Vitamin B12 B

Vitamin B]2 (cyanocobalamin) is produced by bacteria; B12 generated in the colon, however, is unavailable for absorption (see below). Liver, meat, fish, and milk products are rich sources of the vitamin. The minimal requirement is about 1 jg/d. Enteral absorption of vitamin B12 requires so-called "intrinsic factor" from parietal cells of the stomach. The complex formed with this gly-coprotein undergoes endocytosis in the ileum. Bound to its transport protein, transcobalamin, vitamin B12 is destined for storage in the liver or uptake into tissues.

A frequent cause of vitamin B12 deficiency is atrophic gastritis leading to a lack of intrinsic factor. Besides megalo-blastic anemia, damage to mucosal linings and degeneration of myelin sheaths with neurological sequelae will occur (pernicious anemia).

Optimal therapy consists in paren-teral administration of cyanocobal-amin or hydroxycobalamin (Vitamin

B]2a; exchange of -CN for -OH group). Adverse effects, in the form of hyper-sensitivity reactions, are very rare.

Folic Acid (B). Leafy vegetables and liver are rich in folic acid (FA). The minimal requirement is approx. 50 jg/d. Polyglutamine-FA in food is hydrolyzed to monoglutamine-FA prior to being absorbed. FA is heat labile. Causes of deficiency include: insufficient intake, malabsorption in gastrointestinal diseases, increased requirements during pregnancy. Antiepileptic drugs (phenytoin, primidone, phenobarbital) may decrease FA absorption, presumably by inhibiting the formation of monogluta-mine-FA. Inhibition of dihydro-FA reductase (e.g., by methotrexate, p. 298) depresses the formation of the active species, tetrahydro-FA. Symptoms of deficiency are megaloblastic anemia and mucosal damage. Therapy consists in oral administration of FA or in folinic acid (p. 298) when deficiency is caused by inhibitors of dihydro—FA—reductase.

Administration of FA can mask a vitamin B12 deficiency. Vitamin B12 is required for the conversion of methyltet-rahydro-FA to tetrahydro-FA, which is important for DNA synthesis (B). Inhibition of this reaction due to B]2 deficiency can be compensated by increased FA intake. The anemia is readily corrected; however, nerve degeneration progresses unchecked and its cause is made more difficult to diagnose by the absence of hematological changes. Indiscriminate use of FA-containing multivitamin preparations can, therefore, be harmful.

Inhibition of DNA

synthesis

(cell multiplication)

Vit. B12 deficiency

Folate deficiency

A very few large hemoglobin-rich erythrocytes

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