NAT2基因型和肼嗪治疗临床药物遗传学实施联合指南。

IF 5.5 2区 医学 Q1 PHARMACOLOGY & PHARMACY
Michael T Eadon, David W Hein, Michael A Andersen, Arlene B Chapman, Rhonda M Cooper-DeHoff, Zeruesenay Desta, Julio D Duarte, Amanda L Elchynski, Andrea Gaedigk, Seth E Karol, Nita A Limdi, Christelle Lteif, Laura Sosinski, Pablo Zubiaur, Michelle Whirl-Carrillo, Teri E Klein, Kelly E Caudle, Roseann S Donnelly, José A G Agúndez
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引用次数: 0

摘要

Hydralazine是一种血管扩张剂,通常用于治疗顽固性高血压和心力衰竭。n -乙酰转移酶2 (NAT2)催化肼代谢成无活性代谢产物。与NAT2快速和中间代谢者(分别称为“快速乙酰化者”和“中间乙酰化者”)相比,NAT2代谢不良者(历史上称为“慢乙酰化者”)的血浆肼浓度预计会增加,这可能导致临床疗效和不良反应的增加,包括药物引起的系统性红斑狼疮。本指南总结了与NAT2/肼嗪相关的文献证据,并根据NAT2基因型预测的乙酰化表型提供了肼嗪处方的建议(更新于www.cpicpgx.org)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Clinical Pharmacogenetics Implementation Consortium Guideline for NAT2 Genotype and Hydralazine Therapy.

Hydralazine is a vasodilator typically used in the treatment of resistant hypertension and heart failure. N-acetyltransferase 2 (NAT2) catalyzes the metabolism of hydralazine into inactive metabolites. NAT2 poor metabolizers (historically referred to as "slow acetylators") are predicted to have increased plasma hydralazine concentrations compared with NAT2 rapid and intermediate metabolizers (historically referred to as "rapid acetylators" and "intermediate acetylators," respectively), which may lead to both increased clinical efficacy and adverse effects, including drug-induced systemic lupus erythematosus. This guideline summarizes the evidence from the literature relevant to NAT2/hydralazine and provides recommendations for hydralazine prescribing based on NAT2 genotype-predicted acetylator phenotype (updates at www.cpicpgx.org).

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来源期刊
CiteScore
12.70
自引率
7.50%
发文量
290
审稿时长
2 months
期刊介绍: Clinical Pharmacology & Therapeutics (CPT) is the authoritative cross-disciplinary journal in experimental and clinical medicine devoted to publishing advances in the nature, action, efficacy, and evaluation of therapeutics. CPT welcomes original Articles in the emerging areas of translational, predictive and personalized medicine; new therapeutic modalities including gene and cell therapies; pharmacogenomics, proteomics and metabolomics; bioinformation and applied systems biology complementing areas of pharmacokinetics and pharmacodynamics, human investigation and clinical trials, pharmacovigilence, pharmacoepidemiology, pharmacometrics, and population pharmacology.
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