Theuretzbacher Ursula, Ihle Franziska, Derendorf Hartmut
Center for Anti-Infective Agents, Vienna, Austria.
Clin Pharmacokinet. 2006;45(7):649-63. doi: 10.2165/00003088-200645070-00002.
Voriconazole is the first available second-generation triazole with potent activity against a broad spectrum of clinically significant fungal pathogens, including Aspergillus,Candida, Cryptococcus neoformans, and some less common moulds. Voriconazole is rapidly absorbed within 2 hours after oral administration and the oral bioavailability is over 90%, thus allowing switching between oral and intravenous formulations when clinically appropriate. Voriconazole shows nonlinear pharmacokinetics due to its capacity-limited elimination, and its pharmacokinetics are therefore dependent upon the administered dose. With increasing dose, voriconazole shows a superproportional increase in area under the plasma concentration-time curve (AUC). In doses used in children (age < 12 years) voriconazole pharmacokinetics appear to be linear. Steady-state plasma concentrations are reached approximately 5 days after both intravenous and oral administration; however, steady state is reached within 24 hours with voriconazole administered as an intravenous loading dose. The volume of distribution of voriconazole is 2-4.6 L/kg, suggesting extensive distribution into extracellular and intracellular compartments. Voriconazole was measured in tissue samples of brain, liver, kidney, heart, lung as well as cerebrospinal fluid. The plasma protein binding is about 60% and independent of dose or plasma concentrations. Clearance is hepatic via N-oxidation by the hepatic cytochrome P450 (CYP) isoenzymes, CYP2C19, CYP2C9 and CYP3A4. The elimination half-life of voriconazole is approximately 6 hours, and approximately 80% of the total dose is recovered in the urine, almost completely as metabolites. As with other azole drugs, the potential for drug interactions is considerable. Voriconazole shows time-dependent fungistatic activity against Candida species and time-dependent slow fungicidal activity against Aspergillus species. A short post-antifungal effect of voriconazole is evident only for Aspergillus species. The predictive pharmacokinetic/pharmacodynamic parameter for voriconazole treatment efficacy in Candida infections is the free drug AUC from 0 to 24 hour : minimum inhibitory concentration ratio.
伏立康唑是首个可用的第二代三唑类药物,对包括曲霉属、念珠菌属、新型隐球菌及一些较罕见霉菌在内的多种临床上重要的真菌病原体具有强大活性。伏立康唑口服给药后2小时内迅速吸收,口服生物利用度超过90%,因此在临床适当时可在口服和静脉制剂之间转换。由于其消除存在容量限制,伏立康唑呈现非线性药代动力学,其药代动力学因此取决于给药剂量。随着剂量增加,伏立康唑血浆浓度-时间曲线下面积(AUC)呈超比例增加。在儿童(年龄<12岁)使用的剂量下,伏立康唑的药代动力学似乎呈线性。静脉和口服给药后约5天达到稳态血浆浓度;然而,以静脉负荷剂量给药时,伏立康唑在24小时内达到稳态。伏立康唑的分布容积为2 - 4.6 L/kg,表明其广泛分布于细胞外和细胞内 compartments。在脑、肝、肾、心、肺组织样本以及脑脊液中均检测到伏立康唑。血浆蛋白结合率约为60%,且与剂量或血浆浓度无关。清除通过肝脏细胞色素P450(CYP)同工酶CYP2C19、CYP2C9和CYP3A4进行N - 氧化,经肝脏代谢。伏立康唑的消除半衰期约为6小时,约80%的总剂量在尿液中回收,几乎全部以代谢物形式存在。与其他唑类药物一样,药物相互作用的可能性很大。伏立康唑对念珠菌属呈现时间依赖性抑菌活性,对曲霉属呈现时间依赖性缓慢杀菌活性。伏立康唑仅对曲霉属具有明显的短抗真菌后效应。伏立康唑治疗念珠菌感染疗效的预测性药代动力学/药效学参数是0至24小时的游离药物AUC与最低抑菌浓度之比。