Venous thromboembolism in a patient with persistent inhibitor to coagulation factor V – a case report

2016 ◽  
Vol 54 (9) ◽  
pp. e269-e271 ◽  
Author(s):  
Peter Rief ◽  
Gerald Hackl ◽  
Franz Hafner ◽  
Reinhard Bernd Raggam ◽  
Albert Wölfler ◽  
...  
2004 ◽  
pp. 259-263 ◽  
Author(s):  
S Moverare ◽  
S Skrtic ◽  
MK Lindberg ◽  
K Dahlman-Wright ◽  
C Ohlsson

OBJECTIVES: Both oral estrogen-based hormone-replacement therapy and contraceptives increase the risk of venous thromboembolism. Several circulating factors involved in coagulation/fibrinolysis are expressed mainly in the liver whilst some are expressed in extrahepatic tissues, including bone marrow. The aim of this study was to identify estrogen-responsive target genes involved in the pathogenesis of estrogen-induced venous thromboembolism. METHODS: Ovariectomized mice were treated with 17beta-estradiol and possible effects on the expression of genes related to coagulation/fibrinolysis were investigated using DNA microarray analyses. RESULTS: None of the selected genes was regulated by 17beta-estradiol in the liver. Interestingly, 17beta-estradiol increased mRNA levels of coagulation factor V in the bone marrow/bone. Furthermore, this stimulatory effect of 17beta-estradiol on coagulation factor V expression can be mediated via both estrogen receptor-alpha and -beta. CONCLUSIONS: The expression of bone marrow-derived, but not liver-derived, coagulation factor V is increased by estrogen treatment in mice. The pathophysiological importance of this finding for estrogen-induced venous thromboembolism remains to be determined.


2021 ◽  
pp. 100058
Author(s):  
Hideo Wada ◽  
Akitada Ichinose ◽  
Katsuya Shiraki ◽  
Hideto Shimpo ◽  
Motomu Shimaoka

1999 ◽  
Vol 81 (05) ◽  
pp. 684-689 ◽  
Author(s):  
Sam Schulman ◽  
Margareta Sten-Linder ◽  
Björn Wiman ◽  
Nils Egberg ◽  
Hans Johnsson ◽  
...  

SummaryThe results concerning the risk of recurrent venous thromboembolism (VTE) in carriers of the G1691A mutation in the coagulation factor V gene are not consistent and this risk in carriers of the G20210A polymorphism in the prothrombin gene has hitherto not been reported. We followed 534 patients for 48 months after their first episode of objectively documented VTE. The prevalence of the G1691A allele in 467 (87.5%) of the patients and in 207 controls was 25.3% and 8.2%, respectively, in heterozygote form and 2.4% and 0.5%, respectively, in homozygote form. The adjusted odds ratio (OR) for the first VTE was 4.4 (95% CI 2.6-7.8). The risk of recurrent VTE in heterozygotes was not statistically different from non-carriers (17.8% vs 17.6%), with 85% power to detect a hazard ratio of 2.35. Homozygotes had a significantly increased risk (p = 0.036) of recurrent VTE. The prevalence of the G20210A allele in 456 patients and 207 controls was 6.1% and 1.4%, respectively. The adjusted OR was 4.6 (95% CI 1.6-19.3) for the first VTE in 28 carriers of this polymorphism. The risk of recurrent VTE for these was not statistically different from non-carriers with an OR of 0.9 (95% CI 0.2-2.9).


Haemophilia ◽  
2010 ◽  
Vol 17 (1) ◽  
pp. 168-170 ◽  
Author(s):  
H. SHANMUGAM ◽  
S. JAYARANEE ◽  
G. I. EOW

1998 ◽  
Vol 80 (08) ◽  
pp. 344-345 ◽  
Author(s):  
Pasra Arnutti ◽  
Motofumi Hiyoshi ◽  
Wichai Prayoonwiwat ◽  
Oytip Nathalang ◽  
Chamaiporn Suwanasophon ◽  
...  

1996 ◽  
Vol 75 (02) ◽  
pp. 267-269 ◽  
Author(s):  
H Engel ◽  
L Zwang ◽  
H H D M van Vliet ◽  
J J Michiles ◽  
J Stibbe ◽  
...  

SummaryThe currently used activated Protein C resistance test demonstrated to be of limited diagnostic value for the detection of the mutant Factor V Leiden. Moreover, this assay is not useful for patients under anticoagulant therapy. A modification of the APC resistance test, applying Factor V deficient plasma is described which demonstrates a specificity and sensitivity of 1.0. The superiority of the modified APC resistance test over the existing APC resistance test was verified by genotyping.For that purpose, the Amplification Refractory Mutation System (ARMS) was applied to the detection of the G to A mutation at position 1691 in the gene encoding coagulation Factor V. The mutation at that position could be easily detected by using each of two allele-specific oligonucleotide primers concomitantly with one common primer in two separate polymerase chain reactions, thereby amplifying a fragment of 186 base-pairs of the Factor V gene.


1997 ◽  
Vol 78 (01) ◽  
pp. 427-433 ◽  
Author(s):  
Jan Rosing ◽  
Guido Tans

1982 ◽  
Vol 257 (8) ◽  
pp. 4557-4563
Author(s):  
G P Tuszynski ◽  
P N Walsh ◽  
J R Piperno ◽  
A Koshy

1982 ◽  
Vol 257 (11) ◽  
pp. 6556-6564 ◽  
Author(s):  
K Suzuki ◽  
B Dahlbäck ◽  
J Stenflo

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