[1] |
石富国, 古明, 马世平. 一线主要抗结核药不良反应分布特点文献分析. 中国药物警戒, 2011,8(7):434-437.
|
[2] |
陈羽, 刘映, 王静, 等. 抗结核病药物治疗老年肺结核的不良反应及影响因素. 中国老年学杂志, 2015,35(8):2079-2081. doi: 10.3969/j.issn.1005-9202.2015.08.032.
|
[3] |
张明媛, 雷建平, 闫世明, 等. 抗结核药物所致肝损伤及肝病患者抗结核药物治疗——大陆地区诊治建议与台湾《结核病诊治指引》相关介绍. 临床肝胆病杂志, 2015,31(11):1776-1781. doi: 10.3969/j.issn. 1001-5256.2015.11.004.
|
[4] |
尤媛媛, 任鹏飞, 陈永芳. 初治肺结核患者抗结核治疗所致药物性肝损伤的危险因素. 河南医学研究, 2020,29(7):1173-1176. doi: 10.3969/j.issn.1004-437X.2020.07.008.
|
[5] |
蒋博峰, 马晨晨, 陈阳贵, 等. 抗结核药物不良反应发生率及其影响因素分析. 中华疾病控制杂志, 2017,21(2):160-163. doi: 10.16462/j.cnki.zhjbkz.2017.02.013.
|
[6] |
言洁, 曹毅敏. 抗结核药物不良反应发生率及危险因素分析. 北方药学, 2017,14(12):177-178. doi: 10.3969/j.issn.1672-8351.2017.12.144.
|
[7] |
邵海峰. 抗结核病药物治疗老年肺结核的不良反应及影响因素研究. 实用中西医结合临床, 2017,17(7):157-158. doi: 10.13638/j.issn.1671-4040.2017.07.102.
|
[8] |
Wu S, Wang YJ, Tang X, et al. Genetic Polymorphisms of Glutathione S-Transferase P1 (GSTP1) and the Incidence of Anti-Tuberculosis Drug-Induced Hepatotoxicity. PLoS One, 2016,11(6):e0157478. doi: 10.1371/journal.pone.0157478.
|
[9] |
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.
|
[10] |
Henderson CJ, Wolf CR. Disruption of the glutathione transferase pi class genes. Methods Enzymol, 2005,401:116-135. doi: 10.1016/S0076-6879(05)01007-4.
|
[11] |
Zhang M, Wu SQ, He JQ. Are genetic variations in glutathione S-transferases involved in anti-tuberculosis drug-induced liver injury? A meta-analysis. J Clin Pharm Ther, 2019,44(6):844-857. doi: 10.1111/jcpt.13006.
|
[12] |
Wang YM, Chai SC, Brewer CT, et al. Pregnane X receptor and drug-induced liver injury. Expert Opin Drug Metab Toxicol, 2014,10(11):1521-1532. doi: 10.1517/17425255.2014.963555.
|
[13] |
Yang M, Pan H, Chen H, et al. Association between NR1I2 polymorphisms and susceptibility to anti-tuberculosis drug-induced hepatotoxicity in an Eastern Chinese Han population: A case-control study. Infect Genet Evol, 2020,83:104349. doi: 10.1016/j.meegid.2020.104349.
|
[14] |
Wang Y, Xiang X, Huang WW, et al. Association of PXR and CAR Polymorphisms and Antituberculosis Drug-Induced Hepatotoxicity. Sci Rep, 2019,9(1):2217. doi: 10.1038/s41598-018-38452-z.
|
[15] |
Zhang J, Zhao Z, Bai H, et al. Genetic polymorphisms in PXR and NF-κB1 influence susceptibility to anti-tuberculosis drug-induced liver injury. PLoS One, 2019,14(9):e0222033. doi: 10.1371/journal.pone.0222033.
|
[16] |
Santos EA, Gonçalves JCS, Fleury MK, et al. Relationship of anti-tuberculosis drug-induced liver injury and genetic polymorphisms in CYP2E1 and GST. Braz J Infect Dis, 2019,23(6):381-387. doi: 10.1016/j.bjid.2019.09.003.
|
[17] |
Chen R, Wang J, Zhang Y, et al. Key factors of susceptibility to anti-tuberculosis drug-induced hepatotoxicity. Arch Toxicol, 2015,89(6):883-897. doi: 10.1007/s00204-015-1473-1.
|
[18] |
Jaswal A, Sharma M, Raghuvanshi S, et al. Therapeutic Efficacy of Nigella Sativa Linn. against Antituberculosis Drug-Induced Hepatic Injury in Wistar Rats. J Environ Pathol Toxicol Oncol, 2016,35(1):59-71. doi: 10.1615/JEnvironPatholToxicolOncol.2016013789.
|
[19] |
Verma AK, Yadav A, Singh SV, et al. Corrigendum to “Isoniazid induces apoptosis: Role of oxidative stress and inhibition of nuclear translocation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2)” [Life Sci 119 (2018) 23-33]. Life Sci, 2020,240:117136. doi: 10.1016/j.lfs.2019.117136.
