Increased incidence of neonatal vitamin K deficiency resulting from maternal anticonvulsant therapy

Am J Obstet Gynecol. 1993 Mar;168(3 Pt 1):923-8. doi: 10.1016/s0002-9378(12)90846-7.

Abstract

Objective: The null hypothesis of our study is that the incidence of vitamin K deficiency in mother-infant pairs exposed to anticonvulsant drugs is not higher than in controls.

Study design: In this multicenter observational case-control study, 25 pregnant women receiving anticonvulsant therapy and 25 pregnant controls were studied for PIVKA-II (protein induced by vitamin K absence of factor II) and vitamin K1 concentrations at 32 weeks' gestation and at delivery.

Results: PIVKA-II was detectable in 54% of cord samples of the anticonvulsant group and in 20% of controls (chi 2, p = 0.01). In both groups vitamin K1 cord blood levels were predominantly below the detection limit. Maternal vitamin K1 concentrations were lower in women with epilepsy than in controls (Wilcoxon's rank sum test, p < 0.05), but PIVKA-II was rarely present.

Conclusions: The incidence of vitamin K deficiency is increased in neonates exposed to anticonvulsant drugs prenatally. Their mothers, however, are rarely vitamin K deficient.

Publication types

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

MeSH terms

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

Substances

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