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Gastric atrophy

Clinical features ml

Health

Subclinical gastritis

Pernicious anemia with neurologic complications

Figure 2 The end-stage of autoimmune gastritis is gastric atrophy. This results in malabsorption of vitamin B12 and pernicious anemia with neurologic complications when vitamin B12 deficiency is severe. The histologic appearance of autoimmune gastritis is that of chronic inflammation.

In addition to autoantibodies to gastric antigens, patients with pernicious anemia have a substantially higher than normal frequency of antibodies to components of cells which are targets in diseases associated with autoimmune gastritis (Table 1). These autoantibodies include those reactive with thyroid peroxidase, thyroglobulin, pancreatic islet cells, adrenal cortical cells and ovarian cells and indicate the patient either has or is predisposed to the associated disease in which these antibodies occur.

Cell-mediated immunity to gastric antigens

The contribution of cell-mediated immunity to the gastric lesion in the body of the stomach is poorly understood. Increased numbers of T lymphocytes of the CD4 and CD 8 lineages as well as a greatly increased number of B cells have been observed in the gastric lesion. It is presumed that T cells provide help required for the production of the gastric autoantibodies because these antibodies are predominantly of the immunoglobulin G (IgG) isotype, and that they also participate in the destruction of the gastric cells. One elegant study by electron microscopy showed T lymphocytes lined up against the membranes of gastric parietal cells and chief cells as if poised to destroy these cells.

Both gastric parietal cells and chief cells become greatly reduced in numbers as the inflammation progresses. Why there is accompanying loss of chief cells is, as yet, an enigma because the autoimmune attack is not thought to be directed at chief cells. Levels of serum gastrin are high probably because gastrin production by antral cells is under the control of gastric acidity and when acid is insufficient due to the absence of the parietal cells an essential feedback mechanism fails and levels of gastrin rise.

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