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In the population studied, advancing age had no influence on gastric acid secretion in H. pylori-negative subjects. Gastric acid secretion decreases with age in H. pylori-positive subjects because of the increasing prevalence of FAG with age.

Gastric MALT lymphoma shows unique features including regression by Helicobacter pylori eradication and API2-MALT1 fusion. We performed a molecular and clinicopathologic study for 115 cases. All eradication-responsive cases were devoid of API2-MALT1 fusion. All tumors positive for the fusion and all negative for H. pylori infection were nonresponsive to the eradication. Consequently, gastric MALT lymphomas were divided into three groups: Eradication-responsive and fusion-negative (group A, n = 72), eradication-nonresponsive and fusion-negative (group B, n = 22), and eradication-nonresponsive and fusion-positive (group C, n = 21). Group A tumors were characterized by low clinical stage and superficial gastric wall involvement, and group C tumors by low H. pylori infection rate, advanced clinical stage, and nuclear BCL10 expression. All group C tumors showed exclusively low-grade histology. Group B tumors, which have not been well recognized, frequently showed nodal involvement, deep gastric wall involvement, and advanced clinical stage, and sometimes an increased large cell component. A multivariate discriminant analysis revealed that responsiveness to the eradication could be predicted accurately by negative API2-MALT1 fusion, positive H. pylori infection, low clinical stage, and superficial gastric wall invasion, the former being the most important factor for the prediction. This 3-group categorization may be helpful for a comprehensive understanding of gastric MALT lymphoma.

Although the incidence of gastric carcinoma in Japan has declined in the past several decades, there is no information about trends in helicobacter pylori infection. The purpose of the study was to clarify trends in H. pylori infection and in histologic gastritis in young Japanese subjects evaluated between 1975 and 1978 (the 1970s) versus 1991 and 1994 (the 1990s). The prevalence of H. pylori infection and the grade of gastritis in biopsy specimens were evaluated in 173 young Japanese without localized lesions in the upper gastrointestinal tract. Findings in 75 specimens obtained from subjects in the 1970s were compared with those of 98 specimens obtained from subjects in the 1990s. The prevalence of H. pylori infection in the 1970s (54.7%) was significantly higher than that in the 1990s (28.6%) (p < 0.01). The grade of inflammation and the prevalence of both mucosal atrophy and intestinal metaplasia also were significantly higher in the 1970s than in the 1990s (p < 0.01 and p < 0.05). Our data thus show a trend toward a reduced prevalence of H. pylori infection and of histologically apparent gastritis (especially atrophic gastritis). This decrease may be linked to the reported decline of gastric carcinoma in Japan.

Abstract. BACKGROUND: Recently, many study have shown that Helicobacter pylori infection is crucial in development of atrophic gastritis, which is closely associated with gastric cancer. We con ducted a long-term endoscopic prospective follow-up study to investigate the development of gastric cancer in H. pylori-positive and -negative patients. METHODS: 1603 patients who underwent endos -copy and were assessed as to the presence of H. pylori infection by histology, rapid urease test and serologic test between April 1990 and March 1993 were entered. We prospectively studied 1246 sub jects with and 280 subjects without H. pylori infection for a mean follow-up of 7.8 years (range 1-10.6 years). RESULTS: Gastric cancer of both the intestinal and diffuse type developed in 36 (2.9%) infected patients but in none of the uninfected patients during follow-up. There was an increased risk for gastric cancer in infected patients with severe gastric atrophy and corpus predominant gastritis and intestinal metaplasia. Gastric cancer was detected in 21 (4.7%) of the patients with non ulcer dyspepsia, in 10 (3.4%) of those with gastric ulcer and in 5 (2.2%) of those with gastric hyperplastic polyp, at en rollment. No gastric cancer was detected in duodenal ulcer patients. CONCLUSION: These results suggest that the development of both types of gastric cancer is caused by H. pylori-associated gastritis, and the risk for development of gastric cancer in H. pylori-negative subjects is extremely low. Subjects having H. pylori-positive gastric mucosa with severe atrophy and/or corpus gastritis may be at partic ularly high risk for gastric cancer.

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.

These results suggest that early rectal carcinomas should be resected surgically if they 1) show massive submucosal invasion, 2) are classified as moderately differentiated adenocarcinomas, and 3) are larger than 10 mm in diameter. In patients with both scanty submucosal invasion and features of well-differentiated adenocarcinoma or intramucosal carcinoma and if no other risk factors for LN metastasis are present, such as lymphatic invasion by the primary lesion, surveillance may suffice after endoscopic resection.