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Title: Is there a relationship between Helicobacter pylori and gastric autoimmunity? Author: Erdoğan A, Yilmaz U. Journal: Turk J Gastroenterol; 2011; 22(2):134-8. PubMed ID: 21796548. Abstract: BACKGROUND/AIMS: Helicobacter pylori-associated corpus atrophy and autoimmune gastric atrophy share similar histopathologic and clinical aspects. In our study, the relation between Helicobacter pylori and autoimmune gastritis was investigated. METHODS: Eighty-two consecutive histologically and serologically Helicobacter pylori-positive and 96 Helicobacter pylori-negative patients were enrolled in the study. All patients underwent diagnostic upper esophagogastroduodenal endoscopy. Three biopsy specimens from the antrum and corpus greater curvature were obtained for histologic evaluation. Serum samples were collected for detection of anti-parietal cell antibody, anti-Helicobacter pylori IgG and vitamin B12. Statistical analyses were determined with Student t-test and chi-square test. Statistical significance was determined with a p-value <0.05. RESULTS: Of 82 Helicobacter pylori-positive patients, 45 were female and 36 were male, with a mean age 45.1 ± 15.1. There was no significant difference in age, gender and corpus atrophy between the Helicobacter pylori-positive and -negative groups. Eleven Helicobacter pylori-positive patients (13.4%) and 14 (14.6%) Helicobacter pylori-negative patients were positive for anti-parietal cell antibody; the difference between the two groups was not statistically significant (p>0.05). Differences in esophagogastroduodenal endoscopy findings, antrum and corpus inflammation, antrum and corpus atrophy, and vitamin B12 levels were found to be insignificant between parietal cell antibody-positive and -negative groups (p>0.05). CONCLUSIONS: We did not find any relation between Helicobacter pylori infection and anti-parietal cell antibody, a marker of autoimmune gastritis. Long-term follow-up of Helicobacter pylori-infected patients and also determination of the relation between eradication of Helicobacter pylori and autoimmune atrophic gastritis are needed.[Abstract] [Full Text] [Related] [New Search]