Original Articles
Copyright ©The Author(s) 2000. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Dec 15, 2000; 6(6): 789-792
Published online Dec 15, 2000. doi: 10.3748/wjg.v6.i6.789
Long term omeprazole therapy for reflux esophagitis: Follow-up in serum gastrin levels, EC cell hyperplasia and neoplasia
Pankaj Singh, Anant Indaram, Ronald Greenberg, Vernu Visvalingam, Simmy Bank
Pankaj Singh, Anant Indaram, Ronald Greenberg, Vernu Visvalingam, Simmy Bank Division of Gastroenterology, Albert Einstein Colege of Medicine, Long Island Jewish Medical Center, New Hyde Park, New York
Pankaj Singh, is a second year gastroenterology fellow in Albert Einstein College of Medicine, Long Island Jewish Hospital. He did his residency in medicine from King George Medical College, India and then from State University of New York, NY. He is currently studying the effect of alcohol on apoptosis in pancreatic cells.
Author contributions: All authors contributed equally to the work.
Correspondence to: Dr. Pankaj Singh, Department of Gastroenterology, Long Island Jewish Medical Center, 270-05 76th Ave, New Hyde Park, NY 11040, USA
Telephone: (718)-347-2393
Received: October 13, 2000
Revised: October 19, 2000
Accepted: October 22, 2000
Published online: December 15, 2000
Abstract

AIM: To evaluate the long-term safety of omeprazole 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 periodic gastrin levels, H. pylori infection, gastric biopsies for incidence of ECL cell hyperplasia, carcinoids, gastric atrophy and neoplasia. A total 185 patient follow-up years and 137 gastric biopsies were done.

RESULTS: Among the 33 patients, 36% reached their peak gastrin levels in an average of 8 mo to one year, then drifted Down slowly over 1-2 year period to just above their baseline level, 24% of the patients had a peak gastrin level above 400 ng·L-1 and one patient had a peak level above 1000 ng·L-1. One patient had a mild ECL cell hyperplasia which was self-limiting and did not show any dysplastic changes. Eighteen percent of patients were positive for H. pylori infection. The gastric biopsies did not show gastric atrophy, intestinal metaplasia or neoplastic 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.

Keywords: gastroesophageal reflux; proton pump inhibitors; enterochromaffin cell; hypergastrinemia; carcinoid tumor; biopsy