SynthesisBMC genomic data2024
Pharmacogenomic insights into tuberculosis treatment shows the NAT2 genetic variants linked to hepatotoxicity risk: a systematic review and meta-analysis.
Synthesis in BMC genomic data, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- HBV/HCV coinfection and anti-tuberculosis drug-induced liver injury: from risk assessment and exploration of mechanisms to preventive considerations.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Review
- HBV/HCV coinfection and anti-tuberculosis drug-induced liver injury: from risk assessment and exploration of mechanisms to preventive considerations.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026Review
- Validation of an UHPLC-MS/MS Assay for the Quantification of Isoniazid and Four Major Metabolites in Human Plasma.Biomedical chromatography : BMC · 2026Article
- Genetic Landscape of NAT2 in the Moroccan Population: Implications for Isoniazid Pharmacogenetics in Tuberculosis.Clinical and translational science · 2026Article
- CYP2E1 and CYP2D6 in Anti-Tuberculosis Drug-Induced Liver Injury: Mechanisms, Epigenetic Regulation, and Translational Implications.Clinical and translational science · 2026Review
- Strengthening Pharmacogenomics Implementation in Africa: Challenges and Opportunities - A Narrative Review.Health science reports · 2026Article
- NAT2 rs1495741 and anti-tuberculosis drug-induced liver injury in children: genetic association and risk prediction.Frontiers in pharmacology · 2026Article
- NAT2 Acetylation Phenotypes in India: A Narrative Review of Personalized TB Therapy.Pharmacogenomics and personalized medicine · 2026Article
- Genomics in Health and Biomedicine.Advances in experimental medicine and biology · 2026Review
- Cost-utility analysis of stratified isoniazid dosing by NAT2 genotype compared with isoniazid standard regimen for new patients with pulmonary tuberculosis in Thailand.Frontiers in public health · 2026Article
- Opportunities and Challenges of Population Pharmacogenomics.Annals of human genetics · 2025Review
- Implementing health economics for pharmacogenomics research translation in Africa.Communications medicine · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTuberculosis (TB) patients undergoing anti-tuberculosis treatment often face serious adverse drug reactions, such as hepatotoxicity. Genetic variants of the N-acetyltransferase 2 (NAT2) gene have been linked to an increased risk of these toxic events.
objectiveThis study aims to provide a comprehensive evaluation of the evidence linking NAT2 genetic variants to anti-tuberculosis drug-related hepatotoxicity (ATDH).
methodA comprehensive review and meta-analysis was performed by accessing databases such as PubMed, Scopus, and Web of Science. A total of 24 articles were incorporated into the dataset. Meta-analyses were conducted to gather estimates of the association between the slow acetlylators (SA) genotype and ATDH. The studies were stratified by ethnicity, regimen, genotyping methods, criteria for liver toxicity, and dosage. Also, meta-analysis for the specific SA type that was most likely responsible for the ATDH was also conducted.
resultsThe included studies showed individuals with a slow NAT2 acetylator had a significantly greater risk of experiencing hepatotoxicity ATDH (odds ratio [OR] 2.52 (95% CI: 1.95-3.27; p value < 0.001) compared to individuals with other types of acetylator (i.e., rapid and immediate). Among individuals with slow acetylator NAT2*5/7, NAT2*5/6, and NAT2*6/6 genotypes, there is a greater likelihood of association compared to other variations.
conclusionOur meta-analysis confirms a significant association between slow NAT2 acetylator and increased hepatotoxicity risk. The findings from the present underscore the potential of pharmacogenomic testing to improve TB treatment outcomes. By identifying patients with the slow acetylator NAT2 genotype, healthcare providers can predict an increased risk of anti-tuberculosis drug-induced hepatotoxicity. This allows for personalized treatment strategies, such as adjusting drug dosages or selecting alternative therapies, to minimize adverse effects and optimize efficacy.
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