Key result
Carriers of the CYP2C9*3 allele had a lower chance of achieving stability in the first 6 months of acenocoumarol therapy compared with wild-type subjects (HR 0.62; 95% CI 0.42-0.91; P<.05).
Why the study?
Does the presence of CYP2C9*3 or CYP2C9*2 alleles increase anticoagulation problems and delay stabilization during the initial 6 months of acenocoumarol treatment compared to wild-type?
Population
231 subjects starting acenocoumarol treatment with a standard dose regimen at 2 anticoagulation clinics in…
Comparison
Presence of CYP2C9*3 or CYP2C9*2 allele vs Wild-type CYP2C9*1/*1 genotype
Design
Cohort
Follow-up
6 months
Authors
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CYP2C9*3 carriers may need closer early monitoring on acenocoumarol; leaves open whether genotyping improves outcomes.
Cohort (n=231)
Yes
Does the presence of CYP2C9*3 or CYP2C9*2 alleles increase anticoagulation problems and delay stabilization during the initial 6 months of acenocoumarol treatment compared to wild-type?
Effect estimate: HR 0.62 (95% CI 0.42-0.91)
p-value: p=<.05
CYP2C9*3 carriers starting acenocoumarol have delayed stabilization and a higher risk of severe overanticoagulation compared to wild-type subjects.
Tom Schalekamp (2004) conducted a cohort in Patients starting acenocoumarol treatment (n=231). CYP2C9*3 carrier status vs. Wild-type subjects (CYP2C9*1/*1) was evaluated on Chance to achieve stability in the first 6 months of therapy (HR 0.62, 95% CI 0.42-0.91, p=<.05). Carriers of the CYP2C9*3 allele had a lower chance of achieving stability in the first 6 months of acenocoumarol therapy compared with wild-type subjects (HR 0.62; 95% CI 0.42-0.91; P<.05).
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