ENHANCED CELLULAR PROLIFERATION AND P53 ACCUMULATION IN GASTRIC-MUCOSA CHRONICALLY INFECTED WITH HELICOBACTER-PYLORI

This study evaluated whether the increased risk of development of gast ric carcinoma due to chronic Helicobacter pylori infection could be li nked with elevated cell proliferative activity and expression of p53 a nd bcl-2. Forty-eight patients undergoing therapy for H pylori-positiv e gastroduodenal ulcers were separated into not eradicated (NE; n = 23 ) and eradicated (E; n = 25) groups 6 months after the treatment. Seru m pepsinogen (PG) I:II ratios and histologic changes in the gastric co rpus and the antrum, assessed according to the modified Sydney System, as well as epithelial cell proliferation (mitosis, Ki67, and prolifer ating cell nuclear antigen [PCNA]), and expression of oncoproteins (p5 3 and bcl-2) were examined before and at 3 months and 6 months after t reatment for H pylori. Chronic persistent H pylori infection was assoc iated with a low PG I:II ratio, increased inflammation and activity sc ore, and elevated cell proliferation, as evidenced by the Ki67 and PCN A labeling indexes and the mitotic index in the NE group. Scattered ac cumulation of p53 protein continued to be observed in the NE group aft er treatment but was significantly decreased in the E group. We conclu de that persistent H pylori infection causes gastritis, with epithelia l degeneration and regeneration that result in accentuation of epithel ial cell proliferation and accumulation of p53 protein, presumably hei ghtening the genetic instability consistent with the development of ca rcinoma.