Distinct metaplastic and inflammatory phenotypes in autoimmune and adenocarcinoma‐associated chronic atrophic gastritis

Abstract

Background: Autoimmune gastritis (AIG) and adenocarcinoma-associated chronic atrophic gastritis (CAG) are both associated with oxyntic atrophy, but AIG patients demonstrate an increased risk of carcinoid tumors rather than the elevated risk of adenocarcinoma observed with CAG. We therefore sought to compare the characteristics of the metaplastic mucosa in AIG and CAG patients. Methods: We examined markers for metaplasia (spasmolytic polypeptide expressing metaplasia (SPEM) and intestinal metaplasia) as well as proliferation (Ki67) and immune cell populations (neutrophils, macrophages, and eosinophils) in gastric sections from 16 female patients with autoimmune thyroiditis and AIG and 17 patients with CAG associated with gastric adenocarcinoma. Results: Both AIG and CAG patients demonstrated prominent SPEM and intestinal metaplasia. However, AIG patients displayed significantly lower numbers of infiltrating macrophages and significantly reduced mucosal cell proliferation as compared to CAG patients. Conclusions: These findings indicate that, while both AIG and CAG patients display prominent oxyntic atrophy and metaplasia, the AIG patients do not show proliferative metaplastic lineages that would predispose to adenocarcinoma.

Helicobacter Pylori Infection and Gastric Cancer Precursor Lesions: Prevalence and Associated Factors in a Reference Laboratory in Southeastern Brazil

“…It can, many times, inversely appear in the non-atrophic mucosa resulting in focal atrophy or it can even appear in response to different aggressions to the gastric mucosa (40) . Regardless of the order in which these lesions appear, inflammation is seen as the main driver of these pathological changes that can trigger the carcinogenic cascade suggested by Correa (1988) (11)(12)(13)41,42) . In this scenario, several mechanisms through which the inflammation could promote the development of gastric cancer should be considered, including the induction of the cyclooxygenase-2/ prostaglandin E2 (COX-2/PGE2) pathway and the activation of NF-KB and Stat3, as well as the activation of the signalingviaTLR/ MyD88 (43)(44)(45)(46) .…”

“…The majority of gastric cancer cases are intestinal-type adenocarcinoma, located in the antrum and body of the stomach whose development is usually secondary to gastric atrophy and intestinal metaplasia (11)(12)(13) . However, the diagnosis of such pathology is often performed late, when treatment can be less effective.…”

Metaplasia: tissue injury adaptation and a precursor to the dysplasia–cancer sequence

“…Autoimmune gastritis can also cause atrophic gastritis, SPEM and intestinal metaplasia 34,37 . The foci of gastric intestinal metaplasia tend to appear initially at the antrum–corpus junction.…”

Endogenous glucocorticoids prevent gastric metaplasia by suppressing spontaneous inflammation

“…Eosinophils are cytotoxic granulocytes associated with allergic reaction and antiparasitic immune responses within the intestines, and are a common feature of chronic gastric inflammation and SPEM (32,33). Adrenalectomy robustly induced eosinophil infiltration into the stomach ( Figure 1D and Figure 4).…”