论文部分内容阅读
目的研究药物代谢酶锰超氧化物歧化酶(MnSOD)的基因多态性与抗结核药物肝损害的关系,阐明抗结核药物诱导肝损害的分子机制。方法通过聚合酶链反应-直接测序(PCR-DS)方法分析101例有抗结核药物性肝损害的结核病患者(病例组)及107例无抗结核药物性肝损害的结核病患者(对照组)的MnSOD的基因多态性,并分析它们与抗结核药物性肝损害之间的关系。结果与MnSOD编码基因47位碱基T/T基因型(OR:0.68,P>0.05)、T/C基因型(OR:1.03,P>0.05)比较,47位碱基C/C基因型患者更易发生抗结核药物性肝损害,OR值为5.77(P<0.05)。结论 MnSOD编码基因的47位碱基CC基因型有可能是发生抗结核药物性肝损害的易感基因。
Objective To study the relationship between gene polymorphism of MnSOD and liver damage caused by antituberculosis drugs and elucidate the molecular mechanism of anti-TB drug induced liver damage. Methods 101 patients with tuberculosis with drug-induced liver damage (case group) and 107 with tuberculosis without drug-induced liver injury (control group) were analyzed by polymerase chain reaction-direct sequencing (PCR-DS) MnSOD gene polymorphisms, and analyze their relationship with anti-TB drug-induced liver damage. Results Compared with the 47th base T / T genotype (OR: 0.68, P> 0.05) and T / C genotype (OR: 1.03, P> 0.05) More prone to anti-TB drug-induced liver damage, OR was 5.77 (P <0.05). Conclusion The CC genotype 47 of MnSOD gene may be a susceptible gene to anti-TB drug-induced liver damage.