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

S Jeong, E Choi, CP Petersen… - United European …, 2017 - journals.sagepub.com
S Jeong, E Choi, CP Petersen, JT Roland, A Federico, R Ippolito, FP D'Armiento, G Nardone
United European Gastroenterology Journal, 2017journals.sagepub.com
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 …
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.
Sage Journals