Mitochondrial DNA Variants in Patients with Liver Injury Due to Anti-Tuberculosis Drugs
Journal
Journal of clinical medicine
Journal Volume
8
Journal Issue
8
Date Issued
2019-08-13
Author(s)
Hsu, Chia-Lin
Chang, Hsiu-Ching
Liu, Jia-Luen
Liu, Wei-Lun
Wu, Huei-Shu
Chang, Ching-Nien
Abstract
Hepatotoxicity 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.
Subjects
DNA variants; Drug-induced liver injury; complex I; mitochondria; tuberculosis
SDGs
Other Subjects
alanine 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 hepatitis
Type
journal article