Intestinal metaplasia, not atrophy or achlorhydria, creates a hostile environment for Helicobacter pylori.

A 54-year-old man with dyspepsia, Helicobacter pylori-associated chronic active atrophic gastritis without intestinal metaplasia, and hyperplastic gastric polyps was followed up for 1 year after H. pylori eradication with sequential endoscopic gastric mucosal mapping and gastric function tests. Eradication of H. pylori by triple therapy resulted in the histologic resolution of gastritis. However, the patient's condition, gastric function, and morphology of the polyps were not affected. This case illustrates that: a) in the absence of intestinal metaplasia, H. pylori can infect the stomach with gastric atrophy; b) the absence of acid does not preclude H. pylori infection; c) advanced atrophic gastritis may be an irreversible condition; and (d) the neutrophilic infiltrate in hyperplastic polyps is independent of the presence of H. pylori.