International Journal of Clinical Case Reports 2024, Vol.14, No.1, 55-62 http://medscipublisher.com/index.php/ijccr 60 Figure 3 Transcriptional regulation of CYP2D6 expression For rapid metabolizers, higher doses of antidepressant medications may be necessary to achieve efficacy because the drugs are rapidly metabolized in their bodies. In contrast, slow metabolizers may require lower drug doses to avoid potential drug toxicity. Therefore, understanding the patient's CYP2D6 genotype can assist doctors in better selecting appropriate antidepressant medications and determining the right dosage. Furthermore, CYP2D6 gene polymorphism can also impact the adverse reactions of drugs. Rapid metabolizers may be more prone to experiencing adverse drug reactions due to higher drug concentrations in their bodies. In contrast, slow metabolizers may encounter fewer adverse reactions during drug therapy. 3.2 CYP2C9 and VKORC1 gene polymorphisms and their impact on warfarin therapy CYP2C9 and VKORC1 gene polymorphisms have profound implications for warfarin treatment. These two genes play crucial roles in the metabolism and mechanism of action of warfarin (Figure 4). The genetic makeup of individual patients determines their rate of warfarin metabolism and sensitivity to the drug, directly influencing the therapeutic efficacy and safety of warfarin. Figure 4 Warfarin molecule CYP2C9 is a cytochrome P450 enzyme involved in the metabolism of warfarin. The CYP2C9 gene exhibits polymorphism, where different alleles encode varying enzyme activities. Individuals with alleles associated with lower CYP2C9 activity typically metabolize warfarin more slowly, requiring lower drug doses to achieve anticoagulation effects. Conversely, individuals with alleles linked to higher CYP2C9 activity usually require higher warfarin doses. VKORC1 is the subunit 1 of the vitamin K epoxide reductase complex, serving as the target for warfarin action. VKORC1 gene polymorphism affects the sensitivity of warfarin towards VKORC1. Individuals with a sensitive
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