autoimmune gastritis

Autoimmune gastritis is a chronic inflammatory condition in which autoantibodies target gastric parietal cells and intrinsic factor, predominantly affecting the fundus and body of the stomach while sparing the antrum (unlike H. pylori-associated gastritis, which typically involves the antrum). Destruction of parietal cells leads to decreased gastric acid secretion (achlorhydria) and decreased intrinsic factor production, impairing vitamin B12 absorption in the terminal ileum. This results in pernicious anemia, a megaloblastic anemia with neurological manifestations (subacute combined degeneration) due to B12 deficiency. Achlorhydria causes compensatory hypergastrinemia due to loss of negative feedback on G cells (located in unaffected antrum), which can lead to G-cell hyperplasia and increased risk of gastric carcinoid (neuroendocrine) tumors. Chronic atrophic gastritis with intestinal metaplasia also increases risk of gastric adenocarcinoma. Diagnosis involves serologic testing for anti-parietal cell antibodies and anti-intrinsic factor antibodies, along with elevated serum gastrin and low pepsinogen I levels. Endoscopy with biopsy shows atrophic mucosa in the fundus/body with intestinal metaplasia. Autoimmune gastritis is associated with other autoimmune conditions, particularly autoimmune thyroid disease (Hashimoto thyroiditis), type 1 diabetes mellitus, and vitiligo, reflecting a broader autoimmune polyendocrine syndrome pattern. Management includes B12 supplementation (often parenteral) and surveillance endoscopy due to increased malignancy risk.