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.
Study Type
OBSERVATIONAL
Enrollment
115
University Hospitals
Geneva, Switzerland
Time to achieve stable dosing in days, since the beginning of the anticoagulation
Time frame: 5 weeks
Number of patients with INR > or = 4.0, which indicates overanticoagulation
Time frame: 5 weeks
Time to achieve two consecutive therapeutic INRs
Time frame: 5 weeks
Mean daily dosage of acenocoumarol
Time frame: 5 weeks
Major bleedings and minor bleedings
Time frame: 5 weeks
Thromboembolic events due to infratherapeutic anticoagulation
Time frame: 5 weeks
Length of hospitalisation in days
Time frame: 5 weeks
Potential of other drug interactions, linked to the observed genotype and phenotype of the patient
Time frame: 5 weeks
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