Background: The purpose of the present study was to examine the association between interleukin‐8 (IL‐8) in the gastric body due to Helicobacter pylori infection and histological gastritis, as well as elucidating the effect of acid secretion inhibitors on H. pylori associated body gastritis in duodenal ulcer patients. Methods: Twenty H. pylori‐negative patients, 20 H. pylori‐positive patients with chronic gastritis without peptic ulceration, and 20 H. pylori‐positive duodenal ulcer patients (DU) were studied. Four biopsy samples were taken, each from the greater curvature of the antrum and body of the stomach. Biopsies were histologically investigated by ELISA to determine the density of H. pylori, the degree of neutrophil infiltration and the IL‐8 concentration in the mucosa. Results: In the gastric mucosa of H. pylori‐negative subjects, no IL‐8 and hardly any neutrophil infiltration were observed. In contrast, enhanced IL‐8 production and increased neutrophil infiltration were present in those infected with H. pylori. In H. pylori‐positive patients, a significant correlation was observed between the IL‐8 concentration and the degree of neutrophil infiltration, but no correlation was found in the body mucosa of those with DU. Twelve of 20 DU patients demonstrated hardly any neutrophil infiltration, despite the increased mucosal IL‐8 content in the body. The administration of omeprazole in DU patients markedly increased mucosal neutrophil infiltration even though it did not cause any significant change in the H. pylori density and IL‐8 concentration in the body. Although the effect of omeprazole was transient, a significant increase in neutrophil infiltration continued in comparison with the status before omeprazole administration in those subsequently undergoing maintenance treatment with H2‐blockers. Conclusion: In H. pylori‐positive chronic gastritis, IL‐8 concentration is enhanced in the mucosa of the body, and is associated with increased neutrophil infiltration. However, in DU patients, despite increases in body IL‐8 concentration, neutrophil infiltration is reduced and the gastritis may be localized in the antrum.

There is now strong evidence that Helicobacter pylori infection plays an important role in the pathogenesis of peptic ulcer disease, and many studies have shown that eradicating H. pylori can markedly decrease ulcer relapse. 1±3 A number of studies have reported that the eradication rate achieved using omeprazole in combination with two antimicrobial agents was more than 90%. 4±6 However, such treatment fails in 5±10% of patients.Recent studies have indicated that factors such as the patient's compliance with treatment, as well as age, gender, smoking habits, proton-pump inhibitor pretreatment, and clinical diagnosis have an in¯uence on the ef®cacy of H. pylori eradication therapy. 7±16 Additionally, our previous study demonstrated that eradication of H. pylori by treatment with omeprazole, amoxycillin, and clarithromycin (OAC) was less effective in smokers than in non-smokers. 17 Smoking decreases gastric blood¯ow and mucus secretion, and thus may reduce the ef®cacy of treatment by decreasing the delivery of antibiotics to the gastric mucosa. 18±21 SUMMARYBackground: Our previous study demonstrated that Helicobacter pylori eradication was less effective in smokers than in non-smokers. Cetraxate is an antiulcer drug that increases gastric mucosal blood¯ow. Aim: To evaluate the effect of cetraxate combined with new triple therapy for the eradication of H. pylori in smokers. Methods: This study had a single-centre, double-blind, randomized non-placebo design. A total of 106 consecutive H. pylori-positive smoking patients were randomly allocated to one of two regimens: one group received omeprazole (20 mg), amoxycillin (1500 mg), and clar-