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作 者:王海舰[1] 张凤池[1] 周长月 刘成勇[1] 张利宁[2]
机构地区:[1]徐州市传染病医院,徐州221004 [2]徐州市疾病预防控制中心,徐州221000
出 处:《中国当代医药》2016年第21期33-36,共4页China Modern Medicine
基 金:江苏省第四期"333高层次人才培养工程"资助科研项目(BRA2012042)
摘 要:目的了解我市艾滋病患者抗病毒治疗后免疫学应答、病毒抑制效果、耐药情况,以提高抗病毒治疗效果。方法选取2011年1月~2013年8月在徐州市疾病预防控制中心及徐州市传染病院就治的52例艾滋病患者作为研究对象,以2个核苷类逆转酶抑制剂(NRTI)+1个非核苷类逆转酶抑制剂(NNRTI)抗病毒治疗,观察治疗6、12、18、24个月的CD4+细胞计数、病毒载量,对病毒载量〉1000拷贝/ml的患者进行耐药检测。结果52例接受抗病毒治疗前的CD4+细胞计数平均值为(181±112)个/μl,治疗6个月后的CD4+细胞平均值为(272±106)个/μl,显著高于治疗前,差异有统计学意义(t=2.013,P〈0.05)。抗病毒治疗前大多数患者的病毒载量处于较高水平,71.15%(37/52)的患者经治疗后病毒载量降低到较低水平。治疗6、12、18、24个月的耐药发生率分别为12.5%(1/8)、33.33%(3/9)、35.29%(6/17)、44.44%(8/18)。核苷类耐药的突变位点比较集中,主要出现184V位点变异,对拉米夫定、齐多夫定、司他夫定等高度耐药。非核苷类耐药的突变位点比较分散,181C、103N、101E、190A、108L等位点均可出现变异,对依非韦伦、奈韦拉平高度耐药。结论抗病毒治疗能有效控制病毒血症,提升机体的细胞免疫水平,并有效抑制HIV病毒的复制。随着治疗时间的延长,对核苷类与非核苷类药物的耐药毒株大量出现。耐药突变是病毒抑制失败的结果.服药依从性差是主要原因。Objective To understand the immune response,viral suppression and drug resistance of AIDS patients in our city after antiviral treatment,so as to improve the therapeutic effect.Methods 52 cases of AIDS patients in Xuzhou Center for Disease Control Prevention and Xuzhou Infectious Disease Hospital from January 2011 and August 2013 were selected as the research group,antiviral therapy with 2 nucleoside reverse transcriptase inhibitors (NRTI) and 1 non-nucleoside reverse transcriptase inhibitors (NNRTI) was used to 52 patients,CD4+ cell count and viral load were observed with 6,12,18,24 months,and the drug resistance was detected by 〉1000 copy/ml.Results Before antiviral treatment,the average value of CD4+ cells in 52 patients was (181 ± 112)μl,after 6 months of treatment,the average value of CD4+ cells was (272±106)/μl,which was higher than that before treatment,with significant difference (t=2.013,P〈0.05).Viral load was in a high level in most patients before treatment, 71.15% (37/52) was decreased to a low level after treatment.Drug resistance rate was 12.5% (1/8),33.33% (3/9),35.29% (6/17),and 44.44% (8/18) respectively in the treatment of 6,12,18 and 24 months.The mutation sites of nucleoside resistance were relatively concentrated,mainly in the 184V mutation,and highly resistant to lamivudine,zidovudine,stavudine.The mutation sites of non nucleoside resistance were scattered,probably happened in 181C, 103N,101E,190A and 108L,and highly resistant to efavirenz and nevirapine.Conclusion Antiviral therapy can effectively control the virus disease,improve the level of cellular immunity,and effectiv With the prolongation of treatment time,drug resistant strains to nucleoside ely and non -nuc e replication of HIV virus. leoside drugs are in large numbers.Drug resistance mutation is the result of viral suppression,and the poor compliance is the main reason.
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