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Corpus Gastritis (corpus + gastritis)

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Medical Sciences	100%

Selected Abstracts

Negative Association Between Helicobacter pylori Infection and Reflux Esophagitis in Older Patients: Case-Control Study in Japan

HELICOBACTER, Issue 1 2000
Ken Haruma
Background. Recent studies have clarified a close association between H. pylori infection and gastritis, peptic ulcer disease, and gastric cancer, but there is little information concerning the relationship between H. pylori infection and reflux esophagitis (RE). We investigated the relationship between H. pylori, RE, and corpus gastritis. Subjects and Methods. Ninety-five patients with RE and 190 sex- and age-matched asymptomatic healthy controls demonstrating no localized lesions in the upper GI tract were studied and evaluated for H. pylori infection, histologic gastritis, serum gastrin, and pepsinogens (PGs). Results.H. pylori infection was significantly lower in RE patients than in asymptomatic controls (41% vs. 76%, p < .01). Histologic gastritis of both the antrum and corpus was significantly less frequent (antrum; p < .01, corpus; p < .01), and serum levels of PGI and the PG I/II ratio were significantly higher in RE patients than in controls (PGI; p < .05, PG I/II ratio; p < .01). When the subjects were divided into two age groups (59 years of age and younger and 60 years of age and older), a significant difference was found only among patients over 60 years of age (29% vs. 85%, p < .01). Among subjects in this age group, gastritis in both the antrum and corpus were significantly milder in RE patients than in controls. Although the prevalence of H. pylori infection was similar between the two groups of patients under 59 years of age, corpus gastritis was significantly milder in patients than in controls (p < .05). Conclusions. A significantly low prevalence of H. pylori infection was found in RE patients over 60 years of age but not in those under 59 in comparison with sex- and age-matched controls. The relative lack of corpus gastritis might play a role in the pathogenesis of RE in our population through preservation of the acid secretion area. [source]

Vitamin C inhibits corpus gastritis in Helicobacter pylori -infected patients during acid-suppressive therapy

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 11 2001
Masahiro Yoshinaga
Abstract Background: Previous studies have shown that gastric acid suppression worsens corpus gastritis in Helicobacter pylori (H. pylori) -positive patients. We evaluated the effect of acid-suppressive therapy and vitamin C on H. pylori -associated gastritis. Methods: Forty patients with reflux esophagitis were divided into three groups by the status of H. pylori and therapy: group A (n = 15), H. pylori (+) and omeprazole 20 mg; group B (n = 15), H. pylori (+) and omeprazole 20 mg + vitamin C 1200 mg; and group C (n = 10), H. pylori (,) and omeprazole 20 mg. In all three groups, the mucosal interleukin (IL)-8 contents, H. pylori colonization density, neutrophil infiltration in the corpus, and serum gastrin were evaluated at entry and 2 weeks after starting therapy; in group B, serum vitamin C levels were also measured. Results: In group A, the IL-8 contents and the degree of neutrophil infiltration during therapy exceeded those at entry, whereas in groups B and C, these values did not change significantly with treatment. Helicobacter pylori colonization density during therapy was similar to that at entry in all three groups. The serum gastrin (in all groups) and vitamin C levels (in group B) during therapy exceeded those at entry. Conclusions: Potent acid suppression worsens H. pylori -associated corpus gastritis, although such worsening gastritis may be inhibited by vitamin C. [source]

Treatment with a proton pump inhibitor promotes corpus gastritis in patients with Helicobacter pylori -infected antrum-predominant gastritis

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 1 2002
M. Suzuki
Background: Proton pump inhibitors have been reported to modify the level of Helicobacter pylori gastritis. Aim: To quantitatively investigate the effect of a proton pump inhibitor on the mucosal neutrophil reaction. Methods: Forty-six H. pylori -infected patients (17 duodenal ulcer, 29 gastric ulcer) were enrolled. During endoscopic examination, biopsy samples were obtained from the antrum and the corpus. The tissue content of neutrophil myeloperoxidase was measured by enzyme-linked immunoabsorbent assay, and H. pylori infection was histologically assessed. A proton pump inhibitor was administered orally for 8 weeks. Results: In the patients as a whole, antral myeloperoxidase decreased significantly after proton pump inhibitor treatment, but corpus myeloperoxidase remained largely unchanged. In duodenal ulcer patients, myeloperoxidase significantly decreased in the antrum, but increased in the corpus. In gastric ulcer patients, a significant reduction was observed in antral myeloperoxidase, but corpus myeloperoxidase remained unchanged. In the antral myeloperoxidase > corpus myeloperoxidase subgroup (n=24), antral myeloperoxidase significantly decreased, whereas corpus myeloperoxidase increased. No changes were observed at either site in the corpus myeloperoxidase > antral myeloperoxidase subgroup. Histology showed that the antral bacterial load of H. pylori decreased in all subgroups, but that it was mostly unchanged in the corpus. Conclusions: Proton pump inhibitor treatment stimulated the neutrophil reaction in the corpus mucosa of duodenal ulcer patients and of patients in whom antral neutrophil accumulation was more predominant than that of the corpus. This phenomenon may not be caused by increased bacterial density. [source]