Search

Follicular gastritis is an important histological entity, because it may progress to overt gastric MALT lymphoma. However, there is no universal agreement on whether there is any correlation of follicular gastritis with histological features of the antral mucosa or on the prevalence of follicular gastritis. To shed further light on these issues, we studied antral biopsies obtained from 735 adult patients, who had participated in six consecutive clinical trials. They included 348 patients with duodenal ulcer, 82 with gastric ulcer, and 305 with nonulcer dyspepsia. The Sydney classification system of gastritis was used, using a score of 0-3 to grade degree and activity of inflammation, gland atrophy, intestinal metaplasia, and H. pylori colonization density. Follicular gastritis was defined as prominent lymphoid follicles with no lymphoepithelial lesion. None of the H. pylori-negative patients (N = 159) had follicular gastritis. Among H. pylori-positive patients, 80/340 (23.5%) with duodenal ulcer, 5/77 (6.5%) with gastric ulcer, and 20/159 (12.6%) with nonulcer dyspepsia had follicular gastritis (P < 0.001). Multivariate discriminant analysis selected the following four significant predictor variables for follicular gastritis (Wilks lambda = 0.91, chi2 = 70.6, df = 4, P < 0.001): gastritis sum score, atrophic gastritis, age of the patient, and disease. The prevalence of follicular gastritis was linearly correlated (gamma = 24.55 - 0.98chi, r = -0.62, F1,11 = 6.12, P = 0.03) with the age groups of the 576 H. pylori-positive patients studied. In conclusion, follicular gastritis is highly correlated with H. pylori-caused severe, active gastritis. It is mostly prevalent in the young H. pylori-infected patients with duodenal ulcer.

Despite the fact that the association of Helicobacter pylori with an increased risk of gastric cancer is well documented, the exact mechanisms of this association have not been elucidated. Our aim was to shed some light on these mechanisms by studying the relationship of H. pylori CagA status to gastric cell proliferation and apoptosis, since both play an important role in gastrointestinal epithelial cell turnover and carcinogenesis. We studied fifty patients [32 men, 18 women, median age 39.5 years (range 18-67)], referred for upper gastrointestinal endoscopy, from whom antral biopsies were taken. On biopsy specimens gastritis was estimated by scoring the severity of inflammatory infiltrate, and the presence of atrophy and intestinal metaplasia were also noted. The gastric cell proliferation index (PI) was estimated by AgNOR staining, the epithelial apoptotic index (AI) was measured by special staining for apoptosis, and CagA status was determined serologically by immunoblotting the sera of patients against H. pylori antigens. Thirty-eight (76%) of the 50 patients were H. pylori (positive) and 12 (24%) H. pylori (negative). Among the 38 H. pylori(+) patients, 28 (73.6%) were CagA(+) and 10 (24.6%) CagA(-). In the H. pylori CagA(+) and CagA(-) groups, the PI values [median (ranges)] were 5 (4-7) and 3.7 (3.5-5.5), respectively (P < 0.05). In addition the difference in PI between the H. pylori CagA(+) and H. pylori(-) groups was highly significant (P < 0.001). Concerning apoptosis, in the H. pylori CagA(+) and CagA(-) groups, the values for AI were 1 (1-30) and 5.5 (1-35), respectively (P < 0.05). In addition, the difference in AI between the H. pylori CagA(-) and H. pylori(-) groups, was significant (P < 0.05). We conclude that H. pylori CagA(+) strains induce increased gastric cell proliferation, which is not accompanied by a parallel increase in apoptosis. This might explain the increased risk for gastric carcinoma that is associated with infection by H. pylori CagA(+) strains.

H. pylori has recently been recognized as a novel risk factor of gastric cancer, but its precise role in gastric carcinogenesis is as yet unknown. The aim of the present study was to assess the relationship between H. pylori infection and vitamin C levels in gastric juice and also to examine whether eradication of H. pylori could have any impact on these levels. Gastric juice and plasma vitamin C levels were measured in 88 dyspeptic patients who had an upper gastrointestinal endoscopy. In the subgroup of H. pylori-positive patients, eradication was attempted with triple therapy. This subgroup was studied on two occasions, ie, before and after treatment. There were 58 H. pylori-positive and 30 -negative patients. Gastric juice vitamin C levels in H. pylori-positive patients were statistically lower (P < 0.001) than the levels in the H. pylori-negative patients. Triple therapy achieved eradication in 45 patients (77.6%) of the 58 H. pylori-positive patients. Before H. pylori was eradicated in these 45 patients gastric juice vitamin C levels were significantly (P < 0.001) lower than those after eradication, the latter being no different than the group of 30 H. pylori-negative patients. There was a significant (P < 0.001) improvement of gastritis after eradication, which paralleled the elevation of gastric juice vitamin C levels. No difference was noted in plasma vitamin C levels between H. pylori-negative and -positive patients or in the latter before and after H. pylori treatment.(ABSTRACT TRUNCATED AT 250 WORDS)