Folate (vitamin B9) | Laboratory research

Folic acid (pteroyl monoglutamic acid) Is a substance from which folate is formed, a group of compounds with a similar structure consisting of a pteridine ring, a paraaminobenzoate, and one or more glutamine side chains. Polyglutamic forms predominate in the intracellular space and are more effective in enzymatic reactions. Metabolically active forms are: 5-methyl-tetra-hydro-folate (basic form of the organism), 10-formyl-tetra-hydro-folate and tetra-hydro-folate (which function as donor / receiver of carbon atom, respectively, amino acids and nucleoside metabolites In DNA synthesis).

Folic acid (FA) Is Group B water soluble vitamin (B9), which participates in the growth and development processes of the organism. FA is essential for the differentiation of red blood cells, for the normal functioning of the bone marrow and nervous system, for cell division, and is very important for the proper development of the fetus.

Folic acid metabolism is related With vitamin B12: Cobalamin is involved in the cellular uptake of 5-methyl-tetra-hydro-folate monoglutamate and its intracellular transformation into polyglutamate.

Most plant or animal foods contain FA, but Its deficiency is the most common B avitaminosis In Europe and North America. This is the result of an unbalanced diet with very low levels of fresh fruits and vegetables. In addition, with age, various diseases, specific medications such as cotrimoxazole can cause malabsorption and associated folic acid deficiency. Low levels of FA in the body can be caused by: alcoholism or its antagonists, malabsorption (for example, celiac disease), increased demand for it (for example, during pregnancy, anemia or malignant diseases).

Food folate is a polyglutamate and needs to be converted to a monoglutamate in order to be absorbed by the body, it is less bioavailable compared to synthetic folic acid.

Folic acid is absorbed in the small intestine. After absorption, food folate and reabsorbed bile folate move into the circulation, where they bind non-specifically and with low affinity to albumin; One-third circulates in free form, and only a very small fraction binds to the folate-binding protein obtained from the cell membrane; Circulating follicle monoglutamate is rapidly absorbed at the cellular level via the follicle receptor or by passive diffusion, converted to polyglutamate folate at the cytosolic level, and then transported to organs (35% of intracellular folium is found in mitochondria).

The human body contains 5-10 mg of folate and most (50%) is stored in the liver. Excretion occurs in feces (important for entero-hepatic processing) and urine.

Folic acid is also synthesized by intestinal bacteria.

In the absence of folic acid The following clinical symptoms appear: Weakness, irritability, problems with concentration and loss of appetite, inflammation of the mucous membranes, anemia and severe neurological disorders.

During pregnancy, When the demand for FA doubles, its deficiency can lead to premature birth and severe fetal developmental pathologies (especially spinal and cerebral malformations). Intake of folic acid during pregnancy can reduce the risk of developing neural tube defects by 85%.

Lack of both FA and vitamin B12 can lead to the development of megaloblastic anemia, so it is important to determine the combination of these two vitamins. In this case it is possible to determine exactly which vitamin deficiency caused the disease and to correctly prescribe the appropriate treatment. Otherwise, if megaloblastic anemia is caused by vitamin B12 deficiency, treatment with FA drugs can cause irreversible damage to the central nervous system. FA deficiency is also observed in malignant diseases, sepsis, acute inflammatory diseases (especially of the skin), liver diseases, ulcerative colitis and Crohn's disease.

FA deficiency is one of the leading causes of hyperhomocysteinemia, an independent risk factor for the early development of atherosclerosis.

Low serum folic acid levels are found in patients with neuropsychiatric disorders, neural tube defects in pregnant women, and recent miscarriages in women.

When Should we take a test on folate?

• Differential diagnostics of megaloblastic anemia;
• Chronic alcoholism;
• Women who are planning to become pregnant, especially if they have a child with a neural tube defect;
• Monitoring treatment with anticonvulsants, antifolates (methotrexate), pyrimethamine (antimalarial), sulfasalazine (for inflammatory bowel disease), oral contraceptives;
• Malabsorption syndromes;
• Chronic liver disease;
• An old man on poor nutrition.

How to prepare for the test?

Preferably for the test on empty stomach Presence.

The test should be performed prior to any injection, transfusion, or folic acid treatment with vitamin B12.

Research material

Venous blood

 Possible interpretation of the results

The concentration of folic acid increases:

• Vegetarianism;
• Pernicious anemia (vitamin B12 deficiency);
• Diseases of the distal small intestine;
• Afferent loop syndrome.

The concentration of folic acid decreases:

• Malnutrition: Children who are exclusively on a dairy-free diet without folate, diet with phenylketonuria, malnutrition in the elderly, anorexia nervosa;
• Alcohol abuse;
• Malabsorption: Tropical sprue, celiac disease, Crohn's disease, herpetiform dermatitis, jeo-ileal bypass, intestinal resection;
• Increased demand: Pregnancy, lactation, premature infants, adolescents, chronic hemolytic anemia, myeloproliferative diseases, metastatic carcinoma, hyperthyroidism, exfoliative dermatitis;
• Increased loss: Chronic dialysis;
• Chronic liver disease (Cirrhosis, hepatoma);
• Drugs and toxins: Alcohol, sulfasalazine, anticonvulsants (hydantoins, valproic acid), antifolates (methotrexate), trimethoprim-sulfamethoxazole, oral contraceptives, antacids / H2 receptor blockers.

Folate deficiency is usually multifactorial.

Resources

https://www.synevo.ro/shop/folati-serici/

https://spravochnik.synevo.ua/ru/diagnostica-anemii/folievaia-kislota.html