3509 THE EFFECTS OF ANTI-H. PYLORI THERAPY ON DEVELOPMENT OF ENDOSCOPIC REFLUX ESOPHAGITIS IN PEPTIC ULCER PATIENTS.

Abstract

Background/Aims: H. pylori has been generally accepted as the main pathogenetic factor in chronic gastritis, peptic ulcer disease and gastric cancer. There are many arguments that H. pylori is a protective factor or a risk factor for GERD. In a recent preliminary study, some authors reported a high incidence of reflux esophagitis in patients after H. pylori eradication therapy. We carried out a study to evaluate the effects of H.pylori eradication therapy on development of reflux esophagitis and compare endoscopic findings according to ulcer sites. Material and Methods: 168 patients with endoscopically documented peptic ulcer received a 1 or 2 weeks of triple therapy. Esophageal findings were investigated endoscopically before entry, 1 month, 6, 12, and 24 months after cessation of treatment. H. pylori status was evaluated by Giemsa stain, CLO test, and culture at each examination. Results: The patients were classified into two groups, cured and ongoing infection group. Endoscopic findings of 168 patients were compared before and after the triple therapy: hiatal hernia 9/15, reflux esophagitis 8(GI: 4, GII: 4)/6(GI: 4, GII: 2). Of the 168 patients, H. pylori infection was cured in 125 patients: 12(9.6%) of these developed endoscopically proven hiatal hernia, 4(3.2%) developed reflux esophagitis and 3 who had GERD before the triple therapy showed improvement. In 43 patients with ongoing H. pylori infection: 4(9.3%) of these patients developed endoscopically proven hiatal hernia, 2(4.7%) of these developed reflux esophagitis and 2 showed improvement. There was no difference in the incidence of reflux esophagitis between cured and ongoing infection groups(p=0.757). The estimated incidences of reflux esophagitis within 2 years were 3.2% on cured group and 4.7% on ongoing infection group. Of the 36 GU patients, the incidence of reflux esophagitis in both groups were 2(5.6%)/1(12.5%). Of the 132 DU patients, the incidence of reflux esophagitis in both groups were 2(1.2%)/2(5.9%). Conclusion: H. pylori eradication in patients with peptic ulcer disease is not associated with increment of reflux esophagitis. There are no differences in endoscopic esophageal findings according to ulcer sites after the triple therapy. Background/Aims: H. pylori has been generally accepted as the main pathogenetic factor in chronic gastritis, peptic ulcer disease and gastric cancer. There are many arguments that H. pylori is a protective factor or a risk factor for GERD. In a recent preliminary study, some authors reported a high incidence of reflux esophagitis in patients after H. pylori eradication therapy. We carried out a study to evaluate the effects of H.pylori eradication therapy on development of reflux esophagitis and compare endoscopic findings according to ulcer sites. Material and Methods: 168 patients with endoscopically documented peptic ulcer received a 1 or 2 weeks of triple therapy. Esophageal findings were investigated endoscopically before entry, 1 month, 6, 12, and 24 months after cessation of treatment. H. pylori status was evaluated by Giemsa stain, CLO test, and culture at each examination. Results: The patients were classified into two groups, cured and ongoing infection group. Endoscopic findings of 168 patients were compared before and after the triple therapy: hiatal hernia 9/15, reflux esophagitis 8(GI: 4, GII: 4)/6(GI: 4, GII: 2). Of the 168 patients, H. pylori infection was cured in 125 patients: 12(9.6%) of these developed endoscopically proven hiatal hernia, 4(3.2%) developed reflux esophagitis and 3 who had GERD before the triple therapy showed improvement. In 43 patients with ongoing H. pylori infection: 4(9.3%) of these patients developed endoscopically proven hiatal hernia, 2(4.7%) of these developed reflux esophagitis and 2 showed improvement. There was no difference in the incidence of reflux esophagitis between cured and ongoing infection groups(p=0.757). The estimated incidences of reflux esophagitis within 2 years were 3.2% on cured group and 4.7% on ongoing infection group. Of the 36 GU patients, the incidence of reflux esophagitis in both groups were 2(5.6%)/1(12.5%). Of the 132 DU patients, the incidence of reflux esophagitis in both groups were 2(1.2%)/2(5.9%). Conclusion: H. pylori eradication in patients with peptic ulcer disease is not associated with increment of reflux esophagitis. There are no differences in endoscopic esophageal findings according to ulcer sites after the triple therapy.