ArticleImmunity, inflammation and disease2026
Genetic Variants at the NAT2 and HLA-DOA are Associated With Anti-Tuberculosis Drug-Induced Liver Injury Susceptibility and Clinical Manifestations in Western Chinese Populations.
Article in Immunity, inflammation and disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Genetic Variants at the NAT2 and HLA-DOA are Associated With Anti-Tuberculosis Drug-Induced Liver Injury Susceptibility and Clinical Manifestations in Western Chinese Populations.Immunity, inflammation and disease · 2026Article
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7 authors.
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Abstract
backgroundAnti-tuberculosis drug-induced liver injury (ATDILI) is one of the most prevalent and serious adverse reactions during anti-tuberculosis treatment and can potentially lead to liver failure or mortality. This study aims to investigate whether genetic variants in the N-acetyltransferase 2 gene (NAT2) and the HLA-DOA gene (HLA-DOA) are associated with ATDILI susceptibility and clinical manifestations in a Western Chinese population.
methodsA total of 1358 participants with active tuberculosis were enrolled and genotyped for four NAT2 polymorphisms and five HLA-DOA loci. Associations between candidate genetic variants and ATDILI were evaluated using logistic regression analyses, with multiple comparisons adjusted by Bonferroni correction.
resultsThe overall incidence of ATDILI was 28.4% (385/1358) in this cohort. Under a recessive model, NAT2 rs1799930 was found to increase the risk of ATDILI (odds ratio [OR] = 1.88, 95% confidence interval [CI]: 1.20-2.95, p = 0.006), which remained significant after Bonferroni correction (adjusted p = 0.048). Meanwhile, while HLA-DOA rs1367731 (OR = 0.41, 95% CI: 0.18-0.93, p = 0.033), rs6913008 (OR = 0.39, 95% CI: 0.17-0.89, p = 0.024), and rs9276975 (OR = 0.47, 95% CI: 0.23-0.98, p = 0.045) demonstrated a promising protective genomic characteristic that may mitigate the development of ATDILI. However, none of the reported HLA-DOA associations remained statistically significant after applying Bonferroni corrections. Regarding clinical manifestations, NAT2 rs1799930 and rs1799931 have been linked to poor ATDILI clinical presentations, whereas certain HLA-DOA variants (rs1367731, rs6913008, and rs9276975) were possibly linked to milder ATDILI severity.
conclusionOur findings preliminarily suggest that the NAT2 and HLA-DOA genetic variants may play a role in ATDILI susceptibility and clinical outcomes. NAT2 rs1799930 represents a potential genetic risk marker, while HLA-DOA variants may serve as protective factors warranting further validation. These findings may contribute to the precision management of ATDILI and the prevention of anti-TB drug-associated liver injury.
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