[1] Mao Y, Ma S, Liu C, et al. Chinese guideline for the diagnosis and treatment of drug-induced liver injury: an update. Hepatol Int,2024,18(2):384-419.
[2] 中华医学会结核病学分会. 抗结核药所致药物性肝损伤诊治指南(2024年版). 中华结核和呼吸杂志,2024,47(11):1069-1090.
[3] 罗细林, 覃丽, 李昕, 等. 利福平致肝损伤的毒理机制及中药配伍减毒研究进展. 中国现代应用药学,2021,38(9):1125-1132.
[4] Ezhilarasan D. Antitubercular drugs induced liver injury: an updated insight into molecular mechanisms. Drug Metab Rev,2023,55(3):239-253.
[5] Zhou Y, Li M, Cao Y, et al. Farnesoid X receptor: effective alleviation of rifampicin -induced liver injury. Int Immunopharmacol,2024,139:112799.
[6] Mezler M, Jones RS, Sangaraju D, et al. Analysis of the bile acid composition in a fibroblast growth factor 19-expressing liver-humanized mouse model and its use for CYP3A4-mediated drug–drug interaction studies. Drug Metab Dispos,2023,51(10):1391-1402.
[7] Xu BY, Tang XD, Chen J, et al. Rifampicin induces clathrin-dependent endocytosis and ubiquitin–proteasome degradation of MRP2 via oxidative stressactivated PKC-ERK/JNK/p38 and PI3K signaling pathways in HepG2 cells. Acta Pharmacol Sin,2020,41(1):56-64.
[8] Chen J, Wu H, Tang X, et al. 4-Phenylbutyrate protects against rifampin-induced liver injury via regulating MRP2 ubiquitination through inhibiting endoplasmic reticulum stress. Bioengineered,2022,13(2):2866-2877.
[9] Li D, Li Y, Pan W, et al. Role of dynamin-related protein 1-dependent mitochondrial fission in drug-induced toxicity. Pharmacol Res,2024,206:107250.
[10] Zhuang X, Li L, Liu T,et al. Mechanisms of isoniazid and rifampicin-induced liver injury and the effects of natural medicinal ingredients: a review. Front Pharmacol,2022,13:1037814.
[11] Kainat K, Ansari MI, Bano N, et al. Rifampicin-induced ER stress and excessive cytoplasmic vacuolization instigate hepatotoxicity via alternate programmed cell death paraptosis in vitro and in vivo. Life Sci,2023,333:122164.
[12] Lee EH, Baek SY, Park JY, et al. Rifampicin activates AMPK and alleviates oxidative stress in the liver as mediated with Nrf2 signaling. Chem Biol Interact,2020,315:108889.
[13] Gee RRF, Huber AD, Chen T. Regulation of PXR in drug metabolism: chemical and structural perspectives. Expert Opin Drug Metab Toxicol,2024,20(1-2):9-23.
[14] Basaly V, Bhattacharya A, Guo GL. Insights of direct and indirect regulation of PXR through phosphorylation in fatty liver disease. Mol Pharmacol,2025,107(2):100014.
[15] Yao Y, Shen Y. Cross-talk between gut microbiota and liver steatosis: complications and therapeutic target. Open Life Sci,2023,18(1):20220699.
[16] Li M, Wang Y, Lv TT, et al. Mapping the incidence of drug‐induced liver injury: a systematic review and meta‐analysis. J Dig Dis,2023,24(5):332-339.
[17] 顾瑾, 林明贵, 唐神结. 《抗结核药所致药物性肝损伤诊治指南(2024年版)》更新要点解读. 结核与肺部疾病杂志,2024,32:1-8.
[18] Jiang F, Yan H, Liang L, et al. Incidence and risk factors of anti‐tuberculosis drug induced liver injury (DILI): large cohort study involving 4652 Chinese adult tuberculosis patients. Liver Int,2021,41(7):1565-1575.
[19] Patterson B, Abbara A, Collin S, et al. Predicting drug-induced liver injury from anti-tuberculous medications by early monitoring of liver tests. J Infect,2021,82(2):240-244.
[20] Ruiz-Bedoya CA, Mota F, Tucker EW, et al. High-dose rifampin improves bactericidal activity without increased intracerebral inflammation in animal models of tuberculous meningitis. J Clin Invest,2022,132(6):e155851.
[21] Paton NI, Cousins C, Suresh C, et al. Treatment strategy for rifampin-susceptible tuberculosis. N Engl J Med,2023,388(10):873-887.
[22] Onorato L, Gentile V, Russo A, et al. Standard versus high dose of rifampicin in the treatment of pulmonary tuberculosis: a systematic review and meta-analysis. Clin Microbiol Infect,2021,27(6):830-837.
