APC resistance in neonates and infants: adjustment of the APTT-based method

Thromb Res. 1996 Mar 15;81(6):665-70. doi: 10.1016/0049-3848(96)00043-6.


Resistance to activated protein C (APCR) has emerged as the most important hereditary cause of venous thromboembolism. Using an aPTT-based method together with DNA technique we investigated 120 healthy neonates and infants < 12 months of age and 24 infants with septicaemia for the presence of this mutation. In addition, data of 11 neonates with vascular occlusion, heterozygous (+/-) for the Arg 506 Gln mutation were included. Results of an aPTT-based method (clotting time using the APC/CaCl2 solution obtained in an undiluted, 1:5 and 1:11 dilution with factor V deficient plasma divided by clotting time with CaCl2 in the same plasma dilution) are shown: Whereas 7 (5.5%) out of 120 healthy neonates were (+/-) carriers for the factor V Arg 506 Gln mutation, concordance with the aPTT-based method (cut-off defined as ratio < 2) was found only when using the 1:11 plasma dilution. Six (four) out of 24 infants with sepsis, not carrying the factor V mutation, would have been classified as APC resistant when using the 1:1 (1:5) plasma dilution. Four (two) out of 18 patients, (+/-) for the Arg 506 Gln mutation showed APC ratios > 2 in the 1:1(1:5) plasma dilution.

MeSH terms

  • Case-Control Studies
  • Drug Resistance
  • Humans
  • Infant
  • Infant, Newborn
  • Mutation
  • Partial Thromboplastin Time
  • Protein C / pharmacology*
  • Sepsis / blood*
  • Thromboembolism / blood
  • Thromboembolism / genetics*


  • Protein C