Currently there is controversial evidence that suggests that the accepted incidence of atrophic gastritis of 1.2 to 3.3% in patients with Helicobacter pylori gastritis may be increased by the long-term suppression of acid by a proton pump inhibitor (omeprazole). The purpose of this study is to show whether lesser forms of acid suppression by antacids or H2 receptor antagonists may have an influence on the development of atrophic gastritis. The authors recently reported a study in which a cohort of 36 patients with symptoms of dyspepsia were followed clinically for a period of 7 to 19 years. In that report all subjects underwent upper endoscopy with two biopsy specimens each from the antrum and fundus, on at least two occasions, 7 to 19 years apart. A diagnosis of atrophic gastritis was based on the interpretation of these biopsies by two gastrointestinal pathologists. The presence of H. pylori colonization was determined by tissue sampling and by a campylobacter-like organisms test of the antrum. Of the 36 patients in the authors' previous report, 33 had adequate baseline and follow-up data on medications consumed throughout the period of the study. In their current report they now present the findings of a retrospective review in which they correlate the presence of atrophic gastritis with the sole use of antacids and H2 receptor antagonists throughout the period of the study. In the cohort of 33 patients evaluated from the previous report, the authors found that atrophic gastritis had developed in all 28 patients positive for H. pylori, and in none of the 5 patients negative for H. pylori (p < 0.0001). A retrospective analysis of this previously studied cohort of 33 patients revealed that the use of antacids and H2 receptor antagonists did not predict the development of atrophic gastritis in either H. pylori-negative or -positive subjects. In a retrospective analysis of a cohort of 33 patients followed for an average of 11.7 years, atrophic gastritis developed in H. pylori-positive but not in H. pylori-negative subjects, irrespective of the use and duration of antacids or H2 receptor antagonists.
There is a paucity of data on the long-term behavior of dyspepsia, endoscopic findings, and gastroduodenal histology in patients with or without Helicobacter pylori colonization. We evaluated these parameters during a period of 7 to 19 years (average, 12.3 years) by baseline and follow-up studies. In 36 patients studied, the pattern of gastroduodenal dyspepsia and esophagogastroduodenoscopy findings remained essentially unchanged in 67% and 56% respectively. Dyspepsia patterns did not correlate significantly with either endoscopic or histologic findings, including the severity or location of gastritis in the fundus or antrum, or the presence or absence of H. pylori gastritis. Of 36 patients with adequate biopsies of the fundus and antrum, H. pylori colonization with gastritis was present in 73% but not in 27%. Progression to various degrees of atrophic gastritis was noted in 100% with, and in none without, H. pylori gastritis. In the fundus, atrophy progressed from 14% to 56%, but intestinal metaplasia did not change. In the antrum, atrophy increased from 22% to 64% and intestinal metaplasia increased from 17% to 36%. No patient demonstrated dysplasia, but severe atrophy was seen in the fundus (6%) and antrum (11%). Only two patients (5%) had severe loss of glandular elements and very low pepsinogen I, and thus can be considered to have developed advanced gastric atrophy.
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