Fluconazole but not itraconazole decreases the metabolism of losartan to E-3174
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Objective: Losartan is metabolised to its active metabolite E-3174 by CYP2C9 and CYP3A4 in vitro. Itraconazole is an inhibitor of CYP3A4, whereas ̄uconazole aects CYP2C9 more than CYP3A4. We wanted to study the possible interaction of these antimycotics with losartan in healthy volunteers. Methods: A randomised, double-blind, three-phase crossover study design was used. Eleven healthy volunteers ingested orally, once a day for 4 days, either itraconazole 200 mg, ̄uconazole (400 mg on day 1 and 200 mg on days 2±4) or placebo (control). On day 4, a single 50-mg oral dose of losartan was ingested. Plasma concentrations of losartan, E-3174, itraconazole, hydroxy-itraconazole and ̄uconazole were determined over 24 h. The blood pressure and heart rate were also recorded over 24 h. Results: The mean peak plasma concentration (Cmax) and area under the curve [AUC
0±1] of E-3174 were signi®cantly decreased by ̄uconazole to 30% and to 47% of their control values, respectively, and the t1/2 was increased to 167%. Fluconazole caused only a nonsigni®cant increase (23±41%) in the AUC and t1/2 of the unchanged losartan. Itraconazole had no signi®cant eect on the pharmacokinetic variables of losartan or E-3174. The ratio AUC
0±1)E-3174/AUC
0±1losartan was 60% smaller during the ̄uconazole than during the placebo and itraconazole phases. No clinically signi®cant changes in the eects of losartan on blood pressure and heart rate were observed between ̄uconazole, itraconazole and placebo phases. Conclusion: Fluconazole but not itraconazole interacts with losartan by inhibiting its metabolism to the active metabolite E-3174. This implicates that, in man, CYP2C9 is a major enzyme for the formation of E-3174 from losartan. The clinical signi®cance of the ̄uconazole±losartan interaction is unclear, but the possibility of a decreased therapeutic eect of losartan should be kept in mind.