文章摘要
周震宇江伟骏顾怡雯张楠刘畅.胃食管反流病患者餐后近端胃内酸分布及 与食管酸暴露的关系[J].,2014,14(20):3914-3917
胃食管反流病患者餐后近端胃内酸分布及 与食管酸暴露的关系
The Postprandial Proximal Gastric Acid Distribution of GastroesophagealReflux Disease Patients and its Relationship with Esophageal Acid Exposure
  
DOI:
中文关键词: 胃内酸分布  锑电极  胃食管反流病  pH 监测
英文关键词: Gastric acid distribution  Antimony electrode  Gastroesophageal reflux disease  pH monitoring
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作者单位
周震宇江伟骏顾怡雯张楠刘畅 上海同仁医院消化科上海200050 
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中文摘要:
      摘要目的:探讨餐后胃食管反流病(GERD)病人近端胃内酸度的分布状态及其和食管酸暴露的相关性。方法:抽选我院12 例 GERD患者,应用3 级锑电极对定位于LES 上缘近侧5 cm(食管)和LES 上缘远侧5 cm的贲门下(近端胃内)、LES 上缘远侧10 cm 的近端胃远侧(近端胃内)进行pH监测,监测时间为空腹1 h和餐后4 h,同期抽选健康志愿者12例为对照组,计算两组患者 食管酸暴露以及胃内整合酸度(IA)。结果:两组空腹时近端胃内IA 和食管酸暴露比较无显著性差异(P>0.05);对照组中,试检者 餐后1、2、3、4 h贲门下IA 均显著低于近端胃远侧部位(P<0.05),但GERD组中IA 部位差异不明显(P>0.05);餐后2 h,两组近端 胃内IA 均有所回升,但是对照组未超过基线(P>0.05),而GERD 组明显高于基线水平(P<0.05);两组食管酸暴露均主要在餐后 2h 发生,并且两组比较差异显著(P<0.05);在餐后各时段,两组中食管酸暴露与IA 均无显著相关性。结论:GERD餐后晚期近端 胃酸分泌增高,扩大了酸性近端胃池,可部分解释GERD 进食后食管过度酸暴露。
英文摘要:
      ABSTRACT Objective:To investigate the postprandial proximal gastric acid distribution of gastroesophageal reflux disease (GERD) patients and its correlation with esophageal acid exposure. Methods:12 patients with GERD were selected in this study. The 3-level antimony electrode was used to monitor the pH value of LES on the edge of proximal 5cm, LES on the edge of 5cm, LES on the edge of the far side of the distal 10cm. The monitoring time was at fasting 1 h and postprandial 4 h. Over the same period,12 healthyvolunteers were selected as control group. The esophageal acid exposure and gastric integrated acidity (IA) were calculated and compared between the two groups. Results:The intragastric IA and proximal esophageal acid exposure were not significantly different between the two groups on an empty stomach (P>0.05). In the control group, at the 1 h, 2 h, 3 h, 4 h after meal, the IA levels cardia of stomach were significantly lower than those of the proximal distal gastric part (P<0.05), but such difference was found in GERD group (P>0.05). At 2 h after meal, the proximal gastric IA level rebounded in both groups, but it exceed the baseline in GERD group(P<0.05) while not in control group (P>0.05). The esophageal acid exposure were observed mainly at the postprandial 2 h in both groups, and the difference between the two groups was significant (P<0.05). At each meal period, the esophageal acid exposure had no significant correlation with IA in both groups.Conclusion: GERD patients after meal had proximal gastric acid secretion increased, expanded the acidic proximal gastric pool. This can partly explain the excessive esophageal acid exposure of GERD patients after meal.
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