Atrophy, acid suppression and Helicobacter pylori infection

Abstract

Much of what is currently accepted regarding Helicobacter pylori-associated gastritis and its relationship with gastric adenocarcinoma rests on the assumption that atrophic gastritis can be correctly identified and reproducibly recognized. Several studies have indicated that pathologists have a low level of agreement on this topic, and the terms 'gastric atrophy' and 'atrophic gastritis' remain imprecisely defined and poorly understood. Furthermore, the genesis and progression of the atrophic changes that take place in the gastric mucosa of some individuals infected with H. pylori are incompletely characterized. The lack of a strict definition of atrophic gastritis is at least partially responsible for recent concerns regarding the effects of prolonged pharmacological gastric acid inhibition in patients with H. pylori infection. One recent paper concluded that patients with reflux oesophagitis and H. pylori infection who are treated with longterm acid inhibition have an increased risk of atrophic gastritis. As this term evokes associations with an increased risk of gastric cancer, the possibility was subsequently raised that anti-secretory maintenance therapy might increase the risk of cancer in H. pylori-positive patients. A second report, however, concluded that long-term acid-inhibitory therapy for an average of three years is no different from fundoplication in the development of gastric atrophy. Also, because no intestinal metaplasia developed in any of the patients, and only atrophic gastritis associated with intestinal metaplasia is considered a precursor of gastric cancer, there is no evidence to support the hypothesis that long-term acid inhibition in individuals with H. pylori infection increases the risk of gastric cancer.