VITAMIN B12 with Intrinsic Factor

When secretion of intrinsic factor in gastric juice is inadequate or absent (e.g., in Addisonian pernicious anemia or after gastrectomy), VITAMIN B12 in physiologic doses is absorbed poorly, if at all. The resulting deficiency of VITAMIN B12 leads to the clinical manifestations of pernicious anemia. Similar megaloblastic anemias may develop in fish tapeworm (Diphyllobothrium latum) infection or after a surgically created small-bowel blind loop; in these situations, treatment requires freeing the host of the parasites or bacteria that appear to compete for the available VITAMIN B12. Strict vegetarianism and malabsorption syndromes may also lead to VITAMIN B12 deficiency. In the latter case, parenteral therapy, or oral therapy with so-called massive doses of VITAMIN B12, may be necessary for adequate treatment of the patient.

Potency of intrinsic factor concentrates is determined physiologically i.e., by their use in patients with pernicious anemia. The liver-stomach concentrate with intrinsic factor and the vitamin B12 contained in 2 capsules provide 1½ times the minimum amount of therapeutic agent, which, when given daily in an uncomplicated case of pernicious anemia, will produce a satisfactory reticulocyte response and relief of anemia and symptoms.

Concentrates of intrinsic factor derived from hog gastric, pyloric, and duodenal mucosa have been used successfully in patients who lack intrinsic factor. For example, Fouts et al. maintained patients with pernicious anemia in clinical remission with oral therapy (liver extracts or intrinsic factor concentrate with VITAMIN B12) for as long as 29 years.

After total gastrectomy, Ficarra found multifactor preparations taken orally to be just as effective in maintaining blood levels as any medication that has to be administered parenterally. His study was based on 24 patients who had survived for 5 years after total gastrectomy for cancer and who had been taking 2 capsules daily.

Folic Acid

Folic acid deficiency is the immediate cause of most, if not all, cases of nutritional megaloblastic anemia and of the megaloblastic anemias of pregnancy and infancy; usually, it is also at least partially responsible for the megaloblastic anemias of malabsorption syndromes, e.g., tropical and nontropical sprue.

It is apparent that in VITAMIN B12 deficiency (e.g., pernicious anemia), lack of this vitamin results in impaired utilization of folic acid. There are other evidences of the close folic acid-VITAMIN B12 interrelationship:

1. VITAMIN B12 influences the storage, absorption, and utilization of folic acid, and
2. as a deficiency of VITAMIN B12 progresses, the requirement for folic acid increases. However, folic acid does not change the requirement for VITAMIN B12.

Iron

A very common anemia is that due to iron deficiency. In most cases, the response to iron salts is prompt, safe, and predictable. Within limits, the response is quicker and more certain to large doses of iron than to small doses. Each capsule furnishes 110 mg of elemental iron (as ferrous fumarate) to provide a maximum response.

Ascorbic Acid

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