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 fa
Tamoxifen-associated venous thrombosis and activated protein C resistance due to factor V leiden
โ Scribed by Ilene C. Weitz; Valerie K. Israel; Howard A. Liebman
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 65 KB
- Volume
- 79
- Category
- Article
- ISSN
- 0008-543X
No coin nor oath required. For personal study only.
โฆ Synopsis
BACKGROUND.
Thromboembolic events are well recognized complications of can-
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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
## 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
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
To the Editor: Hb S (โค6 Glu-Val), Hb D Los Angeles (โค121 Glu-Gln) and Hb O Arab (โค121 Glu-Lys) are the most common variants in Turkish population including Turkish Cypriots [1,2]. Either during screening of the population or to enlighten the reason of anemia; several abnormal hemoglobin variants can