Research progress on susceptibility genes of anti-tuberculous drug-induced liver injury

doi:10.3969/j.issn.1000-6621.2021.02.016

Abstract

Abstract:

The course of tuberculosis chemotherapy is a long, and the first-line anti tuberculosis drugs commonly used (such as isoniazid and rifampicin) are potentially hepatotoxic and easily cause anti-tuberculosis drug-induced liver injury (ATLI), which leads to low treatment efficacy and ineffective drug use, and then induces drug-resistant tuberculosis, increasing the difficulty of treatment and the burden of patients. ATLI has obviously individual difference, which is mainly caused by genes. However, there is no relevant review on the progress of ATLI susceptibility genes research in China, the authors provide a reference for clinical treatment and prevention by reviewing the relevant research progress of ATLI susceptibility genes at home and abroad.

Key words: Tuberculosis, Antitubercular agents, Drug-induced liver injury, Genes, Polymorphism,single nucleotide

CAO Xin-yu, XUE Miao, WEN Yan, LIU Li. Research progress on susceptibility genes of anti-tuberculous drug-induced liver injury[J]. Chinese Journal of Antituberculosis, 2021, 43(2): 190-193. doi: 10.3969/j.issn.1000-6621.2021.02.016

References 35

[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.