Supplementation of vitamin K in pregnant women receiving anticonvulsant therapy prevents neonatal vitamin K deficiency

Am J Obstet Gynecol. 1993 Mar;168(3 Pt 1):884-8. doi: 10.1016/s0002-9378(12)90839-x.


Objective: The null hypothesis of this study is that extra vitamin K administered to pregnant women on a regimen of enzyme-inducing anticonvulsant therapy will not decrease the frequency of symptoms of vitamin K deficiency in their neonates.

Study design: A multicenter case-control study was performed on 16 pregnant women on anticonvulsant therapy who received 10 mg of vitamin K1 daily from 36 weeks of pregnancy onward. Concentrations of PIVKA-II (protein induced by vitamin K absence for factor II) and of vitamin K1 were determined in cord blood and compared with those in 20 controls.

Results: In none of 17 cord samples was PIVKA-II detectable, compared with 13 of 20 in controls (chi 2, p < 0.001). Median cord vitamin K1 level was 530 pg/ml compared with below detection limit in most controls.

Conclusions: Antenatal vitamin K1 treatment decreases the frequency of vitamin K deficiency in neonates of mothers on anticonvulsant therapy.

Publication types

  • Clinical Trial
  • Multicenter Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anticonvulsants / adverse effects
  • Anticonvulsants / therapeutic use*
  • Biomarkers*
  • Case-Control Studies
  • Epilepsy / drug therapy
  • Female
  • Fetal Blood / metabolism
  • Humans
  • Infant, Newborn
  • Pregnancy
  • Pregnancy Complications / drug therapy
  • Prenatal Exposure Delayed Effects
  • Protein Precursors / metabolism
  • Prothrombin / metabolism
  • Reference Values
  • Vitamin K / administration & dosage
  • Vitamin K / blood
  • Vitamin K / therapeutic use*
  • Vitamin K Deficiency / chemically induced
  • Vitamin K Deficiency / prevention & control*


  • Anticonvulsants
  • Biomarkers
  • Protein Precursors
  • Vitamin K
  • acarboxyprothrombin
  • Prothrombin