Role of the factor V Leiden mutation in septic peritonitis assessed in factor V Leiden transgenic mice*

2006 ◽  
Vol 34 (8) ◽  
pp. 2201-2206 ◽  
Author(s):  
Lois W. Brüggemann ◽  
Saskia H. H. F. Schoenmakers ◽  
Angelique P. Groot ◽  
Pieter H. Reitsma ◽  
C Arnold Spek
Keyword(s):  
Transgenic Mice ◽  
Factor V Leiden ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Septic Peritonitis

Role of Factor V Leiden Mutation in Patients with Angiographically Demonstrated Coronary Artery Disease

1998 ◽  
Vol 91 (2) ◽  
pp. 91-99 ◽  
Author(s):  
S.Terence Dunn ◽  
Courtney R. Roberts ◽  
Eliot Schechter ◽  
William E. Moore ◽  
Elisa T. Lee ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Factor V Leiden ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Artery Disease

Evaluation of Role of Factor V Leiden Mutation in Fatal Pulmonary Thromboembolism

1998 ◽  
Vol 91 (1) ◽  
pp. 7-14 ◽  
Author(s):  
S.Terence Dunn ◽  
Stephan Trong
Keyword(s):  
Pulmonary Thromboembolism ◽  
Factor V Leiden ◽  
Factor V ◽  
Factor V Leiden Mutation

Umbilical venous catheterization and development of Banti syndrome: the possible role of the factor V Leiden mutation

1998 ◽  
Vol 157 (8) ◽  
pp. 696-696
Author(s):  
J. Stankovics ◽  
�gnes Nagy ◽  
K. M�hes ◽  
B. Melegh
Keyword(s):  
Factor V Leiden ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Venous Catheterization

scholarly journals The Role of the Factor V Leiden Mutation in Osteonecrosis of the Hip

2012 ◽  
Vol 19 (5) ◽  
pp. 499-503 ◽  
Author(s):  
Charles J. Glueck ◽  
Richard A. Freiberg ◽  
Gail Boriel ◽  
Zia Khan ◽  
Amanpreet Brar ◽  
...  
Keyword(s):  
Factor V Leiden ◽  
Factor V ◽  
Factor V Leiden Mutation

scholarly journals The prognostic role of thrombophilia in the treatment of infertility

2018 ◽  
Vol 91 (1) ◽  
pp. 42-49
Author(s):  
Túrós János Levente ◽  
Kiss Szilárd-Leó ◽  
Bereczky Lujza-Katalin ◽  
Bartha Edina ◽  
Lészai Lehel ◽  
...  
Keyword(s):  
Assisted Reproduction ◽  
Recurrent Miscarriage ◽  
Factor V Leiden ◽  
Heterozygous Mutation ◽  
Coagulation Disorder ◽  
Homozygous Mutation ◽  
Factor V ◽  
Prognostic Role ◽  
Factor V Leiden Mutation

Abstract Thrombophilia refers to a coagulation disorder that predisposes to thrombosis and thus increases the risk of thrombotic events. Both inherited and acquired thrombophilia are associated with vascular thrombosis and pregnancy-related complications, including infertility, recurrent miscarriage, and premature birth. Recently, thrombophilia has been increasingly encountered as an infertility factor, which gives the clinical relevance of the disease. The aim of the study was to investigate the prognostic role of thrombophilia in the treatment of infertility and the pregnancy of thrombophilic women during assisted reproduction procedures. Frequency of abortions increases and effectiveness of in vitro fertilization (IVF) decreases with age. Normal weight has a positive effect on assisted reproduction techniques (ART’s) outcome. Repeat IVF failure is more common in thrombophilia than in healthy women, and the “take home baby” ratio for IVF is 24%. Spontaneous abortion was most commonly observed in the PAI homozygous group followed by MTHFR homozygous mutation, MTHFR heterozygous mutation, and Factor V (Leiden) mutation. The most effective treatment was concomitant therapy with low molecular weight heparin and aspirin.

Thrombophilia and risk of VTE recurrence according to the age at the time of first VTE manifestation

VASA ◽  
2015 ◽  
Vol 44 (4) ◽  
pp. 313-323 ◽  
Author(s):  
Lea Weingarz ◽  
Marc Schindewolf ◽  
Jan Schwonberg ◽  
Carola Hecking ◽  
Zsuzsanna Wolf ◽  
...  
Keyword(s):  
Factor V Leiden ◽  
Cox Proportional Hazards ◽  
First Episode ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Younger Patients ◽  
Risk Of Recurrence ◽  
G20210a Mutation ◽  
Increased Risk ◽  
The Impact