|
[20] |
Yew WW, Chang KC, Chan DP. Oxidative Stress and First-Line Antituberculosis Drug-Induced Hepatotoxicity. Antimicrob Agents Chemother, 2018,62(8):e02637-17. doi: 10.1128/AAC.02637-17.
|
[21] |
Yang M, Zhang H, Tao B, et al. Possible association of HMOX1 and NQO1 polymorphisms with anti-tuberculosis drug-induced liver injury: A matched case-control study. J Clin Pharm Ther, 2019,44(4):534-542. doi: 10.1111/jcpt.12818.
|
[22] |
Chan SL, Chua APG, Aminkeng F, et al. Association and clinical utility of NAT2 in the prediction of isoniazid-induced liver injury in Singaporean patients. PLoS One, 2017,12(10):e0186200. doi: 10.1371/journal.pone.0186200.
|
[23] |
Lu L, Tao B, Wei H, et al. Relevance of NAT2 genotype to anti-tuberculosis drug-induced hepatotoxicity in a Chinese Han population. J Gene Med, 2019,21(6):e3096. doi: 10.1002/jgm.3096.
|
[24] |
Guaoua S, Ratbi I, El Bouazzi O, et al. NAT2 Genotypes in Moroccan Patients with Hepatotoxicity Due to Antituberculosis Drugs. Genet Test Mol Biomarkers, 2016,20(11):680-684. doi: 10.1089/gtmb.2016.0060.
|
[25] |
Khan S, Mandal RK, Elasbali AM, et al. Pharmacogenetic association between NAT2 gene polymorphisms and isoniazid induced hepatotoxicity: trial sequence meta-analysis as evidence. Biosci Rep, 2019,39(1):BSR20180845. doi: 10.1042/BSR20180845.
|
[26] |
Zhang M, Wang S, Wilffert B, et al. The association between the NAT2 genetic polymorphisms and risk of DILI during anti-TB treatment: a systematic review and meta-analysis. Br J Clin Pharmacol, 2018,84(12):2747-2760. doi: 10.1111/bcp.13722.
|
[27] |
Li Y, Tang H, Qi H, et al. rs1800796 of the IL6 gene is associated with increased risk for anti-tuberculosis drug-induced hepatotoxicity in Chinese Han children. Tuberculosis (Edinb), 2018,111:71-77. doi: 10.1016/j.tube.2018.05.011.
|
[28] |
Chen R, Wang J, Tang SW, et al. CYP7A1, BAAT and UGT1A1 polymorphisms and susceptibility to anti-tuberculosis drug-induced hepatotoxicity. Int J Tuberc Lung Dis, 2016,20(6):812-818. doi: 10.5588/ijtld.15.0450.
|
[29] |
Benoit-Biancamano MO, Adam JP, Bernard O, et al. A pharmacogenetics study of the human glucuronosyltransferase UGT1A4. Pharmacogenet Genomics, 2009,19(12):945-954. doi: 10.1097/FPC.0b013e3283331637.
|
[30] |
Sun Q, Liu HP, Zheng RJ, et al. Genetic Polymorphisms of SLCO1B1, CYP2E1 and UGT1A1 and Susceptibility to Anti-Tuberculosis Drug-Induced Hepatotoxicity: A Chinese Population-Based Prospective Case-Control Study. Clin Drug Investig, 2017,37(12):1125-1136. doi: 10.1007/s40261-017-0572-6.
|
[31] |
Huang YS, Chern HD, Su WJ, et al. Cytochrome P450 2E1 genotype and the susceptibility to antituberculosis drug-induced hepatitis. Hepatology, 2003,37(4):924-930. doi: 10.1053/jhep.2003.50144.
|
[32] |
Zhou SF, Liu JP, Chowbay B. Polymorphism of human cytochrome P450 enzymes and its clinical impact. Drug Metab Rev, 2009,41(2):89-295. doi: 10.1080/03602530902843483.
|
[33] |
Bose PD, Sarma MP, Medhi S, et al. Role of polymorphic N-acetyl transferase2 and cytochrome P4502E1 gene in antituberculosis treatment-induced hepatitis. J Gastroenterol Hepatol, 2011,26(2):312-318. doi: 10.1111/j.1440-1746.2010.06355.x.
|
[34] |
Ji G, Huang W, He J. Is anti-tuberculosis drug-induced hepatotoxicity due to a change in pharmacokinetics caused by alterations in antioxidant gene expression and polymorphisms in the NFE2L2 gene? Int J Clin Pharmacol Ther, 2020,58(2):67-73. doi: 10.5414/CP202599.
|
[35] |
Zhao Z, Peng W, Wu L, et al. Correlation between lncRNA AC079767.4 variants and liver injury from antituberculosis treatment in West China. J Infect Chemother, 2020,26(1):63-68. doi: 10.1016/j.jiac.2019.07.003.
|