Development of diffuse carcinomas in the gastric corpus in patients with rugal hyperplastic gastritis

Abstract

Watanabe et al.1 have recently described development of gastric cancers of Laurens diffuse type in patients with rugal hyperplastic (enlarged fold) gastritis, all located in the gastric corpus. We have read their publication with interest. It is proposed that Helicobacter pylori (HP) infection by itself, also in patients without chronic atrophic gastritis, may play a pivotal role in development of gastric cancer. However, gastric atrophy was evaluated only by measuring serum concentrations of pepsinogen I (PGI) and II. The patients were followed by regular endoscopies and it seems peculiar to rely on serology instead of evaluating gastric mucosal changes, including the parietal cell population, in gastric biopsies collected during endoscopic surveillance.HP-positive patients with enlarged fold gastritis have reduced basal and maximal acid output and a large proportion of parietal cells have altered ultrastructure, both parameters normalized after HP eradication.2 These patients also had significant hypergastrinemia (mean 213 pg/ml), which fell (mean 70 pg/ml) after HP eradication.2 Gastrin is the main trophic stimulus of the acid producing mucosa and the effect is mediated through the gastrin receptor on enterochromaffin-like (ECL) cells.3 There is experimental evidence that carcinogenesis caused by HP is mediated by gastrin as it can be prevented by a gastrin receptor antagonist. 4 Furthermore, gastric carcinomas of the diffuse type in patients with atrophic gastritis have neuroendocrine differentiation and have been suggested to develop from ECL cells. 5Altogether, there is a large number of studies suggesting that gastrin may be pivotal for gastric mucosal hyperplasia and carcinogenesis and serum gastrin should have been measured in the study by Watanabe et al.1 The serum concentrations of PGs do not necessarily reflect gastric acidity or degree of atrophy and particularly some persons with reduced gastric acid secretion and, thus, presumed hypergastrinemia may have serum PGI in the normal range.