Most important risk factor for chronic gastritis, including atrophic gastritis
Colonizes mainly antrum of stomach
Pathophysiology
AMAG
Autoimmune destruction of the parietal cells in the gastric corpus and fundus (T-cell induced autoantibodies against H+/K+ ATPase) → achlorhydria → increased release of gastrin (due to loss of negative feedback) → G cell hyperplasia → hypergastrinemia → hyperplasia of enterochromaffin-like cells → ↑ risk of carcinoid tumors.
Achlorhydria impairs the intestinal absorption of inorganic iron → iron deficiency anemia (early manifestation)
Inflammation of the antrum → destruction of D cells → ↓ somatostatin → ↑ gastrin → ↑ production of gastric acids → duodenal ulcers
Inflammation of the gastric body → local destruction of mucosa (via cytotoxins such as ammonia) → ↓ production of mucins and atrophy of the gastric glands → hypochlorhydria → hypergastrinemia and epithelial dysplasia → epithelial metaplasia → ↑ risk of gastric cancers