CHRONIC GASTRITIS INTESTINAL METAPLASIA DYSPLASIA AND HELICOBACTER-PYLORI IN GASTRIC-CANCER - PUTTING THE PIECES TOGETHER

Chronic gastritis may favour the development of gastric cancer more as a condition than as precancerous lesion. Since, in most cases, it is pathologically correlated with Helicobacter pylori infection, it is re asonable to postulate at least an indirect role for this organism in t he pathogenesis of gastric cancer. H. pylori, however, is only one of the risk factors involved, in that additional factors (excess salt, ci garette smoking, deficiency of foodstuffs with an antioxidizing effect ) may facilitate the malignant transformation of chronic atrophic gast ritis into intestinal-type gastric cancer. Gastric carcinogenesis ther efore presents itself as a multifactorial, multistage process, further ed by the occurrence of precancerous lesions which are usually interre lated (type-III intestinal metaplasia, severe dysplasia) and by functi onal alterations such as achlorhydria, which, though it is not enough in itself to cause gastric cancer, promotes abnormal intragastric bact erial development, a condition which may be followed by abnormal intra gastric formation of cancerogenous nitroso compounds. The existence of a close correlation between both gastric cancer and H. pylori infecti on and low socio-economic and hygienic status of the population lends further strength to the hypothesis that an ''H. pylori factor'' is inv olved in gastric carcinogenesis. Consequently, to reduce the risk of g astric cancer, various strategies have been devised to prevent H. pylo ri infection (improvement in socio-environmental conditions, anti-a. p ylori vaccine) and/or to eradicate the organism (by means of therapeut ic regimens including antimicrobial agents, which, however, can be imp lemented only in patients who have not developed diffuse atrophy and/o r dysplasia, in whom H. pylori may no longer be detectable). Definitiv e proof of the real extent of the relationship between H. pylori and g astric cancer and of the efficacy of therapeutic and preventive measur es can be provided only by controlled trials in populations with a hig h prevalence of chronic non-atrophic gastritis which are difficult to organize.