M F Vaezi1, J E Richter. 1. Department of Gastroenterology, Cleveland Clinic Foundation, Ohio 44195, USA.
Abstract
BACKGROUND/AIMS: The role of acid and duodeno-gastro-esophageal reflux (DGER), also termed bile reflux, in esophageal mucosal injury is controversial. Several recent developments, especially availability of the recent bilirubin monitoring device (Bilitec), have resulted in clarifications in this area. In order to better understand the role of acid and DGER in esophageal mucosal injury, we summarized the recent publications in this area. METHODOLOGY: Review of published medical literature (MEDLINE) on the clinical consequence of esophageal exposure to gastric acid or DGER. RESULTS: Recent data suggest that esophageal pH monitoring and pH > 7 is a poor marker for reflux of duodenal contents into the esophagus. DGER in non-acidic environments (i.e., partial gastrectomy patients) may cause symptoms but does not cause esophageal mucosal injury. Acid and duodenal contents usually reflux into the esophagus simultaneously, and may be contributing to the development of Barrett's metaplasia and possibly adenocarcinoma. Proton pump inhibitors decrease acid and DGER by reducing intragastric volume available for reflux and raising intragastric pH. The promotility agent cisapride decreases DGER by increasing LES pressure and improving gastric emptying. CONCLUSIONS: 1) The term "alkaline reflux" is a misnormer and should no longer be used in referring to reflux of duodenal contents. 2) Bilitec is the method of choice in detecting DGER and should always be used simultaneously with esophageal pH-monitoring for acid reflux. 3) DGER alone is not injurious to esophageal mucosa, but can result in significant esophageal mucosal injury when combined with acid reflux. 4) Therefore, controlling esophageal exposure to acid reflux by using proton pump inhibitors also eliminates the potentially damaging effect of DGER.
BACKGROUND/AIMS: The role of acid and duodeno-gastro-esophageal reflux (DGER), also termed bile reflux, in esophageal mucosal injury is controversial. Several recent developments, especially availability of the recent bilirubin monitoring device (Bilitec), have resulted in clarifications in this area. In order to better understand the role of acid and DGER in esophageal mucosal injury, we summarized the recent publications in this area. METHODOLOGY: Review of published medical literature (MEDLINE) on the clinical consequence of esophageal exposure to gastric acid or DGER. RESULTS: Recent data suggest that esophageal pH monitoring and pH > 7 is a poor marker for reflux of duodenal contents into the esophagus. DGER in non-acidic environments (i.e., partial gastrectomy patients) may cause symptoms but does not cause esophageal mucosal injury. Acid and duodenal contents usually reflux into the esophagus simultaneously, and may be contributing to the development of Barrett's metaplasia and possibly adenocarcinoma. Proton pump inhibitors decrease acid and DGER by reducing intragastric volume available for reflux and raising intragastric pH. The promotility agent cisapride decreases DGER by increasing LES pressure and improving gastric emptying. CONCLUSIONS: 1) The term "alkaline reflux" is a misnormer and should no longer be used in referring to reflux of duodenal contents. 2) Bilitec is the method of choice in detecting DGER and should always be used simultaneously with esophageal pH-monitoring for acid reflux. 3) DGER alone is not injurious to esophageal mucosa, but can result in significant esophageal mucosal injury when combined with acid reflux. 4) Therefore, controlling esophageal exposure to acid reflux by using proton pump inhibitors also eliminates the potentially damaging effect of DGER.
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