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Updated: Jun 25, 2026

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A Multicenter MRI Protocol for the Evaluation and Quantification of Deep Vein Thrombosis
Published on: June 2, 2015
Factor V Leiden with deep venous thrombosis
1Wake Forest University School of Medicine, Winston-Salem, NC, USA. jgardner@wfubmc.edu
Summary
Factor V Leiden (FVL) is a common genetic mutation increasing thrombotic event risk. This condition impairs blood clotting but has a lower risk of pulmonary embolism compared to other clotting disorders.
Area of Science:
- Genetics
- Hematology
- Molecular Biology
Background:
- Factor V Leiden (FVL) is an inherited thrombophilia.
- It is caused by an Arg506-->Gly substitution in the Factor V gene.
- FVL affects approximately 5% of the Caucasian population.
Observation:
- The FVL mutation alters the activated protein C cleavage site on Factor V.
- This leads to impaired anticoagulant function.
- No procoagulant modification is observed.
Findings:
- Heterozygous FVL carriers have a seven-fold increased risk of thrombotic events.
- Homozygous FVL carriers face a 50 to 100-fold increased risk.
- Individuals with FVL have an elevated risk for deep venous thrombosis.
Implications:
- FVL significantly increases the risk of venous thromboembolism.
- Despite increased DVT risk, the risk of pulmonary embolism is relatively lower than in other coagulopathies.
- Understanding FVL is crucial for managing thrombotic risk in affected individuals.
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