The impact of antireflux surgery on oxidative stress of esophageal mucosa caused by gastroesophageal reflux disease: 4-yr follow-up study.

Abstract

Oxidative stress to esophageal mucosa plays a key role in the pathogenesis of gastroesophageal reflux disease (GERD), Barrett's esophagus, and adenocarcinoma. We investigated whether successful antireflux surgery eliminates oxidative stress. Oxidative stress of esophageal mucosa was measured in 20 GERD patients, before antireflux surgery and 6 and 48 months after it, and compared with normal controls' mucosa (N = 9). Preoperatively, 12 of the 20 had erosive esophagitis or Barrett's metaplasia. Postoperatively, healing of GERD was verified with endoscopy and 24-h pH monitoring. We measured oxidative stress by myeloperoxidase activity (MPA), superoxide dismutase activity, and glutathione content (GSH) in distal esophagus samples from endoscopy. No patient had reflux symptoms after surgery, and pH measurements had normalized. MPA in the distal esophagus decreased (p < 0.05) after successful antireflux surgery, but remained higher than that of controls both 6 months and 4 yr postoperatively (p < 0.05). At all time-points, MPA was higher in patients with preoperatively detected erosive reflux disease (ERD) as compared to non-erosive reflux disease (NERD) (p < 0.01, p < 0.05, and p < 0.05, respectively). GSH values decreased with time only in NERD. At all time-points, GSH levels in distal esophagus were lower than control levels. Antireflux surgery can heal macroscopic esophagitis but cannot fully reverse the oxidative stress (as reflected by MPA and GSH) upon the distal esophageal mucosa.