【摘 要】
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1.The present study investigated the relationship between antituberculosis (anti-TB) drug-induced hepatotoxicity and genetic polymorphisms of two important drug-metabolizing enzymes involved in the me
【机 构】
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Institute of Tuberculosis Research,309th Hospital of Chinese People's Liberation Army,Beijing,China
【出 处】
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2012科学研究与结核病防治高峰论坛
论文部分内容阅读
1.The present study investigated the relationship between antituberculosis (anti-TB) drug-induced hepatotoxicity and genetic polymorphisms of two important drug-metabolizing enzymes involved in the metabolism of isoniazid,namely N-acetyltransferase 2 (NAT2) and cytochrome P450 2E1 (CYP2E1).2.A polymerase chain reaction direct sequencing approach was used to detect genetic polymorphisms of the NAT2 and CYP2E1 genes in tuberculosis (TB) patients with (n =101) or without (n =107) anti-TB drug-induced hepatotoxicity.Associations between various genetic polymorphisms and anti-TB drug-induced hepatotoxicity were then determined.3.Patients with NAT2 (282TT,590AA and 857GA) alleles had an increased susceptibility to anti-TB drug-induced hepatotoxicity.The slow acetylator NAT2 genotypes (especially NAT2*6A/7B and NAT2*6A/6A) were risk factors for hepatotoxicity (odds ratio (OR) 9.57 (P < 0.001) for NAT2*6A/7B; OR 5.24 (P =0.02) for NAT2*6A/6A).4.The CYP2E1 genotype per se was not significantly associated with the development of anti-TB drug-induced hepatotoxicity.However,the combination of the CYP2E1 C1/C1 genotype with a slow acetylator NAT2 genotype increased the risk of anti-TB drug-induced hepatotoxicity (OR 5.33; P =0.003) compared with the combination of a rapid acetylator NAT2 genotype with either a C1/C2 or C2/C2 genotype.5.Thus,slow acetylators with the NAT2*6A/7B and NAT2*6A/6A genotypes combined with the C1/C1 CYP2E1 genotype may be involved in the pathogenesis of anti-TB drug-induced hepatotoxicity.6.The present findings may be explained,in part,by changes in the metabolism of the anti-TB drug isoniazid induced via NAT2 and CYP2E1,a metabolic process known to produce hepatotaxic intermediates.
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