Summary
The inflammatory spectrum of gastric diseases includes different clinico-pathological
entities, the etiology of which was recently established in the international Kyoto
classification. A diagnosis of gastritis combines the information resulting form the
gross examination (endoscopy) and histology (microscopy). It is important to consider
the anatomical/functional heterogeneity of the gastric mucosa when obtaining representative
mucosal biopsy samples.
Gastritis includes self-limiting and non-self-limiting (long-standing) inflammatory
diseases, and the latter are epidemiologically, biologically and clinically linked
to the onset of gastric cancer (i.e. “inflammation-associated cancer”). Different biological models of inflammation-associated
gastric oncogenesis have been proposed. Helicobacter pylori (H. pylori) gastritis is the most prevalent worldwide, and H. pylori is classified as a first-class carcinogen. On these bases, eradicating H. pylori is mandatory for the primary prevention of gastric cancer. Non-self-limiting gastritis
may also be triggered by the immune-mediated destruction of gastric parietal cells,
resulting in autoimmune gastritis. In both H. pylori-related and autoimmune gastritis, the non-self-limiting inflammation results in atrophy
of the gastric mucosa, which is the main factor promoting gastric cancer. Long-term
follow-up studies consistently demonstrate the prognostic impact of the histological
staging of gastritis in gastric cancer secondary prevention strategies.
Keywords
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Article info
Publication history
Published online: March 28, 2021
Accepted:
March 5,
2021
Received:
January 27,
2021
Identification
Copyright
© 2021 Editrice Gastroenterologica Italiana S.r.l. Published by Elsevier Ltd. All rights reserved.
