ArticlePloS one2017
Association and clinical utility of NAT2 in the prediction of isoniazid-induced liver injury in Singaporean patients.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 2 of them syntheses that pooled it.
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Who cites it
22 citing papers in PubMed, 2 syntheses or guidelines pooled it, 57 citations in OpenAlex.
- Association of genetic polymorphisms ofBMJ open · 2019Pooled it
- The association between the NAT2 genetic polymorphisms and risk of DILI during anti-TB treatment: a systematic review and meta-analysis.British journal of clinical pharmacology · 2018Pooled it
- Characterization of NAT2 Using Long-Read Sequencing: Allele, Diplotype, and Phenotype Call Accuracy Compared to Other Testing Strategies.Clinical pharmacology and therapeutics · 2026Article
- Systematic review on genetic polymorphisms associated with idiosyncratic drug-induced liver injury (iDILI): iDILInet as an interactive visualization tool.Acta pharmaceutica Sinica. B · 2026Article
- Pharmacogenomic heterogeneity ofAnnals of medicine · 2025Observational
- Incidence and associated risk factors of anti-tuberculosis drug induced liver injury among TB patients.BMC infectious diseases · 2025Article
- Anti-tuberculosis drug-induced hepatotoxicity and associated risk factors among patients with pulmonary tuberculosis at a tertiary care hospital in Thailand.IJID regions · 2025Article
- Characterization of NAT, GST, and CYP2E1 Genetic Variation in Sub-Saharan African Populations: Implications for Treatment of Tuberculosis and Other Diseases.Clinical pharmacology and therapeutics · 2025Article
- Impact of Genetic Polymorphisms on the Efficacy and Safety of Isoniazid in Saudi Tuberculosis Patients.International journal of genomics · 2025Article
- Pharmacogenomics of antibiotic-induced hypersensitivity reactions: current evidence and implications in clinical practice.Frontiers in pharmacology · 2025Review
- Advances in drug-induced liver injury research: in vitro models, mechanisms, omics and gene modulation techniques.Cell & bioscience · 2024Review
- Drug-induced hepatotoxicity and association with slow acetylation variants NAT2*5 and NAT2*6 in Cameroonian patients with tuberculosis and HIV co-infection.BMC infectious diseases · 2024Article
- Influencing risk factors of voriconazole-induced liver injury in Uygur pediatric patients undergoing allogeneic hematopoietic stem cell transplantation.BMC pediatrics · 2024Article
- Article
- Gut microbial metabolism of 5-ASA diminishes its clinical efficacy in inflammatory bowel disease.Nature medicine · 2023Article
- Analytical and Omics-Based Advances in the Study of Drug-Induced Liver Injury.Toxicological sciences : an official journal of the Society of Toxicology · 2021Review
- Oxidative Stress in Drug-Induced Liver Injury (DILI): From Mechanisms to Biomarkers for Use in Clinical Practice.Antioxidants (Basel, Switzerland) · 2021Review
- NAT2 Gene rs1041983 is Associated with Anti-Tuberculosis Drug Induced Hepatotoxicity Among Pediatric Tuberculosis in Bandung, Indonesia.The application of clinical genetics · 2021Article
- Phenotype prediction and characterization of 25 pharmacogenes in Thais from whole genome sequencing for clinical implementation.Scientific reports · 2020Article
- Mitochondrial DNA Variants in Patients with Liver Injury Due to Anti-Tuberculosis Drugs.Journal of clinical medicine · 2019Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsIsoniazid (INH) is part of the first-line-therapy for tuberculosis (TB) but can cause drug-induced liver injury (DILI). Several candidate single nucleotide polymorphisms (SNPs) have been previously identified but the clinical utility of these SNPs in the prediction of INH-DILI remains uncertain. The aim of this study was to assess the association between selected candidate SNPs and the risk of INH-DILI and to assess the clinical validity of associated variants in a Singaporean population.
methodsThis was a case-control study where 24 INH-DILI cases and 79 controls were recruited from the TB control unit in a tertiary hospital. Logistic regression was used to test for the association between candidate SNPs and INH-DILI. NAT2 acetylator status was inferred from genotypes and tested for association with INH-DILI. Finally, clinical validity measures were estimated for significant variants.
resultsTwo SNPs in NAT2 (rs1041983 and rs1495741) and NAT2 slow acetylators (SA) were significantly associated with INH-DILI (OR (95% CI) = 13.86 (4.30-44.70), 0.10 (0.03-0.33) and 9.98 (3.32-33.80), respectively). Based on an INH-DILI prevalence of 10%, the sensitivity, specificity, positive and negative predictive values of NAT2 SA were 75%, 78%, 28% and 97%, respectively. The population attributable fraction (PAF) and number needed to test (NNT) for NAT2 SA were estimated to be 0.67 and 4.08, respectively. A model with clinical and NAT2 acetylator status provided significantly better prediction for INH-DILI than a clinical model alone (area under receiver operating characteristic curve = 0.863 vs. 0.766, respectively, p = 0.027).
conclusionsWe show the association between NAT2 SA and INH-DILI in a Singaporean population and demonstrated its clinical utility in the prediction of INH-DILI.
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