HELICOBACTER-PYLORI IN PROMOTION OF GASTRIC CARCINOGENESIS

Gastric atrophy and intestinal metaplasia are considered the earliest phenotypic changes in the cascade of events leading from normal mucosa to intestinal-type gastric cancer, and epidemiological evidence links Helicobacter pylori to gastric epithelial malignancies, To evaluate a ny causal relationship between bacterial infection and atrophic metapl astic lesions, gastric pathology was histologically and histochemicall y evaluated in 267 consecutive, nonulcerous, untreated subjects, with attention given to the phenotypes of intestinal metaplasia. The preval ence of Helicobacter pylori infection was 61%. Intestinal metaplasia ( particularly types II and III) was significantly associated with both Helicobacter pylori detection (chi(LR)(2): P < 0.002) and increasing a ge (chi(LR)(2): P < 0.002). Using logistic regression analysis, the de velopment of intestinal metaplasia proved more significantly linked wi th Helicobacter pylori infection [odds ratio = 4.55 (95% confidence in terval: 1.51-13.7)], than with age [odds ratio 1.03 (95% CI: 1.01-1.06 )], with no interaction. In conclusion, Helicobacter pylori can be con sidered among the major causal agents of mucosal lesions involved in t he multistep process of gastric carcinogenesis, justifying any attempt to eradicate this bacterial infection.