[The physiopathological aspects of chronic gastritis, Helicobacter pylori and precancerous gastric changes].

Chronic gastritis represents the paradigmatic histological condition by means of which the various clinical displays develop. Among the several etiologic factors, Helicobacter pylori (Hp) certainly represents a determining element for the promotion of such condition. Several morpho-functional evaluations (parietal cells, peptic cells, acid secretion, peptic secretion, gastrinemia) point out how Hp has on the mucosa a mainly direct action, without any substantial modifications of the gastric milieu. Certainly, the bacteria help the bodyfundic atrophic gastritis, but seldom this condition contributes to the modification of the gastric pH in such a relevant way so as to prime the fall of events which lead to the preneoplastic/neoplastic modifications. Metaplastic, dysplastic and neoplastic clones may arise, in the course of Hp infection, even in conditions of normochloridria. Such bacterium behaves as a cofactor of various other damaging or predisposing agents, contributing to modulate the risk by acting on host genetic susceptibility.