CYP2C9, SLCO1B1, SLCO1B3, and ABCB11 Polymorphisms in Patients With Bosentan-Induced Liver Toxicity

被引:13
|
作者
Roustit, M. [1 ,2 ]
Fonrose, X. [3 ]
Montani, D. [4 ,5 ]
Girerd, B. [4 ,5 ]
Stanke-Labesque, F. [2 ,3 ]
Gonnet, N. [2 ]
Humbert, M. [4 ,5 ]
Cracowski, J-L [1 ,2 ]
机构
[1] Univ Grenoble Alpes, INSERM UMR HP2 1042, Grenoble, France
[2] Grenoble Univ Hosp, Clin Pharmacol Unit, INSERM CIC1406, Grenoble, France
[3] Grenoble Univ Hosp, Lab Pharmacol, Grenoble, France
[4] Univ Paris Sud, AP HP, Ctr Natl Reference Hypertens Pulm Severe,DHU, Thorax Innovat TORINO,Hop Bicetre,Serv Pneumol, F-94275 Le Kremlin Bicetre, France
[5] Ctr Chirurg Marie Lannelongue, LabEx LERMIT, INSERM UMRS 999, Le Plessis Robinson, France
关键词
MECHANISM; INHIBITION; EXPORT;
D O I
10.1038/clpt.2014.42
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Bosentan is an endothelin receptor antagonist used as a first-line treatment in pulmonary arterial hypertension (PAH). Its main adverse effect is a dose-dependent liver toxicity. CYP2C9*2 has recently been shown to be associated with hepatotoxicity in PAH patients. We conducted a nested case-control study to further explore the relationship between functional polymorphisms of gene products involved in bosentan pharmacokinetics (OATP1B1, OATP1B3, and CYP2C9) or hepatobiliary transporters affected by bosentan (ABCB11) and bosentan-induced liver toxicity.
引用
收藏
页码:583 / 585
页数:3
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