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本文引用的文献

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The need to shift pharmacogenetic research from candidate gene to genome-wide association studies.需要将药物遗传学研究从候选基因转移到全基因组关联研究。
Pharmacogenomics. 2021 Nov;22(17):1143-1150. doi: 10.2217/pgs-2021-0108. Epub 2021 Oct 5.
2
Evaluation of gene validity for CPVT and short QT syndrome in sudden arrhythmic death.评估 CPVT 和短 QT 综合征基因在心律失常性猝死中的有效性。
Eur Heart J. 2022 Apr 14;43(15):1500-1510. doi: 10.1093/eurheartj/ehab687.
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Moving Pharmacogenetics Into Practice: It's All About the Evidence!将药物遗传学付诸实践：关键在于证据！
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The mutational constraint spectrum quantified from variation in 141,456 humans.从 141456 名人类个体的变异中量化的突变约束谱。
Nature. 2020 May;581(7809):434-443. doi: 10.1038/s41586-020-2308-7. Epub 2020 May 27.
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An International, Multicentered, Evidence-Based Reappraisal of Genes Reported to Cause Congenital Long QT Syndrome.一项国际性、多中心、基于证据的对报道引起先天性长 QT 综合征的基因的重新评估。
Circulation. 2020 Feb 11;141(6):418-428. doi: 10.1161/CIRCULATIONAHA.119.043132. Epub 2020 Jan 27.
6
Characterization of the CACNA1C-R518C Missense Mutation in the Pathobiology of Long-QT Syndrome Using Human Induced Pluripotent Stem Cell Cardiomyocytes Shows Action Potential Prolongation and L-Type Calcium Channel Perturbation.使用人诱导多能干细胞心肌细胞对长 QT 综合征的病理生物学中 CACNA1C-R518C 错义突变的特征分析显示动作电位延长和 L 型钙通道扰动。
Circ Genom Precis Med. 2019 Aug;12(8):e002534. doi: 10.1161/CIRCGEN.119.002534. Epub 2019 Aug 20.
7
Genetic susceptibility in pharmacodynamic and pharmacokinetic pathways underlying drug-induced arrhythmia and sudden unexplained deaths.药物致心律失常和不明原因猝死相关的药效动力学和药代动力学途径中的遗传易感性。
Forensic Sci Int Genet. 2019 Sep;42:203-212. doi: 10.1016/j.fsigen.2019.07.010. Epub 2019 Jul 18.
8
Citalopram and the KCNE1 D85N variant: a case report on the implications of a genetic modifier.西酞普兰与KCNE1 D85N变体：关于一种基因修饰剂影响的病例报告
Eur Heart J Case Rep. 2018 Sep 26;2(4):yty106. doi: 10.1093/ehjcr/yty106. eCollection 2018 Dec.
9
A current understanding of drug-induced QT prolongation and its implications for anticancer therapy.当前对药物引起的 QT 间期延长及其对癌症治疗的影响的理解。
Cardiovasc Res. 2019 Apr 15;115(5):895-903. doi: 10.1093/cvr/cvz013.
10
Corrected QT Interval Prolongation in Psychopharmacological Treatment and Its Modulation by Genetic Variation.精神药理学治疗中的校正 QT 间期延长及其遗传变异的调节。
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药物引起的 QT 间期延长的遗传学：评估药效动力学变异的证据。

The genetics of drug-induced QT prolongation: evaluating the evidence for pharmacodynamic variants.

机构信息

Department of Clinical Pharmacy, University of Michigan College of Pharmacy, Ann Arbor, MI 48109, USA.

Division of Cardiovascular Medicine, Hospital of the University of Pennsylvania, Philadelphia, PA 19104, USA.

出版信息

Pharmacogenomics. 2022 Jun;23(9):543-557. doi: 10.2217/pgs-2022-0027. Epub 2022 Jun 14.

DOI:10.2217/pgs-2022-0027
PMID:35698903
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9245591/
Abstract

Drug-induced long QT syndrome (diLQTS) is an adverse effect of many commonly prescribed drugs, and it can increase the risk for lethal ventricular arrhythmias. Genetic variants in pharmacodynamic genes have been associated with diLQTS, but the strength of the evidence for each of those variants has not yet been evaluated. Therefore, the purpose of this review was to evaluate the strength of the evidence for pharmacodynamic genetic variants associated with diLQTS using a novel, semiquantitative scoring system modified from the approach used for congenital LQTS. D85N and -T8A had definitive and strong evidence for diLQTS, respectively. The high level of evidence for these variants supports current consideration as risk factors for patients that will be prescribed a QT-prolonging drug.

摘要

药物引起的长 QT 综合征（diLQTS）是许多常用药物的不良反应，可增加致命性室性心律失常的风险。药效基因的遗传变异与 diLQTS 相关，但尚未评估每种变异的证据强度。因此，本综述的目的是使用改良自先天性长 QT 综合征的方法的新型半定量评分系统评估与 diLQTS 相关的药效遗传变异的证据强度。D85N 和 -T8A 分别与 diLQTS 具有明确和强有力的证据。这些变异的高证据水平支持目前将其视为将开处 QT 延长药物的患者的危险因素的考虑。