Thromboembolic Diseases
Conditions
Brief summary
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.
Interventions
None listed
Sponsors
University Hospital, Geneva
Study design
Time perspective
PROSPECTIVE
Eligibility
Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No
Inclusion criteria
* Every patients with requiring acenocoumarol therapy for at least 4 weeks and a target INR in the low intensity range (INR range 2-3) * Age ≥ 18 years * Signed informed consent
Exclusion criteria
* Severe cognitive impairment * Previous or current treatment with any coumarin
Design outcomes
Primary
| Measure | Time frame |
|---|---|
| Time to achieve stable dosing in days, since the beginning of the anticoagulation | 5 weeks |
Secondary
| Measure | Time frame |
|---|---|
| Time to achieve two consecutive therapeutic INRs | 5 weeks |
| Mean daily dosage of acenocoumarol | 5 weeks |
| Major bleedings and minor bleedings | 5 weeks |
| Number of patients with INR > or = 4.0, which indicates overanticoagulation | 5 weeks |
| Length of hospitalisation in days | 5 weeks |
| Potential of other drug interactions, linked to the observed genotype and phenotype of the patient | 5 weeks |
| Thromboembolic events due to infratherapeutic anticoagulation | 5 weeks |
Countries
Switzerland
Outcome results
None listed