AIM To evaluate the long-term safety ofomeprazole in patients of gastroesophagealreflux disease resistant to treatment with H2receptor antagonist.METHODS We prospectively followed 33patients on omeprazole therapy for severeerosive esophagitis for 5-8 years,with periodicgastrin levels,H.pylori infection,gastricbiopsies for incidence of ECL cell hyperplasia,carcinoids,gastric atrophy and neoplasia.Atotal 185 patient follow-up years and 137 gastricbiopsies were done.RESULTS Among the 33 patients,36% reachedtheir peak gastrin levels in an average of 8months to one year,then drifted Down slowlyover 1-2 year period to just above their baselinelevel,24% of the patients had a peak gastrinlevel above 400ng·L~1 and one patient had apeak level above 1000 ng·L~1.One patient had amild ECL cell hyperplasia which was self limitingand did not show any dysplastic changes.Eighteen percent of patients were positive forH.pylori infection.The gastric biopsies did notshow gastric atrophy,intestinal metaplasia orneoplastic changes.CONCLUSION In a series of 33 patients followed for 5 - 8 years on omeprazole therapy for severe reflux esophagitis, we did not observe any evidence of significant ECL cell hyperplasia, gastric atrophy, intestinal metaplasia, dysplasia or neoplastic changes. AIM To evaluate the long-term safety ofomeprazole in patients of gastroesophageal reflux disease resistant to treatment with H2 receptor antagonist. METHODS We prospectively followed 33 patients on omeprazole therapy for severe erosive esophagitis for 5-8 years, with periodicgastrin levels, H. pylori infection, gastric biopsies for incidence of total 125 patient follow-up years and 137 gastric biopsies were done. RESULTS Among the 33 patients, 36% reached the peak peak gastrin levels in an average of 8 months to one year, then drifted Down slowlyoverver 1-2 year period to just above their baselinelevel, 24% of the patients had a peak gastrinlevel above 400ng · L ~ 1 and one patient had apeak level above 1000 ng · L ~ 1.One patient had amild ECL cell hyperplasia which was self limitingand did not show any dysplastic changes.Eighteen percent of patients were positive for H.pylori infection.The gastric biopsies did notshow gastric atrophy, intestinal metapl asia orneoplastic changes. CONCLUSION In a series of 33 patients followed for 5-8 years on omeprazole therapy for severe reflux esophagitis, we did not observe any evidence of significant ECL cell hyperplasia, gastric atrophy, intestinal metaplasia, dysplasia or neoplastic changes.