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[Impact of pharmacogenetics on interindividual variability in the response to vitamin K antagonist therapy]
1Service d'hématologie-hémostase, Inserm U765, faculté des sciences pharmaceutiques et biologiques, université Paris-Descartes (Paris-V), France. virginie.siguret@cfx.aphp.fr
Abstract:
Vitamin K antagonists (VKA) are difficult to use because of a narrow therapeutic index and of a marked inter- and intra individual variability among patients in the required dosage. Beside well known demographic or environmental factors (advanced age, co-morbid conditions, acute illnesses, concomitant drugs, vitamin K intake), genetic single nucleotide polymorphisms (SNPs) have been identified as strongly affecting the maintenance dosage and its variability. First, SNPs of vitamin K epoxide reductase complex subunit-1 (VKORC1) gene have been identified, affecting the enzyme shown as one of the target of VKA. Secondly, SNPs of cytochrome P450 2C9 (CYP2C9) gene have been shown to decrease the catabolism of coumarin derivatives (acenocoumarol, warfarin). Several recent studies have shown that being carrier of at least one mutated allele of either VKORC1 or CYP2C9 (CYP2C9*2, CYP2C9*3) allele is associated with a hypersensitivity to VKA therapy, i.e. a lower maintenance dose. Moreover, it has been associated with an increased risk of over-anticoagulation, a longer time to achieve the maintenance dose and an increased risk of bleeding. Finally, the combined analysis of VKORC1 and CYP2C9 SNPs with age may account for more than 50% of the individual variability of the warfarin maintenance dosage. Predicting models of warfarin maintenance dosage taking into account these individual parameters are currently developed.
Insights
Genetic factors, including VKORC1 and CYP2C9 gene variants, significantly impact Vitamin K antagonist (VKA) dosage. Understanding these genetic variations can improve VKA therapy and reduce bleeding risks.
Area of Science:
- Pharmacogenomics
- Clinical Pharmacology
- Internal Medicine
Background:
- Vitamin K antagonists (VKA) present challenges due to narrow therapeutic index and patient-specific dosage variability.
- Factors influencing VKA dosage include demographics, environment, and genetic single nucleotide polymorphisms (SNPs).
Purpose of the Study:
- To investigate the impact of VKORC1 and CYP2C9 gene SNPs on VKA maintenance dosage and variability.
- To assess the association between these genetic variants and VKA therapy outcomes, including hypersensitivity and bleeding risk.
Main Methods:
- Analysis of SNPs in the vitamin K epoxide reductase complex subunit-1 (VKORC1) gene.
- Evaluation of SNPs in the cytochrome P450 2C9 (CYP2C9) gene, affecting coumarin derivative metabolism.
- Review of recent studies linking VKORC1/CYP2C9 variants to VKA response.
Main Results:
- VKORC1 and CYP2C9 gene SNPs are strongly associated with VKA maintenance dosage and its variability.
- Carriers of mutated VKORC1 or CYP2C9 alleles (*2, *3) exhibit VKA hypersensitivity, requiring lower doses.
- These genetic factors increase the risk of over-anticoagulation, prolong time to maintenance dose, and elevate bleeding risk.
Conclusions:
- VKORC1 and CYP2C9 gene polymorphisms are key determinants of VKA response.
- Combined analysis of VKORC1, CYP2C9 SNPs, and age explains over 50% of warfarin dosage variability.
- Development of predictive models incorporating these individual parameters is ongoing to optimize VKA therapy.
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