Atrophic gastritis of distinct etiologies: malignant potential in Helicobacter pylori-associated and autoimmune forms

Atrophic gastritis is an important step in the Correa cascading pathway. It forms a pivotal period between chronic inflammation and a biologically-disrupted mucosal epithelial phenotype leading to gastric neoplasia. From a more than superficial perspective, both Helicobacter pylori (H. pylori)-associated atrophic gastritis and autoimmune atrophic gastritis converge on glandular loss and metaplastic reprogramming, but their etiologic pathways, molecular mediators, topographic distribution and neoplastic characteristics differ drastically. H. pylori infection induces multifocal atrophy and incomplete intestinal metaplasia and is the typical path to intestinal-type gastric adenocarcinoma, while autoimmune gastritis results in corpus-restricted oxyntic destruction, severe hypochlorhydria, hypergastrinemia, and a distinctive predisposition to type I gastric neuroendocrine neoplasms. Despite H. pylori eradication, the epigenetic landscape of metaplastic mucosa often persists, requiring risk-adapted surveillance approaches underpinned by histologic systems such as OLGA and OLGIM. This narrative review aggregates mechanistic, epidemiologic and clinical evidence establishing malignant potentials for both etiologies of atrophic gastritis, and offers an integrated framework for surveillance and prevention.