OBJECTIVES: Our objective was to assess the role of reflux of duodenal contents in the genesis of Barrett's esophagus. Therefore, we performed a study to quantify duodenogastric reflux, using 99mTc-HIDA quantification in gastric juice after continuous intravenous infusion of the same. METHODS: The study contained 20 patients with Barrett's esophagus (10 uncomplicated and 10 complicated by ulcers and/or stenosis), 10 patients with peptic esophagitis without Barrett's esophagus (two grade I, four grade II, and four grade III, according to Savary-Miller), and 10 healthy volunteers who made up the control group. Comparisons were made between the groups. RESULTS: When we considered the groups overall, we observed that the 20 patients with Barrett's esophagus had higher reflux rates (p < 0.01) than either the 10 patients with peptic esophagitis without Barrett's esophagus, or the 10 controls. Complicated Barrett's esophagus presented higher reflux rates than uncomplicated Barrett's esophagus, although the differences were not statistically significant. However, on analyzing the results after considering the groups case by case, we see that the mean reflux rate in the Barrett's esophagus groups is due to five patients presenting much higher rates than the rest. CONCLUSIONS: Our results suggest that duodenogastric reflux might be involved in the appearance of Barrett's esophagus and its related complications, although only in certain cases. The pathogenesis of Barrett's esophagus is probably multifactorial, and other factors must be involved.
OBJECTIVES: Our objective was to assess the role of reflux of duodenal contents in the genesis of Barrett's esophagus. Therefore, we performed a study to quantify duodenogastric reflux, using 99mTc-HIDA quantification in gastric juice after continuous intravenous infusion of the same. METHODS: The study contained 20 patients with Barrett's esophagus (10 uncomplicated and 10 complicated by ulcers and/or stenosis), 10 patients with peptic esophagitis without Barrett's esophagus (two grade I, four grade II, and four grade III, according to Savary-Miller), and 10 healthy volunteers who made up the control group. Comparisons were made between the groups. RESULTS: When we considered the groups overall, we observed that the 20 patients with Barrett's esophagus had higher reflux rates (p < 0.01) than either the 10 patients with peptic esophagitis without Barrett's esophagus, or the 10 controls. Complicated Barrett's esophagus presented higher reflux rates than uncomplicated Barrett's esophagus, although the differences were not statistically significant. However, on analyzing the results after considering the groups case by case, we see that the mean reflux rate in the Barrett's esophagus groups is due to five patients presenting much higher rates than the rest. CONCLUSIONS: Our results suggest that duodenogastric reflux might be involved in the appearance of Barrett's esophagus and its related complications, although only in certain cases. The pathogenesis of Barrett's esophagus is probably multifactorial, and other factors must be involved.