The factor V G1691A (factor V Leiden, FVL) and factor II G20210A gain-of-function
mutations are the most frequent forms of inherited thrombophilia [
1
,
2
]. However, considering their prevalence in the healthy Caucasian population (3–10%
depending on the region), the increase in thromboembolic risk is merely 3–5 times
that of non-carriers and the large majority of carriers will not suffer any thromboembolic
event [
1
,
3
]. Therefore, screening for the presence of FVL and G20210A is controversial, particularly
in patients without a strong personal or familial history of thrombosis and those
in whom the results would not have therapeutic implications.Keywords
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References
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- Mortality and causes of death in families with the factor V Leiden mutation (resistance to activated protein C).Blood. 1997; 89: 1963-1967
- Antithrombotic therapy for VTE disease: CHEST guideline and expert panel report.Chest. 2016; 149: 315-352https://doi.org/10.1016/j.chest.2015.11.026
- Influence of hereditary or acquired thrombophilias on the treatment of venous thromboembolism.Curr Opin Hematol. 2012; 19: 363-370https://doi.org/10.1097/MOH.0b013e328356745b
Article info
Publication history
Published online: February 24, 2017
Accepted:
February 21,
2017
Received:
February 16,
2017
Identification
Copyright
© 2017 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.