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We performed this study to determine which biopsy sites in the stomach are suitable for the diagnosis of Helicobacter pylori infection and the assessment of the extent of atrophic gastritis.Endoscopy was performed in 76 H. pylori-positive patients with histologically confirmed chronic gastritis. Biopsies were taken from the following six sites: the lesser curvatures of the mid-antrum (site 1), the angulus (site 2), the middle body (site 3), and the greater curvatures of the mid-antrum (site 4), the angulus (site 5), and the middle body (site 6) of the stomach. The extent of atrophic gastritis was assessed endoscopically as well as histologically, and patients were classified into five groups according to its extent. H. pylori status was assessed histologically. The histological severity of inflammation, activity, atrophy, and intestinal metaplasia was assessed according to the Updated Sydney System. The grades of these items were compared among the six biopsy sites in each group of patients.Site 6 was most reliable for the diagnosis of H. pylori infection, and site 4 was suitable for examining the status of H. pylori colonization in the antrum. Site 1, site 3, and site 6 were suitable for the assessment of the extent of atrophic gastritis.Our results indicate that for an accurate diagnosis and assessment, biopsies should be taken from the following four sites: the lesser curvatures of the mid-antrum (site 1) and middle body (site 3), and the greater curvatures of the mid-antrum (site 4) and middle body (site 6) of the stomach.

Fifty-eight Helicobacter pylori-positive ulcer patients received omeprazole 20 mg (n = 15), or lansoprazole 30 mg (n = 23), lansoprazole 60 mg (n = 13), or E3810 20 mg (n = 7) q.d. Another 63 H. pylori-positive ulcer patients received lansoprazole and clarithromycin for 2 weeks. Patients received lansoprazole 30 mg and clarithromycin 400 mg (group 1, n = 22), lansoprazole 30 mg and clarithromycin 800 mg (group 2, n = 12), or lansoprazole 60 mg and clarithromycin 800 mg (group 3, n = 29). Neither proton pump inhibitor (PPI) was capable of eradication by monotherapy, but the clearance rates in the lansoprazole group were 60.9 and 69.2%, which were higher than those for omeprazole (p < 0.05). In the dual therapy, eradication rates were 50, 50, and 72.4% in groups 1,2, and 3, respectively. Minor side effects were observed in one case each in groups 1 and 3. Lansoprazole monotherapy proved more efficacious than omeprazole monotherapy, but it was unable to eradicate H. pylori. Dual therapy with lansoprazole 60 mg and clarithromycin 800 mg was an efficacious and safe regimen for H. pylori eradication in this study.

An ultrastructural and immunohistochemical study was done to investigate the normal developmental process of rat gastric wall. Neuronal processes were observed on the external side of immature muscle cells on gestational day 15, and Auerbach's plexus was found on gestational day 18, after which neuronal elements extended just under the subepithelial area. Myofilaments appeared in undifferentiated mesenchyme cells on gestational day 15. On day 17, stomach was responsive to Ach stimulation. On the day after the initiation of gastric motility, gastric glands started to form on the mucosal surface. At the same developmental stage, some parts of the mucosal epithelium and the submucosal connective tissues were stained with antiserum against tenascin. Endocrine and parietal cells appeared in the mucosal epithelium on gestational day 19. Dense secretory granules on the apical surface of mucosal epithelium were increased between day 20 and 21. The cytoplasmic organelles gradually developed with advancing fetal age. We suggest that tenascin may play a role in gastric gland formation and that there are some relationships between gastric gland formation and gastric motility. We believe that the development of subepithelial tissues may be closely associated with epithelial growth.

A mechanism of cytoprotection by 16,16-dimethylprostaglandin E2 (16,16-dimethyl-PGE2) was investigated in rats with respect to possible roles of the gastric juice and the mucus gel layer. 16,16-Dimethyl-PGE2 significantly increased the volume of gastric juice and mucus thickness. In a gastric juice-emptied stomach, 16,16-dimethyl-PGE2 protected the gastric mucosa against 30% ethanol, but not against 40% ethanol. Moreover, this agent did not show any cytoprotective action even against 30% ethanol when both gastric juice and mucus gel were removed. In this situation there was no histological change in the depth of injury, whether 16,16-dimethyl-PGE2 was given as pretreatment or not. These results suggest that there are two mechanisms that may play major roles in the cytoprotection of the gastric mucosa by 16,16-dimethyl-PGE2: (a) dilution of necrotizing agents by increased gastric juice and (b) thickening of the mucus gel layer.