ArticleEuropean journal of clinical pharmacology2008
Association of slow N-acetyltransferase 2 profile and anti-TB drug-induced hepatotoxicity in patients from Southern Brazil.
Article in European journal of clinical pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 7 of them syntheses that pooled it.
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Who cites it
46 citing papers in PubMed, 7 syntheses or guidelines pooled it, 126 citations in OpenAlex.
- Pharmacogenomic insights into tuberculosis treatment shows the NAT2 genetic variants linked to hepatotoxicity risk: a systematic review and meta-analysis.BMC genomic data · 2024Pooled it
- Association of genetic polymorphisms ofBMJ open · 2019Pooled it
- The international journal of tuberculosis and lung disease : the official journal of the International Union against Tuberculosis and Lung Disease · 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
- Hepatotoxicity from antituberculous therapy in the elderly: a systematic review.Tuberculosis (Edinburgh, Scotland) · 2015Pooled it
- Slow N-acetyltransferase 2 genotype contributes to anti-tuberculosis drug-induced hepatotoxicity: a meta-analysis.Molecular biology reports · 2013Pooled it
- Pooled it
- Adverse reactions due to directly observed treatment strategy therapy in Chinese tuberculosis patients: a prospective study.PloS one · 2013Trial
- Genetic interaction between NAT2, GSTM1, GSTT1, CYP2E1, and environmental factors is associated with adverse reactions to anti-tuberculosis drugs.Molecular diagnosis & therapy · 2012Trial
- Pharmacogenomic heterogeneity ofAnnals of medicine · 2025Observational
- Characterization of the complex TB pharmacogenomic landscape in Africa using bioinformatic tools.Briefings in bioinformatics · 2025Article
- Pharmacogenetic Study of Anti-TB Drugs in the Native Ancestry Peruvian Population.Pharmacology research & perspectives · 2025Article
- Genetic Landscape of VIP Pharmacogenomic Variants in the Kinh Vietnamese Population.Pharmacogenomics and personalized medicine · 2025Article
- Pharmacogenetic variability of tuberculosis biomarkers in native and mestizo Peruvian populations.Pharmacology research & perspectives · 2024Article
- Human N-acetyltransferase 2 (Frontiers in pharmacology · 2023Article
- Article
- Fluoroquinolone heteroresistance, antimicrobial tolerance, and lethality enhancement.Frontiers in cellular and infection microbiology · 2022Review
- Homozygotes NAT2*5B slow acetylators are highly associated with hepatotoxicity induced by anti-tuberculosis drugs.Memorias do Instituto Oswaldo Cruz · 2022Article
- Oxidative Stress in Drug-Induced Liver Injury (DILI): From Mechanisms to Biomarkers for Use in Clinical Practice.Antioxidants (Basel, Switzerland) · 2021Review
- N-Acetyl Cysteine as an Adjunct in the Treatment of Tuberculosis.Tuberculosis research and treatment · 2020Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo determine the frequency of N-acetyltransferase 2 (NAT2) polymorphisms, the NAT2 acetylation profile and its relation to the incidence of gastrointestinal adverse drug reactions (ADRs), anti-tuberculosis (TB) drug-induced hepatotoxicity, and the clinical risk factors for hepatotoxicity in a population from Brazil.
methodsTwo hundred and fifty-four Brazilian TB patients using isoniazid (INH), rifampicin (RMP), and pirazinamide (PZA) were tested in a prospective cohort study. NAT2 genotyping was performed by direct PCR sequencing. The association between gastrointestinal ADRs/hepatotoxicity and the NAT2 profile genotype was evaluated by univariate analysis and multiple logistic regression.
resultsOf the 254 patients analyzed, 69 (27.2%) were slow acetylators and 185 (72.8%) were fast acetylators. Sixty-five (25.6%) patients were human immunodeficiency virus (HIV)-positive. Thirty-three (13%) and 14 (5.5%) patients developed gastrointestinal ADR and hepatotoxicity, respectively. Of the 14 hepatotoxicity patients, nine (64.3%) were slow acetylators and five (35.7%) were fast acetylators. Sex, age, presence of hepatitis C virus, alcohol abuse, and baseline aminotransferases were not found to be risk factors for hepatotoxicity. However, logistic regression analysis revealed that slow acetylator status and the presence of HIV (p < 0.05) were independent risk factors for hepatotoxicity.
conclusionsOur findings show that HIV-positive patients that have the slow acetylation profile are significantly associated with a higher risk of developing hepatotoxicity due to anti-TB drugs.
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