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A Multicenter MRI Protocol for the Evaluation and Quantification of Deep Vein Thrombosis
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Factor V Leiden with deep venous thrombosis.

Jeff Gardner1

  • 1Wake Forest University School of Medicine, Winston-Salem, NC, USA. jgardner@wfubmc.edu

Clinical Laboratory Science : Journal of the American Society for Medical Technology
|February 18, 2003
PubMed
Summary
This summary is machine-generated.

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.

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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.