Abstract. Background: Whether screening for thrombophilia is useful for patients after a first episode of venous thromboembolism (VTE) is a controversial issue. However, the impact of thrombophilia on the risk of recurrence may vary depending on the patient’s age at the time of the first VTE. Patients and methods: Of 1221 VTE patients (42 % males) registered in the MAISTHRO (MAin-ISar-THROmbosis) registry, 261 experienced VTE recurrence during a 5-year follow-up after the discontinuation of anticoagulant therapy. Results: Thrombophilia was more common among patients with VTE recurrence than those without (58.6 % vs. 50.3 %; p = 0.017). Stratifying patients by the age at the time of their initial VTE, Cox proportional hazards analyses adjusted for age, sex and the presence or absence of established risk factors revealed a heterozygous prothrombin (PT) G20210A mutation (hazard ratio (HR) 2.65; 95 %-confidence interval (CI) 1.71 - 4.12; p < 0.001), homozygosity/double heterozygosity for the factor V Leiden and/or PT mutation (HR 2.35; 95 %-CI 1.09 - 5.07, p = 0.030), and an antithrombin deficiency (HR 2.12; 95 %-CI 1.12 - 4.10; p = 0.021) to predict recurrent VTE in patients aged 40 years or older, whereas lupus anticoagulants (HR 3.05; 95%-CI 1.40 - 6.66; p = 0.005) increased the risk of recurrence in younger patients. Subgroup analyses revealed an increased risk of recurrence for a heterozygous factor V Leiden mutation only in young females without hormonal treatment whereas the predictive value of a heterozygous PT mutation was restricted to males over the age of 40 years. Conclusions: Our data do not support a preference of younger patients for thrombophilia testing after a first venous thromboembolic event.

Coagulation Factor V Leiden Mutation Was Detected in the Patients with Activated Protein C Resistance in Thailand

1998 ◽  
Vol 80 (08) ◽  
pp. 344-345 ◽  
Author(s):  
Pasra Arnutti ◽  
Motofumi Hiyoshi ◽  
Wichai Prayoonwiwat ◽  
Oytip Nathalang ◽  
Chamaiporn Suwanasophon ◽  
...  
Keyword(s):  
Protein C ◽  
Activated Protein C ◽  
Factor V Leiden ◽  
Coagulation Factor ◽  
Factor V ◽  
Activated Protein C Resistance ◽  
Factor V Leiden Mutation ◽  
Coagulation Factor V

High Frequency of Factor V Leiden Mutation and Prothrombin 20210A Variant in Romanies of Eastern Hungary

1999 ◽  
Vol 82 (11) ◽  
pp. 1555-1556 ◽  
Author(s):  
R. Póka ◽  
G. Losonczy ◽  
L. Muszbek ◽  
I. Balogh
Keyword(s):  
High Frequency ◽  
Factor V Leiden ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
Prothrombin 20210A

Low Prevalence of the Factor V Leiden Mutation Among “Severe” Hemophiliacs with a “Milder” Bleeding Diathesis

1995 ◽  
Vol 74 (05) ◽  
pp. 1255-1258 ◽  
Author(s):  
Arnaldo A Arbini ◽  
Pier Mannuccio Mannucci ◽  
Kenneth A Bauer
Keyword(s):  
Hemophilia A ◽  
Factor V Leiden ◽  
Protein S ◽  
Factor Ix ◽  
Hemophilia B ◽  
Factor V ◽  
Bleeding Diathesis ◽  
Mutation Site ◽  
Spontaneous Bleeding ◽  
Factor V Leiden Mutation

SummaryPatients with hemophilia A and B and factor levels less than 1 percent of normal bleed frequently with an average number of spontaneous bleeding episodes of 20–30 or more. However there are patients with equally low levels of factor VIII or factor IX who bleed once or twice per year or not at all. To examine whether the presence of a hereditary defect predisposing to hypercoagulability might play a role in amelio rating the hemorrhagic tendency in these so-called “mild severe” hemophiliacs, we determined the prevalence of prothrombotic defects in 17 patients with hemophilia A and four patients with hemophilia B selected from 295 and 76 individuals with these disorders, respectively, followed at a large Italian hemophilia center. We tested for the presence of the Factor V Leiden mutation by PCR-amplifying a fragment of the factor V gene which contains the mutation site and then digesting the product with the restriction enzyme Mnll. None of the patients with hemophilia A and only one patient with hemophilia B was heterozygous for Factor V Leiden. None of the 21 patients had hereditary deficiencies of antithrombin III, protein C, or protein S. Our results indicate that the milder bleeding diathesis that is occasionally seen among Italian hemophiliacs with factor levels that are less than 1 percent cannot be explained by the concomitant expression of a known prothrombotic defect.

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