Autoimmune Gastritis

Autoimmune gastritis is a chronic gastritis that may remain asymptomatic for many years before progression to gastric atrophy, depletion of stocks of vitamin B 12 with clinical manifestations of pernicious anemia. Autoantibodies to gastric parietal cells, the molecular target of which is the gastric H/K ATPase, is the simplest screening test for autoimmune gastritis. Intrinsic factor autoantibodies, the second autoantibody test, typically segregate with the development of pernicious anemia; these antibodies have two actions – inhibition of vitamin B 12 binding with intrinsic factor in the stomach and prevention of its transport into the body via the terminal ileum. Autoantibodies to gastric parietal cells and to intrinsic factor are present in 90 and 70%, respectively, of patients with pernicious anemia. As the gastritis evolves, the histology of the stomach shows increasing infiltration by lymphocytes accompanied by increasing destruction of parietal cells and zymogenic cells until the loss of mature cells is complete, the mucosa is atrophic, and there is intestinal metaplasia. This histologic evolution is accompanied by biochemical changes: loss of acid, depletion of pepsinogen I, and increased secretion of gastrin by the gastric antrum. Finally, when the stocks of vitamin B 12 are exhausted, clinical and hematologic signs of megaloblastic anemia and its complications become evident. Although immunosuppressive drugs will check the autoimmune reaction allowing maturation of gastric parietal cells, the preferred treatment is vitamin B 12 replacement.