[23] Te Brake LHM,de Jager V, Narunsky K, et al. Increased bactericidal activity but dose-limiting intolerability at 50 mg·kg rifampicin. Eur Respir J,2021,58(1):2000955.
[24] Svensson EM, Svensson RJ, Te Brake LHM, et al. The potential for treatment shortening with higher rifampicin doses: relating drug exposure to treatment response in patients with pulmonary tuberculosis. Clin Infect Dis,2018,67(1):34-41.
[25] Ryckman TS, Salazar-Austin N. High-dose rifampicin to treat tuberculosis infection: potential and pitfalls. Lancet Respir Med,2024,12(6):420-421.
[26] 支阳, 唐洁婷, 茅益民. 药物性肝损伤的遗传易感性. 中华肝脏病杂志,2023,31(6):653-658.
[27] Chen R, Wang J, Tang S, et al. Association of polymorphisms in drug transporter genes (SLCO1B1 and SLC10A1) and anti-tuberculosis drug-induced hepatotoxicity in a Chinese cohort. Tuberculosis,2015,95(1): 68-74.
[28] 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.
[29] Zazuli Z, Barliana MI, Mulyani UA, et al. Polymorphism ofPXR gene associated with the increased risk of drug-induced liver injury in indonesian pulmonary tuberculosis patients. J Clin Pharm Ther,2015,40(6):680-684.
[30] Wei SL, Anthony A, Onn MK, et al. Anti-tuberculosis drug-induced liver injury. BMJ,2023,383:p2806.
[31] Zhong T, Fan Y, Dong XL, et al. An investigation of the risk factors associated with anti-tuberculosis drug-induced liver injury or abnormal liver functioning in 757 patients with pulmonary tuberculosis. Front Pharmacol,2021,12(708522).
[32] Liu Q, Huang L, Yan H, et al. Clinical risk factors for moderate and severe antituberculosis drug-induced liver injury. Front Pharmacol,2024,15:1406454.
[33] Tuohutaerbieke M, Li X, Yin Y, et al. The characteristics, prevalence, and risk factors of drug-induced liver injury among brucellosis inpatients in Xinjiang, China. Front Pharmacol,2021,12:657805.
[34] Ibrahim SM, Pithavala YK, Vourvahis M, et al. A literature review of liver function test elevations in rifampin drug-drug interaction studies. Clin Transl Sci,2022,15(7):1561-1580.
[35] Pan Y, Tang P, Cao J, et al. Lipid peroxidation aggravates anti-tuberculosis drug-induced liver injury: evidence of ferroptosis induction. Biochem Biophys Res Commun,2020,533(4):1512-1518.
[36] Brewer CT, Kodali K, Wu J, et al. Toxicoproteomic profiling of hPXR transgenic mice treated with rifampicin and isoniazid. Cells,2020,9(7):1654.
[37] Jiang L, Gai X, Ni Y, et al. Folic acid protects against tuberculosis-drug-induced liver injury in rats and its potential mechanism by metabolomics. J Nutr Biochem,2023,112:109214.
[38] Tweed CD, Wills GH, Crook AM, et al. Liver toxicity associated with tuberculosis chemotherapy in the REMoxTB study. BMC Med,2018,16(1):46.
[39] Souleymane MB, Kadri S, Piubello A, et al. High rate of adverse drug reactions with a novel tuberculosis re-treatment regimen combining triple doses of both isoniazid and rifampicin. Int J Infect Dis,2023,133:78-81.
[40] Melnychuk L, Perlman-Arrow S, Lisboa BM, et al. A systematic review and meta-analysis of tuberculous preventative therapy adverse events. Clin Infect Dis,2023,77(2):287-294.
[41] Schmitt C, Riek M, Winters K, et al. Unexpected hepatotoxicity of rifampin and saquinavir/ritonavir in healthy male volunteers. Arch Drug Inf,2009,2(1):8-16.
[42] Gausi K, Mugerwa H, Siccardi M, et al. Pharmacokinetics and safety of twice-daily ritonavir-boosted atazanavir with rifampicin. Clin Infect Dis,2024,78(5):1246-1255.
[43] Kendall MA, Lalloo U, Fletcher CV, et al. Safety and pharmacokinetics of double-dose lopinavir/ritonavir + rifampin versus lopinavir/ritonavir + daily rifabutin for treatment of human immunodeficiency virus–tuberculosis coinfection. Clin Infect Dis,2021,73(4):706-715.
[44] Ichai P, Saliba F, Antoun F, et al. Acute liver failure due to antitubercular therapy: strategy for antitubercular treatment before and after liver transplantation. Liver Transpl,2010,16(10):1136-1146. |
