LI-NA LEECHUN-TA HUANGHsu, Chia-LinChia-LinHsuChang, Hsiu-ChingHsiu-ChingChangI-SHIOW JANLiu, Jia-LuenJia-LuenLiuJIN-CHUAN SHEUJANN-TAY WANGLiu, Wei-LunWei-LunLiuWu, Huei-ShuHuei-ShuWuChang, Ching-NienChing-NienChangJANN-YUAN WANG2021-11-232021-11-232019-08-132077-0383https://scholars.lib.ntu.edu.tw/handle/123456789/587697Hepatotoxicity is the most severe adverse effect of anti-tuberculosis therapy. Isoniazid's metabolite hydrazine is a mitochondrial complex II inhibitor. We hypothesized that mitochondrial DNA variants are risk factors for drug-induced liver injury (DILI) due to isoniazid, rifampicin or pyrazinamide.enDNA variants; Drug-induced liver injury; complex I; mitochondria; tuberculosis[SDGs]SDG3alanine aminotransferase; aspartate aminotransferase; bilirubin; bilirubin glucuronide; creatinine; ethambutol; genomic DNA; isoniazid; mitochondrial DNA; pyrazinamide; tuberculostatic agent; adult; Article; body mass; case control study; clinical article; controlled study; DNA extraction; DNA polymorphism; female; gene sequence; genome; genotype; human; male; middle aged; mitochondrial DNA depletion; next generation sequencing; prospective study; respiratory chain; toxic hepatitisjournal article10.3390/jcm8081207314125782-s2.0-85097257644https://api.elsevier.com/content/abstract/scopus_id/85097257644