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Antigastric autoantibodies in Helicobacter pylori infection: role in gastric mucosal inflammation.

作者信息

Basso D, Gallo N, Zambon C F, Baron M, Navaglia F, Stockreiter E, Di Mario F, Rugge M, Plebani M

机构信息

Department of Laboratory Medicine, University Hospital of Padua, Italy.

出版信息

Int J Clin Lab Res. 2000;30(4):173-8. doi: 10.1007/s005990070003.

DOI:10.1007/s005990070003
PMID:11289707
Abstract

UNLABELLED

The aim of the study was to ascertain whether there is an association between the presence of serum parietal cell autoantibodies (PCA) and: (1) Helicobacter pylori infection; (2) the presence and degree of gastritis and intestinal metaplasia; and (3) the H. pylori infecting strain. Gastric mucosal biopsies were obtained from 49 consecutive patients in order to assess and grade gastritis, make a histological diagnosis, and culture and genotype H. pylori. H. pylori infection was present in 26 patients (group 1), had been present in 17 patients (group 2), and the remaining 6 (group 3) had never had the infection. The infecting strain was cagA positive in 21 of 26 group 1 patients. Positive PCA results were found in 84%, 76%, and 14% of patients in groups 1, 2, and 3, respectively. PCA results were correlated with anti-H. pylori antibody titers (P<0.05). In group 2 patients, PCA were associated with the degree of antral gastritis (Fisher's exact test P<0.05). cagA status was not associated with the presence of PCA (chi2=0.68, NS). The frequency of positive findings for PCA in group 2 was higher in patients with (90%) than in those without (50%) intestinal metaplasia.

IN CONCLUSION

(1) H. pylori infection is associated with the production of PCA, which, after eradication of the infection, persist and might contribute to the persistent antral chronic gastritis and intestinal metaplasia; (2) the gastric lesions associated with infections sustained by the more-virulent H. pylori strains do not appear to be due to the induction of antigastric autoantibodies.

摘要

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