Helicobacter pylori, inflammation, mucosal damage, and apoptosis: pathogenesis and definition of gastric atrophy.
Much of what is currently accepted on the natural history of Helicobacter pylori-induced gastritis and its relationship with gastric adenocarcinoma rests on the assumption that atrophic gastritis can be correctly identified and reproducibly recognized. Recently, 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, therefore, poorly understood. Furthermore, the genesis and progression of the atrophic changes taking place in the gastric mucosa of some, but not all, subjects infected with H. pylori are incompletely characterized. This review has three aims: (1) to briefly reexamine our current knowledge of the mechanisms involved in the injury and repair of gastric glands; (2) to present a hypothesis on the development of gastric atrophy; and (3) to propose a new, stringent definition of gastric atrophy that may be usefully applied in the clinical research arena.
Genta
R M
RM
Veterans Affairs Medical Center, Houston, Texas, USA. rmgenta@bcm.tmc.edu
D017209:Apoptosis / Q000502:physiology*; D001284:Atrophy; D005753:Gastric Mucosa / Q000473:pathology*; D005756:Gastritis / Q000382:microbiology*; D016481:Helicobacter Infections / Q000382:microbiology / Q000473:pathology*; D016480:Helicobacter pylori / Q000502:physiology*; D006801:Humans; D013270:Stomach / Q000473:pathology*; D009626:Terminology as Topic