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机构地区:[1]上海交通大学医学院附属仁济医院消化内科上海市消化疾病研究所,200001
出 处:《胃肠病学》2011年第7期435-437,共3页Chinese Journal of Gastroenterology
摘 要:感染后肠易激综合征(PI-IBS)是肠易激综合征(IBS)的常见临床类型。内脏高敏感是PI-IBS的核心机制之一,其形成可能是源于胃肠道传入神经通路的敏感化和抑制性调控内脏痛反应的神经通路功能减退。肠黏膜肥大细胞可通过其脱颗粒产物如5-羟色胺(5-HT)等参与调节内脏高敏感,目前相关制剂已用于IBS的治疗,但疗效尚不确定。因此,深入了解肠黏膜肥大细胞功能改变在PI-IBS内脏高敏感发生机制中的作用,将为阐明PI-IBS的病理生理机制及其临床治疗提供新的思路。Postinfectious irritable bowel syndrome (PI-IBS) is a common clinical type of irritable bowel syndrome (IBS). Visceral hypersensitivity, which is a core mechanism of PI-IBS, might be related to sensitization of gastrointestinal afferent nerve and dysfunction of nerve negatively modulating visceral pain response. Mucosal mast cells participate in the regulation of visceral hypersensitivity through their degranulation products such as 5-hydroxytryptamine (5-HT), and relevant preparations have already been used in curing IBS, while their efficacy remains uncertain. Therefore, in-depth research on functional changes of mucosal mast cells and their roles in visceral hypersensitivity in PI-IBS would provide new insights into pathophysiological mechanism and clinical treatment of PI-IBS.
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