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Introduction: Apixaban and rivaroxaban, two oral direct factor Xa inhibitors DOACs , have become an alternative to vitamin K antagonists because of their ease of use. Methods: This real-life observational study included and hospitalized patients treated with apixaban or rivaroxaban, respectively. CYP3A and P-gp phenotypic activities were assessed with the Geneva cocktail administered orally on the day of the study. CYP3A and P-gp genetic polymorphisms were also measured. Results: Substantial interindividual variability was observed in dose-normalized blood concentrations and AUC of apixaban Log10 AUCfexofenadine reflecting P-gp activity AUCfexofenadine per log10 CYP3A phenotype and SNPs tested had no significant impact on the pharmacokinetics of both molecules of both molecules.
Conclusion: Our study demonstrated the significant impact of P-gp activity on apixaban and rivaroxaban blood concentrations, which could have a clinically relevant impact on drug response. Introduction: Fluoropyrimidines are commonly used in the treatment of cancer.
Prospective genotyping for four genetic variants c. However, substantial fluoropyrimidines-induced toxicity remains, which might be attributed to rare deleterious variants in DPYD. Objectives: In this retrospective analysis of a large prospective study clinicaltrial.
Variants were considered deleterious if predicted so by at least one tool. For toxicity analysis, a matched-pair analysis was performed in which, for each deleterious variant carrier, three matched DPYD wild-type patients were identified based on three clinical criteria, including treatment regimens, tumor type, and disease stage. Results: In the 1, patients included in the primary analysis, 24 non-synonymous genetic variants in DPYD were found. Of these, a total of 7 variants was defined as deleterious.