Abstract

Autoimmune atrophic gastritis is encountered in 20–27% of patients with obscure, or refractory iron deficiency anemia and is 4 to 6 times more common than celiac disease causing unexplained iron deficiency. The unique clinical features of iron deficiency anemia associated with achlorhydria and mucosal atrophy sparing the gastric antrum have all been accurately described by Faber and others over 100 years ago, including its refractoriness to oral iron treatment, female predominance, relatively young age, increased prevalence of thyroid disease and tendency to progress to pernicious anemia. A significant new development is the relation between autoimmune gastritis and Helicobacter pylori infection. H. pylori per se impairs gastric acid secretion and it is quite likely that a proportion of patients described originally as achylia gastrica represented H. pylori and not autoimmune gastritis. The demonstration of H. pylori antibodies in atrophic gastritis directed against epitopes on gastric mucosal cells implies an autoimmune mechanism triggered by H. pylori and directed against gastric parietal cells by antigenic mimicry of H +K +-ATPase, the most common autoantigen in pernicious anemia. These findings introduce a new element into the 100-year-old saga of achylia gastrica and open new options for its prevention and management.

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