The Perspectives in the Management for Warfarin m Resistance and Toxicity Associated with Vitamin K Epoxide Reductase Dysfunction - Juniper Publishers

JUNIPER PUBLISHERS- OPEN ACCESS JOURNAL OF TOXICOLOGY

The Perspectives in the Management for Warfarin m Resistance and Toxicity Associated with Vitamin K Epoxide Reductase Dysfunction


Authored by Ahmed Abdul-Sabour Bader


Abstract
Anticoagulant therapy is being increasingly used the treatment and prevention of thromboembolic events, and warfarin remains the most frequently used agent for longterm anticoagulation in all patient groups. Warfarin, one of oral anticoagulant drugs that exerting its anticoagulant effect by inhibiting the enzyme vitamin K epoxide reductase (VKORC1), thereby preventing vitamin K recycling and vitamin K-dependent carboxylation of the coagulation factors II, VII, IX, and X; where the carboxylation is very critical for biosynthesis of these blood clotting factors leading to a marked decrease in blood coagulation process. Anticoagulation response to a fixed dose of warfarin is notoriously difficult to predict because of interindividual variability in dose requirement. This, together with the drug’s narrow therapeutic window, necessitates maintenance of anticoagulation status within a tight therapeutic range facilitated by frequent international normalized ratio (INR) monitoring to ensure the efficacy and safety of therapy.

Warfarin resistance may develop as a result of noncompliance, exogenous consumption of vitamin K, and concurrent ingestion of other agents known to decrease warfarin’s effects. Unfortunately, an increasing number of genetic variations of enzyme vitamin K epoxide reductase affecting warfarin pharmacodynamics and/or pharmacokinetics were found to have a major impact on the warfarin dose in adults that had been found to produce detrimental harmful effects on body due to either over coagulation or under coagulation (resistance) to its therapeutic action. These genetic variations are found in single nucleotide polymorphisms (SNPs) in VKORC1 that leading to loss of VKORC1 sensitivity to warfarin; making it difficult or impossible to adequately lower vitamin K levels.

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