ABSTRACT
Helicobacter pylori [H .pylori] has been considered as a most important risk factor for gastric cancer by inducing chronic inflammation. CagA positive H.pylori strain is associated with higher levels of gastric inflammation, however there is no universal agreement on the link between H. pylori harboring CagA and the reportedly risk of precancerous lesions. To ascertain whether CagA positive H. pylori infection correlates with higher gastric epithelial cells oxidative DNA damage and precancerous changes. Sixty two dyspeptic patients attending for diagnostic GIT endoscopy were enrolled in this study .10 patients had normal endoscopic findings [group I], 10 cases had non ulcerative gastritis with H. pylori negative [group II], while 25 patients presented with non ulcerative gastritis were positive for H. pylori [group III], and 17 cases had ulcerative gastritis with H. pylori positive [group IV]. All involved individuals were subjected to clinical examination, abdominal ultrasonographic examination, histopathological examination of gastric mucosa and culturing of mucosal biopsies for H. pylori detection. Seroprevalence of H. pylori strains bearing the cytotoxin associated gene A [CagA] in the serum were assessed by ELISA. DNA damage in gastric epithelial cells was investigated by comet assay. H. pylori CagA was detected in 10 cases of group III and 13 cases of group IV. Gastric epithelial cells DNA damage was significantly increased in H. pylori positive groups [III, IV than H. pylori negative group II] [P< 0.001] with the highest values in group IV [P<0.001], also in CagA positive cases either in group III [P< 0.001] and group IV [P<0.001] compared to CagA negative cases with a significant correlation with more severe grade of gastric atrophy [P< 0.001] and intestinal metaplasia [P< 0.001] as precancerous lesions. CagA H. pylori strains sero-positivity was related to more advanced gastric pathology and precancerous changes with increased oxidative DNA damage in the epithelial cells which could represent as cancer prone biological context