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Hepatitis C and not Hepatitis B virus is a risk factor for anti-tuberculosis drug induced liver injury.

ABSTRACT: The risk of anti-tuberculosis (TB) drug-induced liver injury (DILI) in patients with chronic viral hepatitis (CVH) is not clear. The aim of this study was to investigate incidence and risk factors associated with TB DILI in CVH and non-CVH patients.Retrospectively, a total of 128 CVH patients who received anti-TB medication from January 2005 to February 2014 were reviewed. Among these, 83 patients had hepatitis B virus (HBV), 41 patients had hepatitis C virus (HCV) and 4 patients were dual hepatitis B and hepatitis C virus co-infected (HBV + HCV) with 251 non-CVH patients who received anti-TB medication selected as the controls. There were no human immunodeficiency virus co-infected patients. Risk factors for DILI were analyzed using cox regression analysis.The incidence of DILI was significantly higher in the HCV group (13/41 [31.7%], p < 0.001) and HBV + HCV groups (3/4 [75.0%], p = 0.002) compared to the control group (25/251 [10.0%]). The incidence of transient liver function impairment in the hepatitis B virus group was higher than in the control group (18/83 [21.7%] vs. 27/251 [10.8%] p = 0.010), but not in DILI (11/83 [13.3%] vs. 25/251 [10.0%], p = 0.400). In total patients, HCV, HBV + HCV co-infection, older age, and baseline liver function abnormality were independent factors of DILI.It is recommended to carefully monitor for DILI in patients with HCV or HBV/HCV co-infection, older age, and baseline liver function abnormality.

SUBMITTER: Kim WS

PROVIDER: S-EPMC4736472 | biostudies-other | 2016 Feb

REPOSITORIES: biostudies-other

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Project description:BACKGROUND:Pregnane X receptor (PXR) regulates the expression of drug-metabolizing enzymes and transport enzymes. NF-?B not only plays a role in liver homeostasis and injury-healing processes by regulating inflammatory responses but may also regulate the transcription of PXR. Currently, genetic polymorphisms in PXR are associated with adverse drug effects. Because little is known about the association between NF-?B1 genetic polymorphisms and adverse drug reactions, we explored the association between PXR and NF-?B1 single nucleotide polymorphisms (SNPs) and susceptibility to anti-tuberculosis drug-induced liver injury (ATDILI). MATERIALS AND METHODS:A total of 746 tuberculosis patients (118 with ATDILI and 628 without ATDILI) were prospectively enrolled at West China Hospital between December 2014 and April 2018. Nine selected SNPs (rs3814055, rs13059232, rs7643645 and rs3732360 in PXR and rs78872571, rs4647992, rs60371688, rs1598861 and rs3774959 in NF-?B1) were genotyped with a custom-designed 2x48-plex SNP Scan TM Kit. The frequencies of the alleles, genotypes and genetic models of the variants were compared between patients with or without ATDILI, while joint effect analysis of the SNP-SNP interactions was performed using multiplicative and additive models. The odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) were calculated. RESULTS:The T allele of rs3814055 in PXR was associated with a decreased risk for ATDILI (OR 0.61; 95% CI: 0.42-0.89, p = 0.0098). The T alleles of rs78872571 and rs4647992 in NF-?B1 were significantly associated with an increased risk for ATDILI (OR 1.91; 95% CI: 1.06-3.43, p = 0.028 and OR 1.81; 1.06-3.10, p = 0.029, respectively). The allele, genotype and genetic model frequencies were similar in the two groups for the other six SNPs (all P>0.05). There were no multiplicative or additive interactions between the SNPs. CONCLUSION:Our study is the first to reveal that rs3814055 variants in PXR and rs78872571 and rs4647992 variants in NF-?B1 are associated with susceptibility to ATDILI caused by first-line anti-tuberculosis combination treatment in the Han Chinese population.

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Hepatitis C and not Hepatitis B virus is a risk factor for anti-tuberculosis drug induced liver injury.

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