BACKGROUND/AIMS: Several reports suggest that duodenogastroesophageal reflux may produce esophagitis, Barrett's esophagus, and esophageal adenocarcinoma. The purpose of this study was to understand better the relationship of pH (< 4 and > 7), duodenogastroesophageal reflux, and fasting bile acid concentrations in producing esophageal damage. METHODS: Using a spectrophotometric technique to measure bile reflux, four groups were studied: healthy subjects, reflux patients, patients with Barrett's esophagus, and patients with esophageal symptoms after partial gastrectomy. RESULTS: Simultaneous 24-hour pH and bile monitoring of distal esophagus found close association between total percent of time pH < 4 and duodenogastroesophageal reflux (r = 0.78; P < 0.001) but a poor relationship (r = -0.06) with total percent of time pH > 7, suggesting that the term alkaline reflux is a misnomer. Duodenogastroesophageal reflux increased significantly with the severity of reflux disease, being greatest in patients with Barrett's esophagus and comparable with that in patients with partial gastrectomy. Fasting bile acid concentrations did not distinguish patients with Barrett's esophagus from those with reflux. Rather, increased quantity of acid reflux was the single factor most characterizing patients with Barrett's esophagus. Omeprazole (20 mg twice daily) normalized acid reflux parameters (13.8% +/- 1.6% to 0.8% +/- 0.6%) and significantly (P < 0.001) decreased duodenogastroesophageal reflux (32.8% +/- 6.9% to 4.7% +/- 1.7%). CONCLUSIONS: Acid reflux is the primary factor in the development of Barrett's esophagus. Bile reflux parallels acid reflux and, at best, may have a synergistic role. Aggressive acid suppression with omeprazole markedly decreases both.
BACKGROUND/AIMS: Several reports suggest that duodenogastroesophageal reflux may produce esophagitis, Barrett's esophagus, and esophageal adenocarcinoma. The purpose of this study was to understand better the relationship of pH (< 4 and > 7), duodenogastroesophageal reflux, and fasting bile acid concentrations in producing esophageal damage. METHODS: Using a spectrophotometric technique to measure bile reflux, four groups were studied: healthy subjects, reflux patients, patients with Barrett's esophagus, and patients with esophageal symptoms after partial gastrectomy. RESULTS: Simultaneous 24-hour pH and bile monitoring of distal esophagus found close association between total percent of time pH < 4 and duodenogastroesophageal reflux (r = 0.78; P < 0.001) but a poor relationship (r = -0.06) with total percent of time pH > 7, suggesting that the term alkaline reflux is a misnomer. Duodenogastroesophageal reflux increased significantly with the severity of reflux disease, being greatest in patients with Barrett's esophagus and comparable with that in patients with partial gastrectomy. Fasting bile acid concentrations did not distinguish patients with Barrett's esophagus from those with reflux. Rather, increased quantity of acid reflux was the single factor most characterizing patients with Barrett's esophagus. Omeprazole (20 mg twice daily) normalized acid reflux parameters (13.8% +/- 1.6% to 0.8% +/- 0.6%) and significantly (P < 0.001) decreased duodenogastroesophageal reflux (32.8% +/- 6.9% to 4.7% +/- 1.7%). CONCLUSIONS: Acid reflux is the primary factor in the development of Barrett's esophagus. Bile reflux parallels acid reflux and, at best, may have a synergistic role. Aggressive acid suppression with omeprazole markedly decreases both.