Autoimmune gastritides: A critical review

Autoimmune gastritis (AIG) has long been considered a host-related autoimmune disease that results in oxyntic atrophy, leading to Pernicious Anemia and increasing neoplastic risk. Current evidence discloses that gastric autoimmunity includes a spectrum of inflammatory diseases (i.e., Autoimmune Gastritides) with distinct etiologies, comorbidities, clinical presentations, histological phenotypes, and outcomes.

To distinguish the clinical-pathological subtypes of immunomediated gastric disorders.

Gastric autoimmune diseases comprise Type-1 and Type-2 variants. Type-1 atrophic AIG may lead to vitamin B12 malabsorption, resulting in pernicious anemia, and carries a high risk of Type-1 neuroendocrine gastric neoplasia. Type-1a AIG includes two subtypes. Type-1a is the canonical oxyntic-restricted AIG subtype with no history of exposure to H. pylori infection. In this subtype, a T-cell-rich, cytolytic infiltrate targets the corpus/fundus mucosa, resulting in oxyntic-restricted atrophic changes. Type-1b combines autoimmune etiology with prior or current exposure to H. pylori infection. The dual etiology of Type-1b AIG combines autoimmune oxyntic damage with H. pylori-related antral lesions. This condition may lead to extensive (antral and oxyntic) atrophy, necessitating cancer prevention strategies tailored to the histological stage of gastritis. Type-2 AIG is far less frequent than Type-1, presents with mucus-secreting (antral-pyloric) and oxyntic (corpus/fundus) erosive mucosal high-grade pangastritis, and involves symptomatic multiorgan immune-mediated comorbidities, irrespective of H. pylori status. Type-2 combines Type-1-like serology with a wide, variable spectrum of circulating organ-specific and non-organ-specific autoantibodies and requires targeted treatment.

The nosology of autoimmune gastritides should reflect their diverse etio-pathogenesis, clinicopathological presentations, and outcomes.