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The use of oral anticoagulation is marked by an elevated risk of adverse drug events (ADE) due to a narrow therapeutic window leading to important medical and economical consequences. The risk of ADE is increased partly by drug interactions and recently identified genetic factors influencing the metabolism of coumarins (polymorphism of the cytochrome P450 CYP2C9) as well as the target enzyme of the coumarins (polymorphism of the vitamin K epoxide reductase complex subunit 1 (VKORC1).
The objective is to determine the impact of several genotypes on acenocoumarol treatment and on vulnerability to drug-drug interactions.
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