[1] |
中华人民共和国国家卫生和计划生育委员会. 国家卫生计生委医政医管局关于印发《药物代谢酶和药物作用靶点基因检测技术指南((试行)》和《肿瘤个体化治疗检测技术指南(试行)》的通知. 国卫医医护便函〔2015〕240号. 2015-07-29.
|
[2] |
刘诚诚, 金海霞, 徐建, 等. 结核病患者N-乙酰基转移酶2基因型与异烟肼血药浓度关系的研究. 中国防痨杂志, 2013, 35(3):179-182.
|
[3] |
Chen B, Cai W, Li J, et al. Estimating N-acetyltransferase metabolic activity and pharmacokinetic parameters of isoniazid from genotypes in Chinese subjects. Clin Chim Acta, 2009, 405(1/2):23-29. doi: 10.1016/j.cca.2009.03.045.
doi: 10.1016/j.cca.2009.03.045
|
[4] |
Huang YS. Recent progress in genetic variation and risk of antituberculosis drug-induced liver injury. J Chin Med Assoc, 2014, 77(4):169-173. doi: 10.1016/j.jcma.2014.01.010.
doi: 10.1016/j.jcma.2014.01.010
|
[5] |
Chen B, Li JH, Xu YM, et al. The influence of NAT2 genotypes on the plasma concentration of isoniazid and acetylisoniazid in Chinese pulmonary tuberculosis patients. Clin Chim Acta, 2006, 365(1/2):104-108. doi: 10.1016/j.cca.2005.08.012.
doi: 10.1016/j.cca.2005.08.012
|
[6] |
Chen B, Cao X, Li J. Gene dose effect of NAT2 variants on the pharmacokinetics of isoniazid and acetylisoniazid in healthy Chinese subjects. Drug Metabol Drug Interact, 2011, 26(3):113-118. doi: 10.1515/DMDI.2011.016.
doi: 10.1515/DMDI.2011.016
|
[7] |
Hong BL, D’Cunha R, Li P, et al. A Systematic Review and Meta-analysis of Isoniazid Pharmacokinetics in Healthy Volunteers and Patients with Tuberculosis. Clin Ther, 2020, 42(11):e220-e241. doi: 10.1016/j.clinthera.2020.09.009.
doi: 10.1016/j.clinthera.2020.09.009
|
[8] |
Jing W, Zong Z, Tang B, et al. Population Pharmacokinetic Analysis of Isoniazid among Pulmonary Tuberculosis Patients from China. Antimicrob Agents Chemother, 2020, 64(3):e01736-19. doi: 10.1128/AAC.01736-19.
doi: 10.1128/AAC.01736-19
|
[9] |
Fredj NB, Romdhane HB, Woillard JB, et al. Population pharmacokinetic model of isoniazid in patients with tuberculosis in Tunisia. Int J Infect Dis, 2021, 104:562-567. doi: 10.1016/j.ijid.2021.01.033.
doi: 10.1016/j.ijid.2021.01.033
|
[10] |
Donald PR, Sirgel FA, Venter A, et al. The influence of human N-acetyltransferase genotype on the early bactericidal activity of isoniazid. Clin Infect Dis, 2004, 39(10):1425-1430. doi: 10.1086/424999.
doi: 10.1086/424999
|
[11] |
Fukino K, Sasaki Y, Hirai S, et al. Effects of N-acetyltransferase 2 (NAT2), CYP2E1 and Glutathione-S-transferase (GST) genotypes on the serum concentrations of isoniazid and metabolites in tuberculosis patients. J Toxicol Sci, 2008, 33(2):187-195. doi: 10.2131/jts.33.187.
doi: 10.2131/jts.33.187
|
[12] |
Ohno M, Yamaguchi I, Yamamoto I, et al. Slow N-acetyltransferase 2 genotype affects the incidence of isoniazid and rifampicin-induced hepatotoxicity. Int J Tuberc Lung Dis, 2000, 4(3):256-261.
|
[13] |
Hiratsuka M, Kishikawa Y, Takekuma Y, et al. Genotyping of the N-acetyltransferase2 polymorphism in the prediction of adverse drug reactions to isoniazid in Japanese patients. Drug Metab Pharmacokinet, 2002, 17(4):357-362. doi: 10.2133/dmpk.17.357.
