Metabolism and biological role
Once in the body, folic acid is partially synthesized by the intestinal microflora and also obtained from plant and animal foods. Rich sources include grains, legumes, greens, cabbage, liver, and dairy products.
In the liver, the compound undergoes bioactivation, turning into tetrahydrofolic acid. At the cellular level, this vitamin performs key functions:
- Participates in the synthesis of purine and pyrimidine bases, ensuring the synthesis of 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, primarily in hematopoietic tissue. The main causes of deficiency:
- Dietary and absorption factor — poor diet or malabsorption syndrome.
- Drug factor — use of folic acid antagonists (such as methotrexate, trimethoprim, triamterene, or pyrimethamine).
- Increased demand — pregnancy, when the consumption of the vitamin increases significantly.
Clinically, the deficiency manifests as macrocytic hyperchromic anemia, leukopenia, impaired megaloblast maturation, as well as risks of congenital and acquired hyperhomocysteinemia.
Treatment guidelines and important restrictions
To treat hypo- and avitaminosis, folic acid is prescribed orally at a dosage of 0.005 g daily for a course of 20 to 30 days. The drug is also used in combination therapy for tuberculosis, oncological, and neurological disorders.
Critically important safety rule: in pernicious ($B_{12}$-deficiency) anemia, it is strictly 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.
Folic acid + Cyanocobalamin — the ultimate pair in pernicious anemia: give folic acid alone, and you'll clear the blood but miss the brain (neurology)!
Class and exam questions
Why must folic acid not be prescribed separately from vitamin B12 in pernicious anemia?
Isolated administration normalizes blood counts but does not eliminate neurological disorders, leading to their latent progression.
Which drugs act as folic acid antagonists?
These include methotrexate, trimethoprim, triamterene, and pyrimethamine.
What active form does vitamin B9 convert into in the human body?
In the liver, it is metabolized into tetrahydrofolic acid.
What else to study on this topic
- Clinical presentation and diagnosis of megaloblastic anemias
- Pharmacokinetics and mechanisms of action of folic acid antagonists (methotrexate)
- The role of folic acid in the prevention of neural tube defects during pregnancy
- The relationship between homocysteine metabolism, folates, and vitamin B12
- Pharmacological properties of calcium folinate (leucovorin)
Master the entire topic in the «Pharmacology» course
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