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Background: The occurrence of lymphoid follicles in the gastric mucosa was recently considered to be acquired in respose to infection by Helicobacter pylori., Methods: In order to investigate whether there is any correlation between follicular hyperplasia and Helicobacter pylori colonization, a morphological study was performed in antral biopsy specimens from 267 patients with H. pylori-associated gastritis, and from 312 subjects with histological evidence of chronic gastritis, but without H. pylori colonization., Results: Follicular hyperplasia was observed in 33 (12.3%) specimens with H. pylori-associated gastritis, and in 56 (9%) samples from non-infected group (p=ns). In both H. pylori-positive and H. pylori-negative specimens lymphoid follicular hyperplasia showed a significant correlation with the degree of the gastritis. In these two groups the prevalence of follicular hyperplasia was also significantly higher in the elderly., Conclusions: On the basis of these results, we were unable to find any significant correlation between H. pylori infection and occurrence of lymphoid follicular hyperplasia. The appearance of organized follicular structures in the gastric mucosa seems to be acquired in response to multiple events, and not exclusively in consequence of the colonization by Helicobacter pylori.

To investigate the relationship between lymphocytic gastritis and H. pylori infection, antral biopsy specimens from 162 patients with histological evidence of H. pylori infection, and from 177 subjects without colonization were retrospectively examined. Among patients with antral colonization, lymphocytic gastritis was identified in 8 cases (4.9%). Lymphocytic gastritis was not detected in specimens without H. pylori infection. Quantitation of the epithelial lymphocytic infiltration was carried out in all specimens and showed that cases with lymphocytic gastritis had a mean of 35.3 lymphocytes per 100 epithelial cells, compared with a mean of 2.6 and 2.4 respectively in chronic gastritis and normal mucosa. Among the 331 patients without lymphocytic gastritis, specimens colonized by H. pylori had a mean of epithelial lymphocyte counts significantly higher than those observed in both chronic gastritis and normal mucosa. These findings show a positive correlation between antral colonization by H. pylori and occurrence of lymphocytic gastritis, and suggest that the bacteria may have an important role in the induction of such particular form of antral inflammation.

To investigate on the presence and significance of Helicobacter pylori (Hp) in Barrett's mucosa, esophageal biopsy specimens from 34 patients with columnar-lined epithelium were retrospectively examined. The incidence of colonization was compared with that observed in a control group of 76 subjects with normal esophageal mucosa or moderate esophagitis. Three of the 34 Barrett's specimens were Hp-positive and only 1 of these showed evidence of inflamed mucosa (p = NS). We do not find in this study any evidence to support the existence of association between Hp and Barrett's esophagus or esophageal inflammation. The presence of Hp in antral mucosa of all positive cases suggest the possibility that esophageal colonisation might merely be a consequence of reflux from the gastric antrum.

To investigate whether antral colonization by Helicobacter pylori (Hp) modifies gastrin-cell population, the number of G-cells was evaluated in antral biopsy specimens from 22 apparently healthy subjects and from 48 duodenal ulcer patients using a morphometric method. The level of serum immunoreactive gastrin in a sample of fasting serum obtained at the time of biopsy was also measured. In healthy subjects the G-cell count (evaluated according to G/I index) and the serum gastrin levels were not significantly different than those found in duodenal ulcer patients. When the antral colonization by Hp was assessed, we found that, both controls and duodenal ulcer Hp-positive patients had a mean G-cell count and fasting serum gastrin levels not significantly higher than in patients without Hp.

To investigate the possible relation between Helicobacter pylori (HP) colonization and incidence of intestinal metaplasia (IM), antral biopsy specimens from a total of 263 subjects (167 had chronic gastritis, 12 gastric cancer, and 84 no histological changes) were examined. IM was observed in 27.7% of the HP positive specimens and in 18.3% of the HP negative biopsies (p = NS). Histochemical characterization of mucins showed that the percentage of HP colonization was not significantly different within various subtypes of IM. We do not find in this study any evidence to support the existence of a pathogenetic role of HP on the morphogenesis of IM in antral mucosa.

Specimens from twelve patients with Barrett's esophagus and four additional cases of esophageal carcinoma who had Barrett's epithelium were histologically and by mucin histochemistry examined. Specialized epithelium was observed in 10/12 non cancerous patients. In 9 of these either gastric-fundic or junctional epithelium were seen. All patients with carcinoma had evidence of specialized epithelium. Sulphated mucins were preponderant in biopsies from 7 of the 9 patients with dysplasia either alone or associated with carcinoma. In all 5 specimens with specialized epithelium but without dysplasia or carcinoma, sialomucins were predominant.

Biopsy specimens from the gastric antral mucosa of 194 patients with upper gastrointestinal symptoms were studied with the Warthin-Starry silver stain to demonstrate the presence of Campylobacter Pylori (CP). Of these patients, 44 had peptic ulcer visible on endoscopic investigation. Spiral bacteria were detected in 70 out of 75 specimens with histologically active gastritis (93%), in 34 of 54 specimens with inactive form of gastritis (63%) and in 26 of 65 specimens without morphological changes (40%). Of 44 patients found to have gastric or duodenal ulcers, 33 also had bacteria. No significant differences between patients with endoscopically visible peptic ulcer and those without ulcer were seen. Our results indicate a close relationship between the active form of chronic gastritis and Campylobacter; however they do not show a definite association with peptic ulcer.