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Previous studies have noted that atrophic gastritis is the pathological finding most correlated with the development of gastric adenocarcinoma.1 Worldwide, the most common cause of atrophic gastritis is chronic infection with Helicobacter pylori. This general loss of acid-secreting parietal cells is associated with the development in the corpus of metaplastic lineages including pyloric metaplasia (also known as spasmolytic polypeptide-expressing metaplasia (SPEM) or pseudopyloric metaplasia) and intestinal metaplasia as direct sequelae of atrophy. The intestinal metaplasia lineages can develop in both the corpus and the antrum. In contrast with H. pylori infection, direct destruction of parietal cells through the production of anti-parietal cell antibodies (most prominently antibodies against the H/K-ATPase) in patients with autoimmune gastritis induces profound atrophy in the corpus, sparing the antrum. While it has been known that autoimmune gastritis is associated with a higher incidence of enterochromaffin-like (ECL) cell carcinoids in the stomach,2 the risk of adenocarcinoma has been controversial.3–5 Many studies have failed to discriminate between cancer arising from H. pylori infection and that emanating from the primary results of autoimmune gastritis. This has led to confusion in how these patients should be followed up with endoscopy, especially in younger patients.
In Gut, Massimo Rugge and colleagues present the results of an important study which clarifies the …
Contributors JG is the sole author on this commentary.
Funding JG is supported by grants from a Department of Veterans Affairs Merit Review Award (IBX000930, NIH RO1 DK101332 and DOD CA160479).
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.