Secondary prevention of epidemic gastric cancer in the model of Helicobacter pylori-associated gastritis

Dig Dis. 2014;32(3):265-74. doi: 10.1159/000357857. Epub 2014 Apr 10.


Irrespective of its etiology, long-standing, non-self-limiting gastric inflammation (mostly in Helicobacter pylori-associated cases) is the cancerization ground on which epidemic (intestinal-type) gastric carcinoma (GC) can develop. The natural history of invasive gastric adenocarcinoma encompasses gastritis, atrophic mucosal changes, and intraepithelial neoplasia (IEN). The topography, the extent and the severity of the atrophic changes significantly correlate with the risk of developing both IEN and GC. In recent years, both noninvasive (serological) tests and invasive (endoscopy/biopsy) procedures have been proposed to stratify patients according to different classes of GC risk. As a consequence, different patient-tailored GC secondary prevention strategies have been put forward. This review summarizes the histological features of H. pylori-related gastritis and the natural history of the disease. Histological and serological strategies to assess GC risk as well as the clinical management of atrophic gastritis patients are also discussed.

Publication types

  • Review

MeSH terms

  • Carcinogenesis / pathology
  • Gastritis / blood
  • Gastritis / complications
  • Gastritis / microbiology*
  • Gastritis / pathology
  • Helicobacter pylori / physiology*
  • Humans
  • Models, Biological*
  • Secondary Prevention*
  • Stomach Neoplasms / blood
  • Stomach Neoplasms / epidemiology*
  • Stomach Neoplasms / pathology
  • Stomach Neoplasms / prevention & control