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To determine whether there is a relationship between the presence of H pylon and the various subtypes of intestinal metaplasia in the gastric antrum, 2274 antral gastroscopic biopsies from 533 patients were examined. Hpylon was found in 289 patients. Intestinal The extent of intestinal metaplasia as well as

Whenever intestinal metaplasia was present in the mucosa, 5 ,um sections were cut and stained with Alcian blue pH 2.5/periodic acid Schiff (AB pH 2-5/PAS) and high-irondiamine/Alcian blue for subtyping of intestinal

INTRODUCTIONAlthough Helicobacter pylori is probably not implicated in the pathogenesis of re¯ux oesophagitis, usually onethird to one-half of adult patients with re¯ux oesophagitis or endoscopy-negative re¯ux disease are infected with H. pylori.1 This ®gure is comparable with the prevalence of the infection in the same age group. 2 Two major patterns of H. pylori infection have been recognized: the low acid route, with pangastritis, atrophy and metaplasia, and the elevated acid route, with antral gastritis and duodenal ulcer. 3 The low acid route is believed to give rise to an increased risk of cancer. 3Atrophy and intestinal metaplasia are long-term sequelae of H. pylori infection. 4,5 They are considered to be important precursors for gastric carcinoma.6±8 Type I (complete Ð small intestinal type) and type II (incomplete Ð sialomucin-containing goblet cells scattered among gastric-type neutral mucin-secreting cells) metaplasia are believed to carry the lowest risk. Type III metaplasia (incomplete form, with goblet cells secreting SUMMARY Background: Long-term acid suppression is believed to accelerate atrophic gastritis in Helicobacter pyloripositive patients. The in¯uence of long-term therapy with lansoprazole has not been examined. Aim: To study the clinical and endoscopic ef®cacy and histological evolution of gastric mucosa during 5 years of maintenance treatment with lansoprazole, 30 mg. Methods: Seventy-eight patients with endoscopically proven oesophagitis were followed for 5 years. Biopsies taken at the start of the study, during follow-up and after 5 years were available for 73 patients. Results: The total endoscopic relapse rate was 14.1%. At the start of the study, 34 patients were Helicobacter pylori negative and 39 were Helicobacter pylori positive (two atrophy, 25 antral gastritis, 12 pangastritis). At