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Fatal liver complications with flutamide.

作者信息

Osculati Antonio, Castiglioni Claudia

出版信息

Lancet. 2006 Apr 8;367(9517):1140-1. doi: 10.1016/S0140-6736(06)68498-5.

DOI:10.1016/S0140-6736(06)68498-5
PMID:16616550
Abstract
摘要

相似文献

1
Fatal liver complications with flutamide.氟他胺导致的致命性肝脏并发症。
Lancet. 2006 Apr 8;367(9517):1140-1. doi: 10.1016/S0140-6736(06)68498-5.
2
[Fulminant hepatitis associated with treatment with flutamide].
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3
[Hepatotoxicity from flutamide].
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[Toxic hepatitis caused by flutamide and hirsutism].
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[Acute flutamide-induced hepatitis].
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6
[Acute cholestatic hepatitis secondary to flutamide].
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Involvement of Th2 cytokines in the mouse model of flutamide-induced acute liver injury.Th2 细胞因子在氟他胺诱导的急性肝损伤小鼠模型中的作用。
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Hepatotoxicity with flutamide.氟他胺引起的肝毒性。
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9
[Hirsutism, flutamide and hepatotoxicity].[多毛症、氟他胺与肝毒性]
Gastroenterol Hepatol. 2001 Apr;24(4):218. doi: 10.1016/s0210-5705(01)70153-7.
10
Fulminant liver failure associated with flutamide therapy for hirsutism.
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Selenium and Glutathione-Depleted Rats as a Sensitive Animal Model to Predict Drug-Induced Liver Injury in Humans.硒和谷胱甘肽耗竭大鼠作为一种敏感的动物模型预测药物性肝损伤。
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Flutamide Induces Hepatic Cell Death and Mitochondrial Dysfunction via Inhibition of Nrf2-Mediated Heme Oxygenase-1.氟他胺通过抑制 Nrf2 介导的血红素加氧酶-1 诱导肝实质细胞死亡和线粒体功能障碍。
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The expression, induction and pharmacological activity of CYP1A2 are post-transcriptionally regulated by microRNA hsa-miR-132-5p.
细胞色素P450 1A2(CYP1A2)的表达、诱导及药理活性受到微小RNA hsa-miR-132-5p的转录后调控。
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The antiandrogen flutamide is a novel aryl hydrocarbon receptor ligand that disrupts bile acid homeostasis in mice through induction of Abcc4.抗雄激素氟他胺是一种新型芳烃受体配体,可通过诱导Abcc4破坏小鼠体内胆汁酸稳态。
Biochem Pharmacol. 2016 Nov 1;119:93-104. doi: 10.1016/j.bcp.2016.08.021. Epub 2016 Aug 26.
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Comparison of in vitro bioactivation of flutamide and its cyano analogue: evidence for reductive activation by human NADPH:cytochrome P450 reductase.氟他胺及其氰基类似物的体外生物活化比较:人NADPH:细胞色素P450还原酶还原活化的证据。
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Low-dose flutamide for women with androgen excess: anti-androgenic efficacy and hepatic safety.
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