Metabolism and Biological Role
Once in the body, folic acid is partially synthesized by the resident intestinal microflora and also ingested via plant and animal foods. Rich sources include grains, legumes, leafy greens, cabbage, liver, and dairy products.
In the liver, the compound undergoes bioactivation, turning into tetrahydrofolic acid. At the cellular level, this vitamin performs critical functions:
- Participates in the synthesis of purine and pyrimidine bases, providing the building blocks for DNA and RNA;
- Acts as a methyl group donor, converting homocysteine to methionine;
- Regulates amino acid and choline metabolism;
- Ensures normal cell proliferation and division, stimulates erythropoiesis, and improves iron absorption.
Causes and Manifestations of Deficiency
Vitamin B9 deficiency disrupts cell division processes, primarily affecting hematopoietic tissue. The main causes of deficiency include:
- Dietary and absorption factors — poor diet or malabsorption syndrome.
- Drug-induced factor — use of folic acid antagonists (such as methotrexate, trimethoprim, triamterene, or pyrimethamine).
- Increased demand — pregnancy, when the utilization of the vitamin increases significantly.
Clinically, deficiency manifests as macrocytic hyperchromic anemia, leukopenia, impaired megaloblast maturation, and risks of congenital and acquired hyperhomocysteinemia.
Treatment Guidelines and Important Contraindications
For the treatment of hypovitaminosis and avitaminosis, folic acid is administered orally at a dose of 5 mg daily for a course of 20 to 30 days. The drug is also used in combination therapy for tuberculosis, oncological, and neurological disorders.
A critically important safety rule: in pernicious ($B_{12}$-deficiency) anemia, it is forbidden to use folic acid in isolation. It must be prescribed only in combination with cyanocobalamin. Folic acid monotherapy can improve hematological parameters, but it does not correct neurological disorders, allowing severe neurological symptoms to progress unnoticed.