Histopathological, immunohistochemical, and serological prospective study of H. pylori induced chronic gastritis

H.pylori infection is the major cause of non-autoimmune chronic gastritis. Furthermore, recent studies suggest that H.pylori could have a crucial role in the induction and/or maintenance of autoimmunity at the gastric level. Assess the role of H.pylori in the development of the histopathological features, antral G-cells changes, and induction of gastric autoimmune reaction in chronic gastritis. From each one of eighty dyspeptic patients, multiple endoscopical gastric biopsies from antral and body mucosa, and blood sample were collected. The gastric antral and body mucosa biopsies were processed separately and stained by routine [H and E stain], Giemsa stain, and modified triple Genta stains for histopathological examination according to the updated Sydney System. Further sections from antral biopsies were stained by polyclonal antigastrin antibody immunohistochemical stain for immunohistochemical examination. The blood examined serologically by indirect IF- and ELISA- tests to assess the PCA and anti-H.pylori [IgG] respectively. In antral and body mucosa, the density of H.pylori colonization had significant positive correlation with the grade of both chronic inflammation and PMN activity [P<0.05], but it had no significant correlation with the grade of glandular atrophy [P>0.05]. The mean number of antral G-cells in H.pylori positive instances had no significant difference with H.pylori negative ones [P.0.05]. The rate of anti-H.pylori [IgG] in patients with positive PCA statistically was significantly higher than those in patients with negative PCA [P<0.05]. H.pylori is the commonest cause of chronic gastritis. It plays an important role in the development of its histopathological features. It had no effect on the number of antral G-cells. It plays an important role in the development of gastric autoimmune reaction during its chronic infection that leads eventually to autoimmune chronic gastritis