Profile of vitamins B9, B12, D

Profile of B9, B12, D vitamins

Profile of vitamins B9, B12, D - It is informative to examine vitamins in such pathologies as general weakness, fatigue, irritability.

The profile includes the following 3 studies:

General Information

folic acid (B9)

(pteroylmonoglutamic 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 vitamin deficiency in Europe and North America. This is the result of an unbalanced diet, very low in fresh fruits and vegetables. In addition, advanced age, various diseases, specific medications such as cotrimoxazole can cause malabsorption and related folic acid deficiency. A low level 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, concentration problems and loss of appetite, inflammation of 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.

Vitamin B12

Vitamin B12 Belongs to the group of biologically active substances containing cobalt - cobalamins. These include cyanocobalamin itself (vitamin B12), hydroxycobalamin, and two coenzyme forms of vitamin B12: methylcobalamin and 5-deoxyadenosylcobalamin.

Vitamin B12 is a water-soluble vitamin that plays an extremely important role in the formation of red blood cells, cellular metabolism, the functioning of the nervous system, and the production of DNA.

When should we take the test?

Differential diagnostics of macrocytic anemias;
Hyperhomocysteinemia;
Patients with thrombosis;
Chronic inflammatory diseases and anatomical defects of the small intestine, atrophic gastritis;
Gastrectomy;
Chronic alcoholism;
Terminal hip diseases (Crohn's disease, lymphoma, resection);
Diagnosis of congenital forms of vitamin B12 deficiency;
Monitor the condition with a strict vegetarian diet.

Possible interpretation of the results

Increased concentration of vitamin B12:

Liver diseases (acute hepatitis, cirrhosis, liver coma, liver metastases);
Renal failure;
Heart failure;
Diabetes mellitus;
Myeloproliferative diseases (acute and chronic myeloid leukemia, erythromyelosis, monocytic leukemia, lymphocytic leukemia);
Treatment with vitamin B12.
Protein deficiency.

Reduced concentration of vitamin B12:

Insufficient intake of vitamin:

A strict vegetarian diet;
Diet during phenylketonuria;
Low content of vitamin in breast milk;

Malabsorption due to deficiency of internal factor in the gastric mucosa:

Pernicious anemia;
Total gastrectomy;
Toxic damage to the gastric mucosa during chronic alcohol intoxication;

Impaired absorption of vitamin B12 and / or folic acid:

Celiac disease;
Resection of stomach, small intestine;
Infection with Helicobacter pylori;
Chronic inflammatory diseases (Crohn's disease, dysbiosis, chronic enteritis);
Anatomical defects of the small intestine;
Achlorhydria (atrophic gastritis, primary hypothyroidism, HIV infection);
Parasitic infestations;
Infiltrative diseases;
Ileum radiation therapy (lymphomas, scleroderma);
Alzheimer's disease;

Hereditary disorders of cobalamin metabolism:

Transcobalamin deficiency;
Hereditary selective malabsorption of vitamin B12;
Hereditary pernicious anemia.

Vitamin D (total)

Vitamin D deficiency is common especially in adolescents and can cause: rickets, pathology of the cardiovascular system, depression, decreased immunity, autoimmune diseases and others

Compared to the widespread prevalence of vitamin D deficiency, hypervitaminosis D is rare and occurs only in the case of prolonged exposure to high doses of vitamin D. This condition is clinically characterized by anorexia, nausea, vomiting, diarrhea, hypotension, nephrolithiasis, heart problems. Laboratory test results show severe hypercalcemia and hyperphosphatemia, as well as low levels of parathyroid hormone.

How to prepare for the test / rules of material collection

Blood sample Sampling, for profile studies, is essential on empty stomach , in the morning.

Research material

Needed for research Venous blood (One sniff)

Possible interpretation of the results

If the test reveals abnormalities, it may be necessary to use additional, other methods of diagnostics. For this, you must consult a specialist, who, taking into account the symptoms, will correctly select the appropriate examinations to make an accurate diagnostics.

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Resources

https://www.synevo.ro/shop/vitamina-b12/

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

https://www.synevo.ro/shop/25-oh-vitamina-d/