Prospects for intervention in gastric carcinogenesis: reversibility of gastric atrophy and intestinal metaplasia

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Abstract
Atrophy in the stomach is conventionally (and simply) defined as “loss of glands”. Such loss may follow ulceration with destruction of the glandular layer or, more frequently, result from a prolonged inflammatory process in which multiple glandular units separately undergo destruction. However, atrophy can also be thought of as “a loss of specialised cells”. Under this broader definition it is possible to include loss of parietal and chief (zymogenic) cells without glandular destruction. Such partial or “pre-atrophy” has been described in human autoimmune gastritis5 and is frequently encountered in animal models of both autoimmune gastritis6 and chronicHelicobacter infection.7 In these latter situations oxyntic cells are replaced within the intact glandular tubules by mucous neck cells (MNC). More interestingly, partial loss of parietal cells and replacement by MNC is a frequent but largely unrecognised finding in the inflamed corpus inH pylori gastritis.8 MNC were originally considered to be a transit cell population intermediate between stem cells and the fully differentiated parietal and chief cells. However, the repertoire of trefoil peptides and growth factors produced by MNC indicate that they are a distinct cell lineage which share the properties of other mucosally protective cell lineages in the gastrointestinal tract.9 Furthermore, it is apparent that proliferation of MNC explains the appearance of new glands formed in the wake of atrophy, so-called “pyloric metaplasia”.