基础医学与临床 ›› 2008, Vol. 28 ›› Issue (4): 349-353.

• 研究论文 • 上一篇    下一篇

胃食管反流病患者餐后近端胃酸分布及其与酸反流的关系

许大波 孙晓红 王智凤 柯美云   

  1. 北京协和医院消化科 北京协和医院 北京协和医院消化内科 北京协和医院消化内科
  • 收稿日期:2007-02-07 修回日期:2005-06-04 出版日期:2008-04-25 发布日期:2008-04-25
  • 通讯作者: 许大波

Postprandial acid distributions in proximal stomach and its relationship with acid reflux in patients with gastroesophageal reflux disease

Da-bo XU, Xiao-hong SUN, Zhi-feng WANG, Mei-yun KE   

  1. PUMC Hospital, CAMS & PUMC PUMC Hospital,CAMS & PUMC
  • Received:2007-02-07 Revised:2005-06-04 Online:2008-04-25 Published:2008-04-25
  • Contact: Da-bo XU,

摘要: 目的 探讨胃食管反流病(GERD)患者餐后近端胃内酸分布及其与食管酸暴露的关系。方法 应用3通道锑电极在下食管括约肌(LES)上缘近侧5cm、远侧5cm和远侧10cm处(LES~5cm, LES+5cm, LES+10cm),对受试者行空腹1h和餐后4h食管和胃内pH监测。计算食管酸暴露和胃内整合酸度(IA)。健康志愿者(HS)组和GERD组各10例。结果 (1) HS组餐后LES+5cm处总IA有低于LES+10cm处的趋势,但GERD组未发现酸缓冲作用的部位差异。(2) 餐后第2h,HS组LES+5cm和LES+10cm处IA回升未超过基线;GERD组近端胃IA回升高于基线水平:LES+5cm: 5.4 (1.8~6.8) vs. 1.8(0.3~3.1) mmol/Loh(P<0.05);LES+10cm: 5.6(2.4~7.6) vs. 2.3(0.8~3.1) mmol/Loh(P=0.05)。(3) 两组食管酸暴露均主要发生在餐后第2h,但GERD组显著高于HS组。食管酸暴露和胃内酸度无显著性相关关系。结论 餐后近端胃酸分布异常以及胃酸分泌增高,可能部分地解释餐后GERD患者食管过度酸暴露。

Abstract: Objective: To determine the postprandial acid distributions in patients with gastroesophageal reflux disease (GERD), and their relationship with esophageal acid exposure. Methods: Esophageal and gastric pH were recorded in a 1h fasting segment and a 4h postprandial segments using a triple-channel pH catheter with three antimony electrodes, which were positioned 5cm proximal to the upper margin of LES(LES-5cm), 5cm and 10cm distal to the upper margin of LES(LES+5cm and LES+10cm), respectively. Esophageal acid exposure and gastric integrated acidity (IA) were calculated for each ambulatory pH study. Ten healthy subjects (HS) and 10 patients with GERD were enrolled. Results: (1) Total postprandial IA had a trend to be lower at LES+5cm than at LES+10cm in HS, but there was no significant difference between the two positions in patients with GERD. (2) At 2nd hour after meal, there was no significant difference of gastric IAs between 2nd hour after meal and baseline in HS. Whereas gastric IAs in patients with GERD recovered to a higher level than baseline: LES+5cm: 5.4 (1.8-6.8) mmol/Loh vs. 1.8(0.3-3.1) mmol/Loh (P <0.05); LES+10cm: 5.6(2.4-7.6) mmol/Loh vs. 2.3(0.8-3.1) mmol/Loh, (P=0.05). (3) Excessive esophageal acid exposure occurred mainly at 2nd hour after meal both in HS and the patients, but were higher in patients than in HS. There was no statistically significant relationship between esophageal acid exposure and gastric IA on each postprandial segment in the patients with GERD and HS. Conclusion: The present study suggested that abnormal acid distribution in proximal stomach and an enhanced meal stimulated acid secretion may partly elucidates excessive postprandial esophageal acid exposure in patients with GERD.