Dig Liver Dis. 2021 Mar 27:S1590-8658(21)00100-6. doi: 10.1016/j.dld.2021.03.007. Online ahead of print.
ABSTRACT
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.
PMID:33785282 | DOI:10.1016/j.dld.2021.03.007