## BACKGROUND. Thromboembolic events are well recognized complications of can-
Activated protein C resistance and the factor V Leiden mutation in children with thrombosis
โ Scribed by Sifontes, Maria T.; Nuss, Rachelle; Hunger, Stephen P.; Waters, Jill; Jacobson, Linda J.; Manco-Johnson, Marilyn
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 22 KB
- Volume
- 57
- Category
- Article
- ISSN
- 0361-8609
No coin nor oath required. For personal study only.
โฆ Synopsis
To determine the prevalence of activated protein C resistance and the factor V Leiden mutation (position 1691, arginine 506 to glutamine substitution) in children with thrombosis, plasma samples from children with thrombosis were tested for activated protein C resistance. DNA was analyzed for the factor V Leiden mutation. Five of 34 children (15%) had activated protein C resistance; each was heterozygous for the factor V Leiden mutation. All 5 children heterozygous for the factor V Leiden mutation suffered non-CNS venous thromboses comprising 21% of the group of children (5/24) with non-CNS venous thrombotic events. Each of these 5 children had a family history of thrombosis. In conclusion, children with non-CNS venous thrombosis should be evaluated for the factor V Leiden mutation. Children most likely affected are those with a family history of thrombosis.
๐ SIMILAR VOLUMES
The factor V Leiden mutation in 12-children with thrombosis and in 20 controls was investigated. Five heterozygous individuals and 1 homozygous individual among the cases with thrombosis and 1 heterozygous individual among controls were found. Central nervous system thromboses were increased in chil
## Objective: To test a possible association between activated protein C resistance and intrauterine fetal death. Methods: The activated protein C anticoagulant activity and factor V R506Q mutation were assessed in 14 nonpregnant women with a history of intrauterine fetal death and 14 healthy cont
Four hundred and ninety-three consecutive patients referred for arterial or venous thrombosis were screened for congenital and acquired abnormalities of blood coagulation predisposing to thrombosis, and were compared to 341 age-and sex-matched controls. The aim of the study was to determine the prev
Hereditary predisposition to thrombosis due to activated protein C resistance (APCR) has been attributed to a missense mutation in the factor V gene at nucleotide 1691 (G to A), causing replacement of arginine at codon 506 with glutamine. Using an RFLP-PCR assay to detect this mutation, we measured