doi: 10.2133/dmpk.17.357
|
[14] |
Huang YS, Chern HD, Su WJ, et al. Polymorphism of the N-acetyltransferase 2 gene as a susceptibility risk factor for antituberculosis drug-induced hepatitis. Hepatology, 2002, 35(4):883-889. doi: 10.1053/jhep.2002.32102.
doi: 10.1053/jhep.2002.32102
|
[15] |
Cai Y, Yi J, Zhou C, et al. Pharmacogenetic study of drug-metabolising enzyme polymorphisms on the risk of anti-tuberculosis drug-induced liver injury: a meta-analysis. PLoS One, 2012, 7(10):e47769. doi: 10.1371/journal.pone.0047769.
doi: 10.1371/journal.pone.0047769
|
[16] |
Du H, Chen X, Fang Y, et al. Slow N-acetyltransferase 2 genotype contributes to anti-tuberculosis drug-induced hepatotoxicity: a meta-analysis. Mol Biol Rep, 2013, 40(5):3591-3596. doi: 10.1007/s11033-012-2433-y.
doi: 10.1007/s11033-012-2433-y
|
[17] |
Yuliwulandari R, Prayuni K, Susilowati RW, et al. NAT2 slow acetylator is associated with anti-tuberculosis drug-induced liver injury severity in indonesian population. Pharmacogenomics, 2019, 20(18):1303-1311. doi: 10.2217/pgs-2019-0131.
doi: 10.2217/pgs-2019-0131
|
[18] |
Zhang D, Hao J, Hou R, et al. The role of NAT2 polymorphism and methylation in anti-tuberculosis drug-induced liver injury in Mongolian tuberculosis patients. J Clin Pharm Ther, 2020, 45(3):561-569. doi: 10.1111/jcpt.13097.
doi: 10.1111/jcpt.13097
|
[19] |
Azuma J, Ohno M, Kubota R, et al. NAT2 genotype guided regimen reduces isoniazid-induced liver injury and early treatment failure in the 6-month four-drug standard treatment of tuberculosis: a randomized controlled trial for pharmacogenetics-based therapy. Eur J Clin Pharmacol, 2013, 69(5):1091-1101. doi: 10.1007/s00228-012-1429-9.
doi: 10.1007/s00228-012-1429-9
|
[20] |
Donald PR, Parkin DP, Seifart HI, et al. The influence of dose and N-acetyltransferase-2 (NAT2) genotype and phenotype on the pharmacokinetics and pharmacodynamics of isoniazid. Eur J Clin Pharmacol, 2007, 63(7):633-639. doi: 10.1007/s00228-007-0305-5.
doi: 10.1007/s00228-007-0305-5
|
[21] |
Kubota R, Ohno M, Hasunuma T, et al. Dose-escalation study of isoniazid in healthy volunteers with the rapid acetylator genotype of arylamine N-acetyltransferase 2. Eur J Clin Pharmacol, 2007, 63(10):927-933. doi: 10.1007/s00228-007-0333-1.
doi: 10.1007/s00228-007-0333-1
|
[22] |
Kinzig-Schippers M, Tomalik-Scharte D, Jetter A, et al. Should we use N-acetyltransferase type 2 genotyping to personalize isoniazid doses? Antimicrob Agents Chemother, 2005, 49(5):1733-1738. doi: 10.1128/AAC.49.5.1733-1738.2005.
doi: 10.1128/AAC.49.5.1733-1738.2005
|
[23] |
Huerta-García AP, Medellín-Garibay SE, Ortiz-Álvarez A, et al. Population pharmacokinetics of isoniazid and dose recommendations in Mexican patients with tuberculosis. Int J Clin Pharm, 2020, 42(4):1217-1226. doi: 10.1007/s11096-020-01086-1.
doi: 10.1007/s11096-020-01086-1
|
[24] |
Hu Y, Chen S, Yu X, et al. Rapid identification of the NAT2 genotype in tuberculosis patients by multicolor melting curve analysis. Pharmacogenomics, 2016, 17(11):1211-1218. doi: 10.2217/pgs-2016-0026.
doi: 10.2217/pgs-2016-0026
|