标题：Prolonged induction of warfarin metabolism and a paradoxical INR response in a mitral valve replacement patient receiving rifampicin for infective endocarditis
摘要：Case Report Rifampicin induces multiple detoxification pathways, including those mediated by enzymes of the cytochrome P450 (CYP) family such as CYP2C9 and CYP3A4 [1], and is a known perpetrator of metabolic drug-drug interactions (mDDIs). Warfarin is a narrow therapeutic index anti-coagulant drug that is primarily cleared via CYP-mediated metabolism, and as such is a plausible victim of mDDIs with clinically relevant consequences. S-warfarin is primarily cleared by CYP2C9 while R-warfarin is exclusively cleared by CYP3A4 [2]. S-warfarin is 3-5 times more active than R-warfarin and is primarily responsible for the observed anticoagulant activity. While mDDIs involving rifampicin and warfarin have been reported [3-10], the appropriate schedule for warfarin dose reduction post cessation of rifampicin remains poorly defined and patients are at risk of both bleeding and thrombotic events during this period.
