Gastric secretion antibodies

This condition has often been referred to in the past as juvenile pernicious anemia but it appears to be a quite separate entity. Confusion probably arose because there is a deficiency of intrinsic factor resulting in vitamin B12 malabsorption in both conditions. However, it differs from the disease in adults in that free acid is present in the gastric secretion (A8,L3,M5), the gastric mucosa is usually normal, and antibodies to intrinsic factor are not a feature. Megaloblastic anemia usually develops during the first 2 years of life but this depends on the amount of residual intrinsic factor available, and... 

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. 

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Failure of intrinsic factor secretion is commonly a result of autoimmune disease 90% of patients with pernicious anemia have complement-fixing antibodies in the cytosol of the gastric parietal cells. Similar autoantibodies are found in 30% of the relatives of pernicious anemia patients, suggesting that there is a genetic basis for the condition. 

For patients who secrete antiintrinsic factor antibodies in the saliva or gastric juice, oral intrinsic factor will be of no benefit. 

Preprosomatostatin, a 116-amino acid peptide, is encoded on the long arm of chromosome 3. Somatostatin (SS-14), a cyclic peptide with a molecular weight of 1,600, is produced from the 14 amino acids at the C-terminus of this precursor molecule. SS-14 was first isolated from the hypothalamus and named for its ability to inhibit the release of growth hormone (GH, somatotropin) from the anterior pituitary. It also inhibits the release of insulin. In addition to the hypothalamus, somatostatin is also secreted from the D cells (8 cells) of the pancreatic islets, many areas of the central nervous system outside of the hypothalamus, and in gastric and duodenal mucosal cells. SS-14 predominates in the central nervous system (CNS) and is the sole form secreted by the 8 cells of the pancreas. In the gut, however, prosomatostatin (SS-28), which has 14 additional amino acids extending from the C-terminal portion of the precursor, makes up 70 to 75% of the immunoreactivity (the amount of hormone that reacts with antibodies to SS-14). The prohormone SS-28 is 7 to 10 times more potent in inhibiting the release of GH and insulin than is SS-14. 

About 70% of patients also have anti-intrinsic factor antibodies in plasma, saliva and gastric juice. Although the oral administration of partially purified preparations of intrinsic factor will restore the absorption of vitamin B in many patients with pernicious anaemia, this can result eventually in the production of anti-intrinsic factor antibodies, so parenteral administration of vitamin B is the preferred means of treatment. For patients who secrete anti-intrinsic factor antibodies in the saliva or gastric juice, oral intrinsic factor will be useless. 

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