The putative role of inflammation in the irritable bowel syndrome
The putative role of inflammation in the irritable bowel syndrome
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DOI：
10.1136/gut.49.6.743
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发表时间：
2001-12-01
期刊：
影响因子：
24.5
通讯作者：
Rampal, P
中科院分区：
文献类型：
--
作者：
Collins, SM;Piche, T;Rampal, P
肠易激综合征（IBS）可被定义为一种疼痛的慢性腹部综合征，其通常与排便习惯改变有关，并且没有可辨别的潜在结构异常。一般认为，症状是由肠道功能异常产生的，包括感觉知觉改变、运动异常，在一些患者中，还包括上皮功能异常。行为因素很重要，特别是在报告症状时。缺乏的是对改变肠道功能的发病机制的理解。IBS是一种异质性疾病，不仅在其临床表现和病理生理学方面，而且在其发病机制方面。虽然中枢和外周因素都与IBS的发病机制有关，但本文将仅限于评估支持炎症作为IBS肠道功能改变基础的证据。在考虑炎症在IBS中的作用时，提示与哮喘进行比较。像IBS一样，哮喘曾经被认为是一种心身疾病，特别是在非特应性儿童中。50多年来，哮喘的治疗重点是对异常终末器官生理学（即气道高反应性）的药理学纠正，这种方法类似于当前的IBS治疗方法，旨在调节运动活动或感觉知觉。随后在正常无菌的支气管肺泡灌洗液中发现了炎性细胞，从而认识到哮喘是一种炎症性疾病。IBS的类似思维转变之所以难以实现，有两个原因。首先，肠道通常处于受控的炎症状态，识别炎症细胞数量或组成的微妙增加的挑战不容低估。其次，直觉上，IBS比哮喘更具异质性，炎症不太可能是所有情况下的一个因素。然而，有新的证据表明炎症在IBS患者的发病机制中起作用，从临床的角度来看，有两种情况促使人们考虑炎症在IBS发病机制中的作用。第一种是胃肠炎后患者中IBS的发展（感染后IBS（PIIBS））。这发生在7-31%的胃肠炎患者中，这些患者由各种微生物病原体1 -3（包括寄生虫）引起。4一些研究表明，这些患者的结肠固有层和粘膜的细胞结构持续增加，或淋巴细胞增加。综上所述，这些发现表明，对感染的炎症反应，而不是感染因子本身，
The irritable bowel syndrome (IBS) may be defined as a painful chronic abdominal symptom complex which is usually associated with altered bowel habit, and for which there is no discernible underlying structural abnormality. It is generally accepted that symptoms are generated by abnormalities of gut function, including altered sensory perception, abnormal motility and, in some patients, abnormalities of epithelial function. Behavioural factors are important, particularly in the reporting of symptoms. What is lacking is an understanding of the pathogenetic mechanisms that alter gut function. IBS is a heterogeneous condition, not only in its clinical presentation and pathophysiology, but also in terms of its pathogenesis. While both central and peripheral factors have been implicated in the pathogenesis of IBS, this article will restrict itself to an evaluation of the evidence supporting inflammation as a basis for altered gut function in IBS. In considering the role of inflammation in IBS, one is prompted to make a comparison with asthma. Like IBS, asthma was once considered a psychosomatic disorder, particularly in non-atopic children. For more than 50 years the treatment of asthma focused on the pharmacological correction of abnormal end organ physiology (that is, airways hyperresponsiveness), an approach that is similar to current therapeutic approaches to IBS, and which are aimed at modulating motor activity or sensory perception. The subsequent discovery of inflammatory cells in the normally sterile broncheoalveolar lavage led to the recognition of asthma as an inflammatory condition. There are two reasons why a similar shift in thinking in IBS will be diYcult. Firstly, the gut is normally in a state of controlled inflammation and the challenge of identifying a subtle increase in inflammatory cell number or composition is not to be underestimated. Secondly, IBS is intuitively more heterogeneous than asthma, and inflammation is unlikely to be a factor in all cases. Nevertheless, there is emerging evidence for a role of inflammation in the pathogenesis of a least a subset of IBS patients.From a clinical point of view, there are two scenarios that prompt consideration of a role for inflammation in the pathogenesis of IBS. The first is the development of IBS in patients following gastroenteritis (post-infective IBS (PIIBS)). This occurs in 7–31% of patients with gastroenteritis from a variety of microbial agents1–3 including parasites. 4 Some studies have shown a persistent increase in the cellularity of the lamina propria and mucosa or an increase in lymphocytes in the colon of these patients. 5 6 Taken together, these findings suggest that the inflammatory response to infection, rather than the infective agent itself,