Abstract

Background: Atrophic gastritis is one of the long-term sequels of Helicobacter pylori infection, to determine atrophic gastritis caused by H pylori and anti parietal antibodies.
Patients and Methods: 60 atrophic gastritis patients were included. Blood was analyzed for CagA antibodies Immunoglobulin G (IgG) and Parietal cell antibodies using an indirect immunofluorescence technique. C-reactive protein (CRP) was also done for the same patients.
Results: The mean age of 60 patients were 45.67 years ± 15.54 SD. In 37 (61.6%) (p=0.011) patients had Helicobacter Pylori Cag A antibody IgG positive and in 23 (38.3 %) patients had anti parietal cell antibody positive. Odd ratio and relative risk are equal to one. In 39 (65%) patients, atrophic gastritis was seen only in the antrum, 74.3% of them had Helicobacter Pylori Cag A antibody IgG positive, while 25.6 % (P=0.000) had anti parietal cell antibody positive. All atrophic gastritis patients showed positive CRP. Helicobacter Pylori Cag A antibody IgG positive found in 83.3% (p=0.000) with moderate antrum atrophy.
Conclusions: Antiparietal antibody H. pylori infection had a relation with autoimmune gastritis leading to cross reactive gastric T cells activation via molecular mimicry. Atrophic antral gastritis was associated with CagA positive H pylori infection while atrophic corpus gastritis was associated with antiparietal cell antibody.

Key words: Antiparietal antibody, atrophy, autoimmune, gastritis, Helicobacter pylori