What is the pathophysiology of autoimmune atrophic gastritis?

Updated: Jun 07, 2019
  • Author: Akiva J Marcus, MD, PhD; Chief Editor: BS Anand, MD  more...
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Answer

Autoimmune atrophic gastritis is associated with serum anti-parietal and anti–intrinsic factor (IF) antibodies. The gastric corpus undergoes progressive atrophy, IF deficiency occurs, and patients may develop pernicious anemia. [31]

The development of chronic atrophic gastritis (sometimes called type A gastritis) limited to corpus-fundus mucosa and marked diffuse atrophy of parietal and chief cells characterizes autoimmune atrophic gastritis. In addition to hypochlorhydria, autoimmune gastritis is associated with serum anti-parietal and anti-IF antibodies that cause IF deficiency, which, in turn, causes decreased availability of cobalamin, eventually leading to pernicious anemia in some patients. Hypochlorhydria induces G-Cell (Gastrin producing) hyperplasia, leading to hypergastrinemia. Gastrin exerts a trophic effect on enterochromaffin-like (ECL) cells and is hypothesized to be one of the mechanisms leading to the development of gastric carcinoid tumors (ECL tumors). [32, 33]

In autoimmune gastritis, autoantibodies are directed against at least 3 antigens, including IF, cytoplasmic (microsomal-canalicular), and plasma membrane antigens. There are two types of IF antibodies, types I and II. Type 1 antibody prevents the attachment of B12 to IF and Type II antibody prevents attachment of the vitamin B12-intrinsic factor complex to ileal receptors. [34]

Cell-mediated immunity also contributes to the disease. T-cell lymphocytes infiltrate the gastric mucosa and contribute to the epithelial cell destruction and resulting gastric atrophy.


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