Recent developments in the pathophysiology of irritable bowel syndrome
Recent developments in the pathophysiology of irritable bowel syndrome作者机构：Section for Gastroenterology Department of Medicine Stord Hospital Section of Neuroendocrine GastroenterologyDivision of Gastroenterology Department of Clinical MedicineUniversity of Bergen National Centre for Functional Gastrointestinal Disorders Department of Medicine Haukeland University Hospital
出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)
年 卷 期：2015年第21卷第25期
页 面：7621-7636页
核心收录：
基 金：Supported by Grants from Helse-Vest and Helse-Fonna Norway
主 题：Diet Endocrine cells Genetic factors Lowgradeinflammation Microbiota Stem ce
摘 要：Irritable bowel syndrome(IBS) is a common gastrointestinal disorder, the pathophysiology of which is not completely known, although it has been shown that genetic/social learning factors, diet, intestinal microbiota, intestinal low-grade inflammation, and abnormal gastrointestinal endocrine cells play a major role. Studies of familial aggregation and on twins have confirmed the heritability of IBS. However, the proposed IBS risk genes are thus far nonvalidated hits rather than true predisposing factors. There is no convincing evidence that IBS patients suffer from food allergy/intolerance, with the effect exerted by diet seemingly caused by intake of poorly absorbed carbohydrates and fiber. Obesity is a possible comorbidity of IBS. Differences in the microbiota between IBS patients and healthy controls have been reported, but the association between IBS symptoms and specific bacterial species is uncertain. Low-grade inflammation appears to play a role in the pathophysiology of a major subset of IBS, namely postinfectious IBS. The density of intestinal endocrine cells is reduced in patients with IBS, possibly as a result of genetic factors, diet, intestinal microbiota, and low-grade inflammation interfering with the regulatory signals controlling the intestinal stem-cell clonogenic and differentiation activities. Furthermore, there is speculation that this decreased number of endocrine cells is responsible for the visceral hypersensitivity, disturbed gastrointestinal motility, and abnormal gut secretion seen in IBS patients.
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