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

Citation
D. Basso et al., Antigastric autoantibodies in Helicobacter pylori infection: role in gastric mucosal inflammation, INT J CL L, 30(4), 2000, pp. 173-178
Citations number
28
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
INTERNATIONAL JOURNAL OF CLINICAL & LABORATORY RESEARCH
ISSN journal
09405437 → ACNP
Volume
30
Issue
4
Year of publication
2000
Pages
173 - 178
Database
ISI
SICI code
0940-5437(200012)30:4<173:AAIHPI>2.0.ZU;2-N
Abstract
The aim of the study was to ascertain whether there is an association betwe en the presence of serum parietal cell autoantibodies (PCA) and: (1) Helico bacter pylori infection; (2) the presence and degree of gastritis and intes tinal metaplasia; and (3) the H. pylori infecting strain. Gastric mucosal b iopsies were obtained from 49 consecutive patients in order to assess and g rade 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 h ad the infection. The infecting strain was cagA positive in 21 of 26 group I patients. Positive PCA results were found in 84%, 76%, and 14% of patient s in groups 1, 2, and 3, respectively. PCA results were correlated with ant i-H. pylori antibody titers (P < 0.05). In group 2 patients, PCA were assoc iated with the degree of antral gastritis (Fisher's exact test P < 0.05). c agA status was not associated with the presence of PCA (X-2 = 0.68, NS). Th e 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 per sistent antral chronic gastritis and intestinal metaplasia; (2) the gastric lesions associated with infections sustained by the more-virulent H. pylor i strains do not appear to be due to the induction of antigastric autoantib odies.