The majority of cases of vitamin B12 deficiency, particularly severe deficiency, are due to malabsorption. While vitamin B12 is a water-soluble vitamin it is extremely large and only between 1 and 3% of any specific dose will cross the intestinal wall by diffusion. Thus, the normal physiological absorption of vitamin B12 is dependent upon it forming a complex with a glycoprotein that is secreted by the parietal cells of the stomach called intrinsic factor (IF). The most classical case where IF is deficient or absent is in the autoimmune pernicious anemia (PA). The most usual presentation of this condition is where antibodies are produced against the parietal cells rendering them incapable of secretion not only of IF but also hydrochloric acid (HCl) leading to hypochlorhydria. Yet another form sees autoantibodies produced against IF itself rendering it incapable of binding vitamin B12 with consequent malabsorption of the IF-B12 complex in the ileum, where specific receptors are responsible for the active absorption of vitamin B12. There is some evidence that many elderly people, perhaps even the majority, suffer to varying degrees from gastric atrophy. In such circumstances while they may still have an adequate supply of IF they lack a competent secretion of HCl. It is suggested that this acid and the accompanying action of pepsin is necessary to release vitamin B12 from the form in which it is present in food. The consequences would be varying degrees of malabsorption of food-bound vitamin B12 but an ability to absorb the free form of the vitamin present in foods fortified with vitamin B12 or from supplements. Other now infrequent causes of vitamin B12 malabsorption are resections of the stomach or removal of the ileum, the site of absorption.
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