Factor V Leiden and genetic defects of thrombophilia in childhood porencephaly

Arch Dis Child Fetal Neonatal Ed. 1998 Mar;78(2):F121-4. doi: 10.1136/fn.78.2.f121.

Abstract

Aims: To determine to what extent the Arg506 to Gln point mutation in the factor V gene and further genetic factors of thrombophilia affect the risk of porencephaly in neonates and infants.

Methods: The Arg506 to Gln mutation, factor V, protein C, protein S, antithrombin, antiphospholipid antibodies and lipoprotein (a) (Lp(a)) were retrospectively measured in neonates and children with porencephaly (n = 24).

Results: Genetic risk factors for thrombophilia were diagnosed in 16 of these 24 patients: heterozygous factor V Leiden (n = 3); protein C deficiency type I (n = 6); increased Lp (a) (n = 3); and protein S type I deficiency (n = 1). Three of the 16 infants had two genetic risk factors of thrombophilia: factor V Leiden mutation combined with increased familial Lp (a) was found in two, and factor V Leiden mutation with protein S deficiency type I in one.

Conclusions: The findings indicate that deficiencies in the protein C anticoagulant pathway have an important role in the aetiology of congenital porencephaly.

MeSH terms

  • Adolescent
  • Brain Diseases / blood
  • Brain Diseases / embryology*
  • Brain Diseases / genetics*
  • Child
  • Child, Preschool
  • Cysts / blood
  • Cysts / embryology*
  • Cysts / genetics*
  • Factor V / genetics*
  • Female
  • Humans
  • Infant
  • Infant, Newborn
  • Lipoprotein(a) / blood
  • Magnetic Resonance Imaging
  • Male
  • Point Mutation*
  • Protein C Deficiency
  • Protein S Deficiency / genetics
  • Retrospective Studies
  • Risk Factors
  • Thrombophilia / genetics*

Substances

  • Lipoprotein(a)
  • factor V Leiden
  • Factor V