![]() Vitamin K 1 is transformed to more polar metabolites, such as phytomenadione-2,3-epoxide. ![]() Systemic availability following intramuscular administration is about 50%. Following an intramuscular dose of 10mg vitamin K, plasma concentrations of 10–20mcg/l are produced (normal range 0.4–1.2mcg/l). Vitamin K 1 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. ![]() A single 1mg IM dose results in comparable vitamin K 1 concentrations at 1 month as two 2 mg doses (one given at birth and the other at one week). Absorption is limited in the absence of bile.Īfter intramuscular administration vitamin K 1 release into the circulation is prolonged, i.e. The systemic availability following oral dosing is approximately 50%, with a wide range of interindividual variability. In the mixed micelle solution, vitamin K 1 is solubilised by means of a physiological colloidal system consisting of lecithin and a bile acid.įollowing oral administration vitamin K 1 is absorbed from the small intestine. A comparison was also made between K 1 levels 24 hours after oral K 1 administration with those of 14 healthy newborns given the same dose. Main outcome measures were serum concentrations of vitamin K 1 and undercarboxylated prothrombin (PIVKA-II) before and for up to 4 days after a single dose of mixed micellar K 1 1 mg intravenously or 2 mg orally. The pharmacokinetics and efficacy of oral versus intravenous mixed micellar vitamin K prophylaxis in infants with cholestatic liver disease was compared. Paediatric populationĪ 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). Vitamin K 1 administration, which promotes synthesis of the above-mentioned coagulation factors by the liver, can reverse an abnormal coagulation status due to vitamin K 1 deficiency. Lack of vitamin K 1 leads to an increased tendency to haemorrhagic disease in the newborn. Vitamin K 1 does not readily cross the placental barrier from mother to child and is poorly excreted in breast milk.
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