Association Between CYP2C9 Genetic Variants and Anticoagulation-Related Outcomes During Warfarin Therapy

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Abstract
Warfarin is an anticoagulant agent used for the prevention of thromboembolic events in patients with chronic conditions such as atrial fibrillation, and is prescribed to more than 1 million patients in the United States annually.1 Because warfarin has a narrow therapeutic range and may increase the risk of bleeding events, therapy is individualized by monitoring the prothrombin time international normalized ratio (INR), a measure of anticoagulation status. The management of warfarin therapy is challenging because of variability in patient response due to a multitude of factors including drug, diet, and disease-state interactions.1 In addition, genetic variation of the hepatic microsomal enzyme CYP2C9, the activity of which constitutes the primary pathway for the metabolism of S-warfarin, may lead to significant differences in patient response to warfarin.