schneider A. Mehring M. et al.Incidence of irritable bowel syndrome and chronic fatigue following GI infection: a population-level study using routinely collected claims data.Gut. 2018; 67: 1078-1086Crossref PubMed Scopus (38) Google Scholar as well as the changes in the gut including immune activation, impaired barrier function and altered 5-HT metabolism. This raises the important issue of how much of all IBS is postinfectious? One small early study reported that the proportion ranged from 6% to 17%,21Longstreth G.F. Hawkey C.J. Mayer E.A. et al.Characteristics of patients with irritable bowel syndrome recruited from three sources: implications for clinical trials.Aliment Pharmacol Ther. 2001; 15: 959-964Crossref PubMed Scopus (105) Google Scholar a figure similar to the 13.3% reported in a recent much larger survey of 7811 patients with IBS.2Card T. Enck P. Barbara G. et al.Post-infectious IBS: defining its clinical features and prognosis using an internet-based survey.United European Gastroenterol J. 2018; (2050640618779923)Crossref Scopus (28) Google Scholar One key question remains: Have these insights led to specific therapies targeted at underlying mechanisms rather than the current symptom-directed therapies? The observations of immune activation in PI-IBS encouraged a small pilot study of prednisolone in PI-IBS; however, this agent showed no benefit.22Dunlop S.P. Jenkins D. Neal K.R. et al.Randomized, double-blind, placebo-controlled trial of prednisolone in post-infectious irritable bowel syndrome.Aliment Pharmacol Ther. 2003; 18: 77-84Crossref PubMed Scopus (154) Google Scholar Keating et al23Keating C. Beyak M. Foley S. et al.Afferent hypersensitivity in a mouse model of post-inflammatory gut dysfunction: role of altered serotonin metabolism.J Physiol. 2008; 586: 4517-4530Crossref PubMed Scopus (77) Google Scholar showed that Trichinella infection in mice was followed by enhanced afferent discharge in response to distension, an example of visceral hypersensitivity which could be blocked by a 5-HT receptor antagonist, ondansetron. Because patients with PI-IBS had been shown to have exaggerated postprandial 5-HT release, a small pilot study of ondansetron in IBS with diarrhea (IBS-D) was performed which showed relief of IBS symptoms, particularly urgency.24Garsed K. Chernova J. Hastings M. et al.A randomised trial of ondansetron for the treatment of irritable bowel syndrome with diarrhoea.Gut. 2014; 63: 1617-1625Crossref PubMed Scopus (158) Google Scholar Immune activation in IBS-D is another potential therapeutic target which has been tested. A randomised placebo-controlled trial of the anti-inflammatory agent mesalazine in IBS-D showed no benefit overall; however, post hoc analysis showed that a small subgroup with PI-IBS seemed to respond.25Lam C. Tan W. Leighton M. et al.A mechanistic multicentre, parallel group, randomised placebo-controlled trial of mesalazine for the treatment of IBS with diarrhoea (IBS-D).Gut. 2016; 65: 91-99Crossref PubMed Scopus (64) Google Scholar Furthermore, open-label treatment of E coli O147 infection with mesalazine seemed to decrease the risk of developing PI-IBS,26Andresen V. Lowe B. Broicher W. et al.Post-infectious irritable bowel syndrome (PI-IBS) after infection with Shiga-like toxin-producing Escherichia coli (STEC) O104:H4: A cohort study with prospective follow-up.United European Gastroenterol J. 2016; 4: 121-131Crossref PubMed Scopus (27) Google Scholar but this finding needs confirming in randomized, controlled trials. Against this, a small pilot study of mesalazine in PI-IBS failed to show any difference from placebo, although it was undoubtedly underpowered.26Andresen V. Lowe B. Broicher W. et al.Post-infectious irritable bowel syndrome (PI-IBS) after infection with Shiga-like toxin-producing Escherichia coli (STEC) O104:H4: A cohort study with prospective follow-up.United European Gastroenterol J. 2016; 4: 121-131Crossref PubMed Scopus (27) Google Scholar, 27Tuteja A.K. Fang J.C. Al-Suqi M. et al.Double-blind placebo-controlled study of mesalamine in post-infective irritable bowel syndrome - a pilot study.Scand J Gastroenterol. 2012; 47: 1159-1164Crossref PubMed Scopus (32) Google Scholar Rodent models of Campylobacter infection showed small intestinal bacterial overgrowth could follow gastroenteritis.28Pimentel M. Chatterjee S. Chang C. et al.A new rat model links two contemporary theories in irritable bowel syndrome.Dig Dis Sci. 2008; 53: 982-989Crossref PubMed Scopus (67) Google Scholar Whether this occurs in humans is unclear, but recent studies in India have suggested that PI-IBS may overlap with tropical sprue in which bacterial overgrowth is common.29Ghoshal U.C. Gwee K.A. Post-infectious IBS, tropical sprue and small intestinal bacterial overgrowth: the missing link.Nat Rev Gastroenterol Hepatol. 2017; 14: 435-441Crossref PubMed Scopus (48) Google Scholar Trials with rifaximin in IBS-D have shown a benefit in about 1 in 11 of patients. What is now needed is a large randomized, controlled trial that tests all participants for small intestinal bacterial overgrowth and links the result to outcome of rifaximin therapy. As can be seen, most of the literature to date on PI-IBS has been descriptive. What is now needed are large, randomized trials in PI-IBS of specific treatments in which participants are subdivided according to the underlying mechanisms (Figure 1). The response of each subgroup will allow more accurate definition of what is the main driver of symptoms and what is mere epiphenomena. Only then will we achieve the precision medicine we all aspire to. Rome Foundation Working Team Report on Post-Infection Irritable Bowel SyndromeGastroenterologyVol. 156Issue 1PreviewThe 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. Full-Text PDF" @default.
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• W2900541686 title "Significance of Postinfectious Irritable Bowel Syndrome?" @default.
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• W2900541686 cites W2043676278 @default.
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• W2900541686 cites W2099814399 @default.
• W2900541686 cites W2114058582 @default.
• W2900541686 cites W2114455930 @default.
• W2900541686 cites W2121782849 @default.
• W2900541686 cites W2129997920 @default.
• W2900541686 cites W2135313371 @default.
• W2900541686 cites W2137119327 @default.
• W2900541686 cites W2144481594 @default.
• W2900541686 cites W2158018898 @default.
• W2900541686 cites W2159108878 @default.
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• W2900541686 cites W2293101337 @default.
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