Parietal cells defects

Vitamin B] deficiency is commonly caused by pernicious anemia (PA). TA is an autoimmune disease resulting from the body s production of antibodies that recognize inlrinsic factor or other proteins of the parietal cell. The binding of antibodies to these proteins results in loss of their function. The parietal cells may be destroyed and be undetectable in patients with PA. The major defect in PA is gastric atrophy. 1 here may be a lack of all gastric secretions, including intrinsic factor, gastric acid, and pepsin. 

Pernicious anemia, a deficiency of intrinsic factor, is a relatively common problem caused by malabsorption of dietary cobalamin. It may result from an inherited defect that leads to a decreased ability of gastric parietal cells to synthesize intrinsic factor or from partial resection of the stomach or of the ileum. Production of intrinsic factor often declines with age and may be low in elderly individuals. An alternative circumstance that leads to the development of a B12 deficiency is pancreatic insufficiency or a high intestinal pH, which would result from too little acid being produced by the stomach. Both of these conditions prevent the degradation of the R-binder-B12 complex as a result, B12 will not be released from the R-binder protein and, therefore, cannot bind to intrinsic factor. 

Vitamin B12 deficiency results more commonly from a stomach defect than from a dietary deficiency. Before it can be absorbed the vitamin B12 (extrinsic factor) that is released from associated peptides and proteins in the stomach must combine with the intrinsic factor, a small glycoprotein secreted by the parietal cells. Subjects who suffer from pernicious anaemia fail to produce intrinsic factor with the result that the vitamin is not absorbed and must be given by injection. Vitamin B]2 produced by microbes in the lower reaches of the intestine is of no use to the body. 

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