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The recommended treatment regimen for tuberculosis is a combination of agents with antitubercular activity, during which hepatotoxicity is one of the most common side effects. In addition to the  N -acetyltransferase 2 ( NAT2 ) genotype,  rs3814055  in nuclear receptor subfamily 1, group I, member 2 ( NR1I2 ) has been demonstrated to be associated with anti-tuberculosis drug-induced hepatotoxicity (ATDH), but previous results have been inconsistent.A retrospective nested hospital-based case–control study was performed to investigate the association between genetic polymorphisms and the risk of ATDH. Fifteen genetic variants (13 SNPs and two null genotypes) in cytochrome P450 2E1,  NR1I2 , UDP-glucuronosyltransferase 1A1,  NAT2 , superoxide dismutase 1, superoxide dismutase 2, and glutathione  S -transferases ( GSTT1 ,  GSTM1 ,  GSTP1)  were genotyped. Odds ratios with 95% confidence intervals were calculated with drug doses, body mass index comorbidity of diabetes mellitus, and baseline alanine transaminase value as covariates.Conditional logistic regression demonstrated that the  NAT2  slow acetylation genotype and the  T  allele of  rs3814055  in  NR1I2  may contribute to susceptibility to ATDH.Stratified association analysis demonstrated that in  NAT2  non-slow acetylators, the  T  allele of  rs3814055  was a risk factor for ATDH, whereas the  T  allele did not increase the susceptibility to ATDH in slow acetylators. The recommended treatment regimen for tuberculosis is a combination of agents with antitubercular activity, during which hepatotoxicity is one of the most common side effects. In addition to the  N -acetyltransferase 2 ( NAT2 ) genotype,  rs3814055  in nuclear receptor subfamily 1, group I, member 2 ( NR1I2 ) has been demonstrated to be associated with anti-tuberculosis drug-induced hepatotoxicity (ATDH), but previous results have been inconsistent. A retrospective nested hospital-based case–control study was performed to investigate the association between genetic polymorphisms and the risk of ATDH. Fifteen genetic variants (13 SNPs and two null genotypes) in cytochrome P450 2E1,  NR1I2 , UDP-glucuronosyltransferase 1A1,  NAT2 , superoxide dismutase 1, superoxide dismutase 2, and glutathione  S -transferases ( GSTT1 ,  GSTM1 ,  GSTP1)  were genotyped. Odds ratios with 95% confidence intervals were calculated with drug doses, body mass index comorbidity of diabetes mellitus, and baseline alanine transaminase value as covariates. Conditional logistic regression demonstrated that the  NAT2  slow acetylation genotype and the  T  allele of  rs3814055  in  NR1I2  may contribute to susceptibility to ATDH. Stratified association analysis demonstrated that in  NAT2  non-slow acetylators, the  T  allele of  rs3814055  was a risk factor for ATDH, whereas the  T  allele did not increase the susceptibility to ATDH in slow acetylators.

Relevance of gene polymorphisms of NAT2 and NR1I2 to anti-tuberculosis drug-induced hepatotoxicity