Intestinal metaplasia: types, mechanisms of origin, and role in gastric cancer histogenesis

Abstract

Intestinal metaplasia (IM) is by far the most frequent metaplastic change occurring in the gastric mucosa. True pyloric type metaplasia of oxyntic glands and pancreatic metaplasia of the cardia and oxyntic glands is relatively infrequent and focally restricted. So-called ‘pseudopyloric metaplasia’ of oxyntic glands, a prominent component of diffuse corpus-fundus (type A) atrophic gastritis, is better interpreted as mucous-neck cell hyperplasia with lack of acid-peptic differentiation, rather than as true metaplasia¹. Three types of IM are usually considered: (1) type I or complete or small intestine type, composed of columnar crypt/absorptive enterocytes with sparse globet cells, with or without Paneth cells and intestinal type endocrine cells; (2) type II or incomplete sulphomucin-negative type, consisting of goblet cells scattered among gastric foveolar and neck cells; and (3) type III or incomplete sulphomucin-positive type, showing goblet cells scattered among sulphomucin-producing columnar cells. The latter cells show gastric or hybrid gastric/intestinal cell patterns under histochemical and ultrastructural investigation and overlie a relatively immature proliferative component, often sulphomucin-negative but CAR-5 (an intestinal oncofetal antigen) positive, whose expansion apparently leads to dysplasia². Cytokeratin 7-positive glands or microcysts, mainly non-proliferative, are sometimes found at the bottom of type III or mixed complete/incomplete types of metaplasia, often combined with Brunner-type glands.