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胃食管反流病的病理生理学。

Pathophysiology of gastroesophageal reflux disease.

机构信息

Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.

出版信息

Best Pract Res Clin Gastroenterol. 2013 Jun;27(3):339-51. doi: 10.1016/j.bpg.2013.06.002.

DOI:10.1016/j.bpg.2013.06.002
PMID:23998973
Abstract

The gastroesophageal junction is structurally complex and functionally designed to ensure the acid secreted by the most proximal gastric mucosa flows towards the stomach and not up onto the oesophageal squamous mucosa. The pattern and mechanism of reflux vary with the severity of reflux disease and this probably represents different ends of a spectrum rather than distinct pathophysiological mechanisms. Nearly all patients with severe reflux disease have hiatus hernia, however, a substantial proportion of patients with mild reflux disease do not, and this may be a result of intermittent or partial hiatus hernia undetectable by current available tools. The acid pocket is an area of post-prandial unbuffered gastric acidity immediately distal to the gastroesophageal junction and which is enlarged in patients with hiatus hernia. The acid pocket provides a reservoir of acid available to reflux when the intrinsic sphincter fails. Central obesity is an important factor in the aetiology of reflux and does this by the increased abdomino-thoracic pressure gradient inducing hiatus hernia and increasing the rate of flow of reflux when sphincter opens. Central obesity also induces short segment intrasphincteric reflux and thereby columnar metaplasia of the most distal oesophagus.

摘要

胃食管交界处结构复杂,功能设计旨在确保最近端胃黏膜分泌的胃酸流向胃,而不是反流到食管鳞状黏膜。反流的模式和机制因反流病的严重程度而异,这可能代表着不同的极端情况,而不是不同的病理生理机制。几乎所有严重反流病患者都有食管裂孔疝,但相当一部分轻度反流病患者没有,这可能是由于目前可用的工具无法检测到间歇性或部分食管裂孔疝。酸袋是胃食管交界处远端餐后无缓冲胃酸的区域,在食管裂孔疝患者中会扩大。当内在括约肌失效时,酸袋为反流提供了一个可用的酸储备。中心性肥胖是反流发病机制中的一个重要因素,它通过增加腹胸压力梯度引起食管裂孔疝,并增加括约肌打开时反流的流速来实现。中心性肥胖还会引起短段括约肌内反流,从而导致最远端食管柱状化生。

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