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Definition, Etiology, PathogenesisTop
Autoimmune gastritis (autoimmune metaplastic atrophic gastritis [AMAG]) is a chronic inflammation of the gastric mucosa leading to irreversible atrophy. It is associated with circulating antibodies against parietal cells (90% of patients) and against intrinsic factor, which are responsible for vitamin B12 deficiency; this leads to the development of pernicious anemia in some patients. Associated autoimmune diseases such as thyroiditis, Addison disease, Sjögren syndrome, type 1 diabetes mellitus, hypoparathyroidism, or rheumatoid arthritis may coexist and are associated with elevated risk of gastritis. Patients of North European or Scandinavian ancestry are also at increased risk of autoimmune gastritis.
Clinical Features and Natural HistoryTop
Clinical features associated with autoimmune gastritis are nonspecific. Patients may be asymptomatic or may develop symptoms related to pernicious anemia, such as neurologic abnormalities, cognitive impairment, angular cheilitis, and atrophic glossitis. Even individuals with total mucosal atrophy and intestinal metaplasia may remain asymptomatic, which suggests that endoscopic findings may not completely correlate with clinical presentation.
There is a small increased risk for the development of gastric adenocarcinoma and gastric carcinoid.
DiagnosisTop
Routine blood tests may be helpful in identifying megaloblastic anemia as the first sign of a potential autoimmune etiology and low vitamin B12 levels (see Cobalamin Deficiency). Serum vitamin B12 and autoantibody studies should be completed in the setting of suspected autoimmune gastritis. Antibodies to intrinsic factor and parietal cell are highly sensitive for pernicious anemia. Patients with confirmed pernicious anemia should usually undergo endoscopy to evaluate for the presence of potential gastric malignancy (the risk is a few times higher compared with the general population). In early disease numerous pseudopolyps may be observed in the gastric body and fundus. At later stages gastric fold flattening or absence and atrophic mucosa with vascular abnormalities may be seen.
TreatmentTop
Vitamin B12 supplementation (see Cobalamin Deficiency). Patients should be monitored to confirm their response to supplementation.
