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Folic Acid Injection

Folic acid is a water-soluble, B-complex vitamin found in a variety of foods including liver, yeast, and leafy greens. Folic acid can also be taken orally or parenterally. A deficiency can bring hematologic complications including megaloblastic and macrocytic anemias. In addition to treating these conditions, this vitamin can also be used to diagnose folate deficiency. Researchers have recently discovered that adequate folic acid intake can substantially decrease the risk of congenital neural tube defects that appear in utero. Unlike some derivatives, folic acid does not offset the action of folate reductase inhibitors because it requires the enzyme dihydrofolate reductase for activation. Also, folic acid cannot be used to treat aplastic and normocytic anemias. In 1998, the recommended dietary allowance for all women of child bearing age who are capable of becoming pregnant was increased to 400 mcg of folic acid daily. As of that year, the FDA has required food manufacturers to fortify enriched grain products with folic acid to reduce the risk of congenital defects.

Folic acid, a biochemically inactive compound, is the precursor for tetrahydrofolic acid and methyltetrahydrofolate. Tetrahydrofolic acid, methyltetrahydrofolate, and other folic acid congeners are essential for the maintenance of normal erythropoiesis and are also required cofactors for the synthesis of purine and thymidylate nucleic acids. They are also necessary for the interconversion of amino acids such as the metabolism of histidine to glutamic acid and the interconversion of serine and glycine. Folic acid congeners are transported across cells by receptor-mediated endocytosis where they function and are stored. Other processes involving folate coenzymes include generation and use of formate and methylation of transfer RNA. Impaired thymidylate synthesis, which leads to faulty DNA synthesis, is responsible for megaloblastic and macrocytic anemias.

Mechanism of Action

Folic acid causes the formation of methionine from homocysteine using vitamin B12 as a cofactor. Adequate intakes can normalize high homocysteine levels by increasing the remethylation of homocysteine to methionine via 5-methyltetrahydrofolate-homocysteine methyltransferase. Reduced intake is associated with hyperhomocysteinemia, which is recognized as an independent risk factor for artherosclerosis. There is mounting evidence that elevated plasma homocysteine (and therefore decreased serum methionine) contributes to congenital neural tube defects. High serum homocysteine levels may also contribute to the development of colon cancer, diabetic retinopathy, and other diseases.

Pharmacokinetics
Contraindications/Precautions
Pregnancy/ Breastfeeding
Adverse Reactions/ Side Effects
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