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HIV/AIDS合并肺结核患者抗结核分枝杆菌治疗肝毒性的危险因素
引用本文:卜岚,白轩.HIV/AIDS合并肺结核患者抗结核分枝杆菌治疗肝毒性的危险因素[J].中华实验和临床感染病杂志(电子版),2018,12(2):183-188.
作者姓名:卜岚  白轩
作者单位:1. 710061 西安市,西安市第八医院感染一科 2. 710061 西安市,西安市精神卫生中心临床心理二科
摘    要:目的探讨人类免疫缺陷病毒感染/获得性免疫缺乏综合征(HIV/AIDS)合并肺结核患者抗结核分枝杆菌治疗肝毒性的危险因素。 方法收集201年8月至2015年5月西安市第八医院收治的321例HIV/AIDS合并肺结核患者的全血及临床资料,并于患者抗结核分枝杆菌治疗后随访4个月。检测患者N-乙酰化转移酶2(NAT2)基因型。Logistic回归分析患者抗结核分枝杆菌治疗肝毒性的影响因素。 结果321例HIV/AIDS合并肺结核患者失访96例,剩余225例患者中73例(32.4%)发生药物性肝毒性(肝毒性组),152例(67.6%)未发生药物性肝毒性(无肝毒性组)。两组患者身体质量指数(BMI)(χ2 = 0.830、P = 0.003)、NAT2基因型(χ2 = 7.361、P = 0.025)、CD4细胞计数(χ2 = 4.380、P = 0.036)以及氟康唑治疗患者数(χ2 = 9.924、P = 0.002)差异均具有统计学意义。BMI、NAT2基因型和氟康唑治疗均为患者抗结核分枝杆菌治疗肝毒性的独立危险因素(P均< 0.05)。 结论低BMI、慢乙酰型NAT2基因型HIV/AIDS合并肺结核患者抗结核分枝杆菌治疗易发生肝毒性,建议慎重同时使用抗结核分枝杆菌治疗药物和氟康唑。

关 键 词:人类免疫缺陷病毒感染/获得性免疫缺乏综合征  结核  抗结核分枝杆菌治疗  肝毒性  危险因素  
收稿时间:2017-06-05

Clinical analysis of the risk factors of hepatotoxicity during treatment for Mycobacterium tuberculosis in patients with human immunodeficiency virus infection/acquired immune deficiency syndrome
Lan Bu,Xuan Bai.Clinical analysis of the risk factors of hepatotoxicity during treatment for Mycobacterium tuberculosis in patients with human immunodeficiency virus infection/acquired immune deficiency syndrome[J].Chinese Journal of Experimental and Clinical Infectious Diseases(Electronic Version),2018,12(2):183-188.
Authors:Lan Bu  Xuan Bai
Institution:1. Department of Infectious Diseases, The Eighth Hospital of Xi'an, 710061 Xi’an, China 2. Department of Clinical Psychology, