Related Experiment Video For Atrophic gastritis
Updated: Aug 8, 2025
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Published on: February 16, 2024
Exploring the spectrum of incidental gastric polyps in autoimmune gastritis
Sara Massironi1, Alessandra Elvevi2, Camilla Gallo2
1Division of Gastroenterology and Center for Autoimmune Liver Diseases, European Reference Network on Hepatological Diseases (ERN RARE-LIVER), San Gerardo Hospital, ASST Monza, Via G.B. Pergolesi 33, Monza e Della Brianza (MB), Monza, Italy; Department of Medicine and Surgery, University of Milano-Bicocca, Monza, Italy.
Background:
Gastric polyps represent an abnormal proliferation of the gastric mucosa. Chronic atrophic autoimmune gastritis (CAAG) targets parietal cells and results in hypo-achlorhydria and hypergastrinemia, which exerts a proliferative effect on the gastric mucosa.
Aims:
We investigate the incidence of gastric polyps in CAAG patients.
Methods:
This is a single-center retrospective study examining patients with confirmed CAAG from January 1990 until June 2022. Demographic, clinical, biochemical, and serological data were collected for each included patient. The histopathological characteristics of the detected polyps were recorded.
Results:
A total of 176 CAAG patients were included. Eighty-nine (50.5%) had 163 incidental polyps. Seventy-six patients (85%) had 130 non-endocrine lesions, among which 118 (90.7%) were inflammatory, 6 (4.6%) adenomatous, and 4 (3%) fundic; 33 patients (37%) had gastric neuroendocrine neoplasms (gNENs), and 21 (23.6%) both; one had MALToma and one gastric adenocarcinoma. Higher circulating levels of gastrin and chromogranin A were observed among patients with polyps (median 668 vs 893 pg/ml p = 0.0237, 146 vs 207 ng/ml p = 0.0027, respectively).
Conclusion:
CAAG implies a high incidence of gNENs and exocrine lesions. Gastrin plays a possible trophic role on the mucosa. Further evidence is needed to validate its predictive role for increased polyp risk in CAAG.
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