Chemical formula: C₃₁H₄₆O₂ Molecular mass: 450.696 g/mol PubChem compound: 5284607
The presence of vitamin K (i.e. vitamin K or substances with vitamin K activity) is essential for the formation within the body of prothrombin, factor VII, factor IX and factor X. Lack of vitamin K leads to an increased tendency to haemorrhage. When an antidote to an anticoagulant is necessary it is essential to use vitamin K1 itself, as vitamin K analogues are much less effective.
Vitamin K1 does not readily cross the placental barrier from mother to child and is poorly excreted in breast milk.
Lack of vitamin K1 leads to an increased tendency to haemorrhagic disease in the newborn. Vitamin K1 administration, which promotes synthesis of the above-mentioned coagulation factors by the liver, can reverse an abnormal coagulation status due to vitamin K1 deficiency.
A prospective randomised controlled study included 44 infants (1-26 weeks of age) with conjugated hyperbilirubinaemia (idiopathic neonatal hepatitis – 17 patients, biliary atresia – 13, total parenteral nutrition cholestasis – 3, Alagille’s syndrome – 2, alpha 1 antitrypsin deficiency – 2, inspissated bile syndrome – 2, and 5 miscellaneous diagnoses (fructosaemia, galactosaemia, choledochal cyst, necrotising enterocolitis, cytomegalovirus hepatitis). The pharmacokinetics and efficacy of oral versus intravenous mixed micellar vitamin K prophylaxis in infants with cholestatic liver disease was compared.
Main outcome measures were serum concentrations of vitamin K1 and undercarboxylated prothrombin (PIVKA-II) before and for up to 4 days after a single dose of mixed micellar K1 1 mg intravenously or 2 mg orally. A comparison was also made between K1 levels 24 hours after oral K1 administration with those of 14 healthy newborns given the same dose.
In the mixed micelle solution, vitamin K1 is solubilised by means of a physiological colloidal system consisting of lecithin and a bile acid.
Following oral administration vitamin K1 is absorbed from the small intestine. The systemic availability following oral dosing is approximately 50%, with a wide range of interindividual variability. Absorption is limited in the absence of bile.
After intramuscular administration vitamin K1 release into the circulation is prolonged, i.e. the IM route acts as a depot. A single 1mg IM dose results in comparable vitamin K1 concentrations at 1 month as two 2 mg doses (one given at birth and the other at one week).
Vitamin K1 accumulates predominantly in the liver, is up to 90% bound to lipoproteins in the plasma and is stored in the body only for short periods of time. Following an intramuscular dose of 10mg vitamin K, plasma concentrations of 10–20mcg/l are produced (normal range 0.4–1.2mcg/l). Systemic availability following intramuscular administration is about 50%.
Vitamin K1 is transformed to more polar metabolites, such as phytomenadione-2,3-epoxide.
The half-life of vitamin K1 in plasma is approximately 72 hours in neonates and about 1.5 to 3 hours in adults. Vitamin K1 is excreted in bile and urine as the glucuronide and sulfate conjugates.
None applicable.
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