Vitamin K (phylloquinone): deficiency of vitamin K

Vitamin K (phylloquinone) is a food vitamin K. The fat of food enhances its absorption. Additions of vitamin K are added to formula formulas for infants. Vitamin K refers to the group of compounds (menaquinones) synthesized by intestinal bacteria; the amount synthesized does not satisfy the need for vitamin K.

Vitamin K monitors the formation of clotting factors II (prothrombin), VII, IX and X in the liver. Other vitamin K-dependent factors of blood coagulation are proteins C, S and Z; proteins C and S - anticoagulants. Metabolic transformations contribute to the preservation of vitamin K; as soon as vitamin K took part in the formation of coagulation factors, the reaction product, the vitamin K epoxide, is enzymatically converted to the active form, vitamin K hydroquinone.

For the manifestation of the action of vitamin K-dependent proteins, Ca is required. Vitamin K-dependent proteins, osteocalcin and matrix block containing the γ-carboxyglutamine protein, play an important role in bones and other tissues.

Hypovitaminosis of Vitamin K

Deficiency of vitamin K is a consequence of extremely inadequate intake with food, malabsorption of lipids or the use of anticoagulants of the coumarin group. Deficiency is especially prevalent in children who are breastfeeding. Hypovitaminosis K contributes to the deterioration of blood clotting. The diagnosis can be suspected on the basis of the data of standard studies of blood coagulability and confirm with the effect of taking vitamin K. Treatment consists in prescribing vitamin K orally. In the case where the cause of deficiency is malabsorption of lipids or a high risk of bleeding, vitamin K is injected parenterally.

Vitamin K deficiency reduces levels of prothrombin and other vitamin K-dependent clotting factors, causing coagulation disorders and, potentially, bleeding.

Causes of Vitamin K deficiency

Worldwide, vitamin K deficiency can cause an increase in childhood morbidity and mortality. Deficiency of vitamin K causes hemorrhagic disease of the newborn, which usually manifests itself on the 1-7th day after birth. In such newborns, birth trauma can cause intracranial hemorrhage and bleeding. Newborns are prone to vitamin K deficiency, because:

1. the placenta is relatively poor in lipid and vitamin K;
2. the synthesis of prothrombin in an as yet immature liver is imperfect;
3. in breast milk, a low vitamin K content is approximately 2.5 μg / l (cow milk contains 5000 μg / l) and
4. The intestines of newborns are sterile during the first few days of life.

Late hemorrhagic disease (3-8 weeks after birth) is usually associated with breastfeeding, malabsorption or liver disease. If the mother took anticonvulsant drugs of the phenytoin group, anticoagulants of the coumarin group or antibiotics of the cephalosporin series, the risk of developing both types of hemorrhagic disease increases.

In healthy adults, vitamin K deficiency is rare, because vitamin K is widely distributed in green vegetables, and intact intestinal bacteria synthesize menaquinones. Blockage of the biliary tract, malabsorption, cystic fibrosis and small bowel resection contribute to vitamin K deficiency.

Anticoagulants of the coumarin group interfere with the synthesis of vitamin K-dependent coagulation factors (II, VII, IX and X) in the liver. Certain antibiotics (especially certain cephalosporins and other broad-spectrum antibiotics), salicylates, vitamin E supernodes and hepatic insufficiency increase the risk of bleeding in patients with vitamin K deficiency.

[1], [2], [3], [4], [5], [6], [7]

Symptoms of vitamin K deficiency

Bleeding is the most common manifestation. Characterized by the ease of formation of hematomas and bleeding of mucous membranes (especially nasal bleeding, gastrointestinal bleeding, menorrhagia and hematuria). Blood can leak from incisions or puncture sites.

In infants, hemorrhagic neonatal disease and late hemorrhagic disease can lead to cutaneous, gastrointestinal, intrathoracic and, in worst cases, intracerebral hemorrhages. With mechanical jaundice, bleeding - if it happens - usually begins after 4-5 days. Bleeding can begin as a slow seepage from a surgical wound, gums, nose, mucous membrane of the gastrointestinal tract, or as a massive gastrointestinal.

Hypervitaminosis (intoxication) of vitamin K

Vitamin K ₁ (phylloquinone) is nontoxic when ingested, even in large quantities. However, menadione, a synthetic water-soluble vitamin K precursor, can cause intoxication and should not be used to treat vitamin K deficiency.

Diagnosis of vitamin K deficiency

Deficiency of vitamin K or antagonism (caused by the use of coumarinic anticoagulants) can be suspected in the case when patients at risk are observed pathological bleeding. Studies of blood clotting phases can pre-confirm the diagnosis. Prothrombin time (MI), currently MHO (international normalized ratio) is prolonged, but partial thromboplastin time (TTH), thrombin time, platelet count, bleeding time, fibrinogen levels, fibrin degradation products and D-dimer are normal. If intravenous injection of 1 mg of phytonadione (analogue name of vitamin K), PV decreases significantly within 2-6 hours, then the cause of liver disease is unlikely, and thus the diagnosis of vitamin K deficiency is confirmed. Some centers can determine vitamin K deficiency more exactly, by measuring the level of vitamin in the blood plasma. The plasma level of vitamin K varies from 0.2 to 1.0 ng / ml in healthy people who consume adequate amounts of vitamin K (50-150 μg / day). Knowing the amount of vitamin K consumed can help interpret its plasma levels; Recent consumption affects plasma levels, but not in tissues.

At the present time, more sensitive indicators of the status of vitamin K - PIVKA (Protein Induced in Vitamin K Absence or Antagonism - a protein induced in the absence or antagonism of vitamin K) or immature (non-carboxylated) osteocalcin are under study.

[8], [9], [10], [11], [12], [13]

Treatment of vitamin K deficiency

Whenever possible, phytonadione should be administered orally or subcutaneously. The usual dose for adults is 5-20 mg. (Rarely, even if phytonadione is correctly diluted and injected slowly, a substitution for intravenous administration can lead to anaphylactic shock or anaphylactic reactions.) MHO usually decreases within 6-12 hours. The dose can be repeated after 6-8 hours if there has not been a sufficient reduction in MHO. Phytonadione in a dose of 2.5-10 mg orally is prescribed to correct (not emergency) elongated MHO in patients taking anticoagulants. Correction usually comes in 6-8 hours. When only partial correction of MHO is desired (for example, when MHO should remain slightly elevated due to an artificial heart valve), lower doses (1-2.5 mg) of phytonadione can be administered.

Infants who are bleeding due to a deficiency are prescribed phytonadione 1 mg once or subcutaneously or intramuscularly to correct them. The dose is repeated if the MHO remains elevated. Doses can be higher if the mother took oral anticoagulants.

Prevention of vitamin K deficiency

Intramuscular injection of phytonadione in a dose of 0.5-1 mg is recommended for all newborns within the first hour of birth in order to reduce the degree of intracranial hemorrhage during birth trauma. This method is also used for preventive purposes before surgical interventions. Some clinicians recommend that pregnant women taking anticonvulsant drugs take 10 mg of phytonadione either orally once a day for 1 month or 20 mg orally once a day for 2 weeks before the delivery. Because of the low content of vitamin K in the breast milk of the mother, it can be increased, recommending taking with food up to 5 mg / day of phylloquinone.