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Additional recommended knowledge
Upon entry into the stomach, vitamin B12 becomes bound to one of two B12 binding proteins present in gastric juice. In the less acidic environment of the small intestine, these proteins dissociate from the vitamin, enabling it to bind to intrinsic factor and enter the portal circulation through a receptor in the ileal mucosa specific for the B12-intrinsic factor complex.
In pernicious anemia, an autoimmune disease, autoantibodies directed against intrinsic factor or parietal cells themselves lead to an intrinsic factor deficiency, malabsorption of vitamin B12, and subsequent megaloblastic anemia. Atrophic gastritis can also cause intrinsic factor deficiency and anemia through damage to the parietal cells of the stomach wall. Pancreatic exocrine insufficiency can interfere with normal dissociation of vitamin B12 from its binding proteins in the small intestine, preventing its absorption via the intrinsic factor complex.
Bariatric surgery is a known risk factor in the development of pernicious anemia. Other risk factors contributing to this condition are stomach tumors, gastric ulcers, and excessive consumption of alcohol.
Patients experiencing an insufficiency in their intrinsic factor levels cannot benefit from a low dose oral vitamin B-12 supplement, because it will not absorb through the wall of the small intestine. Historically, the disease was thought untreatable before the discovery that it could be managed with regular injections of vitamin B-12, thus bypassing the digestive tract. More recently, Swedish researchers discovered that sufficiently large doses of B-12 can also be absorbed sublingually, so injections are necessary only for those unable to take pills by sublingual administration.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Intrinsic_factor". A list of authors is available in Wikipedia.|