Hypercoagulability is a less frequent but important contributor to thrombosis.
Primary causes of hypercoagulability are genetic.
Mutations in the factor V gene (the Leiden mutation) affect 2-15% of Caucasians. The mutation promotes resistance to protein C-mediated inactivation. This leads to increased Va presence.
Heterozygotes have a 7x increase of DVT, a 35x risk with the BCP, and a 50x increase with homozygotes.
Among patients with recurrent deep vein thrombosis, carrier frequency can approach 60%.
A single nucleotide change in the prothrombin is present in 1-2% of the population and is associated with an almost 3x risk of venous thrombosis.
Elevated levels of homocysteine contribute to arterial and venous thrombosis, as well as the development of atherosclerosis, likely due to inhibition of antithrombin III and endothelial thrombomodulin. Elevated homocysteine levels may also increase ROS levels, causing endothelial damage.
Increased homocysteine levels can result from genetic mutations, as well as
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