Background: Helicobacter pylori infection is associated with variable clinical outcomes, including gastroduodenal diseases, and genetic factors may be relevant in this process. Aims: We investigated the effects of an interleukin 8 (IL-8) gene polymorphism on the risk of gastroduodenal diseases, the degree of H pylori induced gastritis, and IL-8 gene transcription. Subjects: The study was performed in 244 healthy control subjects and 690 H pylori positive patients with non-cardia gastric cancer, gastric ulcer, duodenal ulcer, or gastritis. Methods: We identified the IL-8 2251 A/T polymorphism by direct sequence analysis, and measured the gastritis score and serum pepsinogen (PG). The transcriptional promoter activity of the IL-8 gene was assessed by luciferase assay. Results: IL-8 2251A was associated with a higher risk of gastric cancer and gastric ulcer. Patients carrying IL-8 2251A showed an increased risk of gastric cancer (odds ratios (OR) 2.01 (95% confidence interval (CI) 1.38-2.92)) and gastric ulcer (OR 2.07 (95% CI 1.37-3.12)). Compared with patients younger than 49 years, atrophy and metaplasia scores in the antrum were significantly higher and the PG I/II ratio significantly lower in 2251A carriers than in T/T carriers. In the in vitro assay, IL-8 2251A showed enhanced promoter activity in response to IL-1b or tumour necrosis factor a. Conclusions: The IL-8 2251A allele may be associated with progression of gastric atrophy in patients with H pylori infection, and may increase the risk of gastric cancer and gastric ulcer in Japanese people.

Background-It remains controversial whether or not Helicobacter pylori infection causes altered gastric acid secretion. A novel test for evaluating gastric acid secretion (endoscopic gastrin test; EGT) has recently been developed. Aim-To investigate by EGT the eVects of H pylori eradication on the state of gastric acid secretion in patients with peptic ulcer. Methods-Twenty six patients with duodenal ulcer and 33 with gastric ulcer, for all of whom H pylori infection had been documented, were studied by EGT, histological examination of gastric mucosa, and measurement of plasma gastrin levels before and one and seven months after H pylori eradication. Results-In patients with duodenal ulcer, the mean EGT value before H pylori eradication was higher than that in H pylori negative controls, but it had decreased significantly seven months after the treatment. In contrast, the mean EGT value of patients with gastric ulcer before H pylori eradication was lower than that in H pylori negative controls, but it had increased one month after the treatment; this was followed by a slight decrease at seven months. In both groups, mean EGT values seven months after the treatment were not significantly diVerent from the mean control value. Conclusions-The reduced acid secretion in gastric ulcer patients and gastric acid hypersecretion in duodenal ulcer patients were both normalised after the clearance of H pylori.

INTRODUCTIONRecent studies have shown that re¯ux oesophagitis may develop after the successful treatment of Helicobacter pylori infection.1, 2 We and others have reported previously that H. pylori eradication causes an alteration in gastric acid secretion.3±8 Although gastric acid secretion has been accepted as a key factor in the pathogenesis of re¯ux oesophagitis, the relationship between changes in acid secretion and the development of re¯ux oesophagitis after H. pylori eradication is not well known. Recently, we have developed a convenient method for measuring stimulated gastric acid secretion. The method, named endoscopic gastrin test, can be performed in a short time concomitantly with the routine endoscopic examination.10 It has been con®rmed in a previous study that the results of the endoscopic gastrin test are highly reproducible and are correlated signi®-cantly with the peak acid output determined by the conventional gastric acid stimulation test. In the present study, using the endoscopic gastrin test, we investigated whether changes in gastric acid secretion after H. pylori eradication play a role in the development of re¯ux oesophagitis. In addition, we investigated the in¯uence of the presence or absence of hiatal hernia, an important pathogenic factor of re¯ux oesophagitis. 11±13 SUBJECTS AND METHODS SubjectsA total of 105 with H. pylori infection in whom re¯ux oesophagitis had been ruled out endoscopically (76 men and 29 women, mean age 51.5 years) were followed up SUMMARY Background: The role of acid secretion in re¯ux oesophagitis which may develop after H. pylori eradication is not well known. Aim: To investigate the participation of altered gastric acid secretion and the presence of hiatal hernia in the development of re¯ux oesophagitis after eradication therapy for H. pylori. Subjects and Methods: A total of 105 patients with H. pylori infection, but without re¯ux oesophagitis at the time of eradication therapy, were followed prospectively for 7 months after the clearance of this microorganism.

These findings suggest that most cases of reflux esophagitis in Japan occur in the absence of H. pylori infection and atrophic gastritis, and it may also tend to occur in patients with milder gastritis even in the presence of H. pylori infection. Therefore, H. pylori infection may be an inhibitory factor of reflux esophagitis through inducing atrophic gastritis and concomitant hypoacidity.

Curative treatment of H. pylori infection is useful in preventing ulcer recurrence. Gastric ulcer is more likely to relapse than duodenal ulcer. Recurrent ulcer tended to recur at the site of the original ulcers.