Pernicious anemia is an autoimmune disorder caused by production of autoantibodies against the parietal cell antigen, H+/K+-ATPase, and against the parietal cell secretory product, intrinsic factor, resulting in the loss of parietal cells in the fundus and body of the stomach. The loss of these cells is associated with achlorhydria, vitamin B12 deficiency and megaloblastic anemia.58
Macroscopically, it is characterized by loss of mucosal folds and thinning of the gastric mucosa. Histology shows a marked infiltration into the submucosa by mononuclear cells, including autoantibody-containing plasma cells, T and B cells, which can extend into the lamina propria between the glands. Cellular infiltration of the mucosa is accompanied by degenerative change in parietal cells. In the fully established lesion, as mentioned, there is a marked reduction in number of gastric glands and the parietal cells are replaced by mucus-containing cells. Recently, studies in murine models of autoimmune gastritis have suggested that macrophages and CD4+ T cells might play a role in the pathogenesis of the disease and that the interaction between the Fas antigen on the target cells and its ligand on the effector cells might be responsible for target cell destruction.59
In children the 'adult form' of pernicious anemia has been reported in association with other autoimmune diseases, such as thyroiditis and diabetes mellitus, and with precancerous and malignant lesions. In childhood, pernicious anemia has been attributed to dietary lack of cobal-amin, to absence of cobalamin in the ileum or to so-called juvenile pernicious anemia. The last is characterized by absent or very low levels of intrinsic factor in the gastric juice, in the absence of achlorhydria and the absence of intrinsic factor or H+/K+-ATPase autoantibodies.58 It has been suggested that this defect could be due to abnormal synthesis and biological elaboration in the gastric lumen of intrinsic factor.
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