General characteristics and properties of vitamins
Vitamins are low-molecular-weight organic substances that are not synthesized by the human body and must be continuously supplied through diet. They possess a number of specific properties:
- do not serve as an energy source for cells;
- are not used as structural building materials;
- exhibit marked biological activity in extremely small quantities;
- are incorporated into the structure of enzyme complexes and regulatory hormones.
Biocatalytic properties are exerted not by the original molecules themselves, but by the products of their internal transformation — coenzymes. In clinical practice, ready-to-use coenzyme forms (e.g., cocarboxylase, pyridoxal phosphate, flavinat, cobalamide) are used in metabolic pharmacotherapy due to their natural origin and low toxicity.
Features of fat-soluble vitamin metabolism
The group of lipophilic compounds includes vitamins A, D, E, and K, which are insoluble in aqueous media. The process of their assimilation completely mirrors the metabolic pathway of dietary lipids:
- Emulsification and micelle formation in the intestinal lumen under the action of bile acids.
- Incorporation into chylomicrons of the intestinal epithelium.
- Transport via lymphatic vessels into the systemic circulation.
| Vitamin | Deficiency manifestations upon blood level decrease |
|---|---|
| Vitamin A | Dry skin, impaired dark adaptation ("night blindness") |
| Vitamin D | Bone demineralization, osteoporosis, osteomalacia, Ca/P metabolic disorders |
| Vitamin E | Reduced antioxidant defense, risks of erythrocyte hemolysis |
| Vitamin K | Hemorrhagic syndrome, drop in blood clotting factors |
Causes of decreased blood vitamin concentrations
A drop in serum vitamin concentrations and the development of hypovitaminosis regularly occur in hepatobiliary and gastrointestinal disorders:
- Cholelithiasis and acholia: cause impaired fat emulsification, steatorrhea, and combined deficiency of A, D, E, and K;
- Chronic pancreatitis: leads to decreased serum concentrations of lipophilic vitamins, although clinical presentation may rarely manifest;
- Cholestasis during parenteral nutrition: inadequate bile supply blocks normal absorption;
- Metabolic polyneuropathies: deficiency states (e.g., B12 deficiency along with homocysteine fluctuations) provoke primarily axonal damage to sensory nerve fibers and distal muscle weakness.
ADEK-quate fat: fat-soluble vitamins — A, D, E, K — are absorbed only together with lipids and bile.
Class and exam questions
Why does the deficiency of fat-soluble vitamins develop slower than that of water-soluble ones?
Lipophilic vitamins A, D, E, and K have the ability to be stored in body tissues — predominantly in the liver and adipose tissue. For the same reason, excessive intake can lead to the development of hypervitaminosis.
Which laboratory parameter is monitored during treatment with vitamin K antagonists?
Patients receiving therapy with vitamin K antagonists are indicated for regular determination of the international normalized ratio (INR) in a biochemical blood test.
What are the consequences of bile deficiency in the intestine for the vitamin balance?
In acholia or cholestasis syndrome, micelle formation and fat absorption are impaired, which entails multiple hypovitaminosis A, D, E, K with clinical signs of vision, bone mineralization, and hemostasis disorders.
What else to study on this topic
- Electroneuromyographic differences between metabolic PNP and CIDP
- The role of homocysteine and vitamin B12 in the genesis of distal muscle weakness
- Timing and list of mandatory examinations after surgical correction of heart defects
- CIDP associated with diabetes mellitus: EAN/PNS criteria
- Use of coenzyme preparations (flavinat, pyridoxal phosphate) in metabolic therapy
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