title: Etiology and importance of alkaline esophageal reflux.
abstract: While an alkaline component to esophageal reflux disease is known to be present, little is known about its etiology and harmful effects. Simultaneous gastric and esophageal 24-hour pH monitoring was performed in 81 patients with foregut symptoms. The presence of a mechanically defective lower esophageal sphincter was determined by manometry and duodenogastric reflux by computer-assisted discriminant analysis of the gastric pH record. Heartburn, dysphagia, and regurgitation occurred more frequently in those with a mechanically defective sphincter (p < 0.05) and epigastric pain in those with duodenogastric reflux (p < 0.05). Esophagitis was more common and severe in those with a mechanically defective sphincter (p < 0.05). In these patients, the percentage of time over 24 hours that the esophageal pH was less than 4 was 40.5% in patients without duodenogastric reflux but only 10.2% in those with duodenogastric reflux (p < 0.005), suggesting acid damage in the former and alkaline damage in the latter. To establish the origin of the esophageal alkaline exposure, episodes of elevated fasting gastric pH greater than 4 lasting longer than 1 minute were searched for and identified in 45 patients. Esophageal pH tracings were compared for 30 minutes before and after these events. The esophageal pH was higher following these episodes in duodenogastric reflux patients (p < 0.05), suggesting a gastroduodenal origin of the esophageal alkalinization. This study shows that esophageal damage may be due to acid or alkaline reflux. The alkaline component of gastroesophageal reflux is important and should be considered in the evaluation of patients with foregut symptoms so that appropriate medical or surgical therapy can be instituted.
authors.affiliation: Department of Surgery, Creighton University, Omaha, Nebraska 68131.
authors.forename: K M
authors.initials: KM
authors.lastname: Lin
authors.forename: R K
authors.initials: RK
authors.lastname: Ueda
authors.forename: R A
authors.initials: RA
authors.lastname: Hinder
authors.forename: H J
authors.initials: HJ
authors.lastname: Stein
authors.forename: T R
authors.initials: TR
authors.lastname: DeMeester
mesh_terms: D004942:Esophagitis, Peptic / Q000209:etiology / Q000503:physiopathology; D004943:Esophagogastric Junction / Q000503:physiopathology; D004947:Esophagus / Q000503:physiopathology; D005745:Gastric Acidity Determination; D005764:Gastroesophageal Reflux / Q000209:etiology* / Q000503:physiopathology; D006801:Humans; D006863:Hydrogen-Ion Concentration