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Genetic polymorphism of factor V (Leiden) and factor II (Prothrombin) is of no importance for warfarin anticoagulation therapy dose optimizing

Warfarin is an anticoagulant therapy drug often associated with unwanted side effects such as serious bleeding. Drug therapy optimization includes careful titration to avoid the risk of bleeding. The warfarin anticoagulation effect is monitored by the prothrombin time (PT) over therapy period. It is known that PT is influenced by coagulation factor II and factor V activity. The aim of our study was to test if genetic polymorphism within these genes is of importance for optimized warfarin therapy dose differences. We genotyped 181 patients by the use of commercial LightCycler Mutation Detection Kit for the presence of G1691A factor V (Leiden) and G20210A (factor II) mutations. Genotype between factor V patients did not differ significantly from our previous results for healthy controls (N=121). Genotype frequencies for wild type homozygous patients were 92.3% and heterozygotes 7.7% compared to 92.7% and 7.3% in controls, respectively (P=0.900). Similarly, genotype between factor II patients did also not differ from controls for wild type (96.7% homozygous, and 3.3% heterozygous) compared to 98.2% and 1.8% among controls, respectively (P=0.614). Results for factor V influence on warfarin dose showed no significant difference between warfarin median daily doses between wild type homozygous compared to heterozygous genotype (4, 0mg compared to 4, 33mg, respectively ; P=0.338). Warfarin median daily dose between factor II wild type homozygous compared to heterozygous genotype also did not differ significantly (4.15mg compared to 4.25mg, respectively ; P=0.855). Results of our investigation, suggest that genetic polymorphism of coagulation factors V and II are of no importance in optimizing warfarin anticoagulant drug therapy.

warfarin; factor II; factor V; genetic polymorphism; drug therapy optimization; side effects

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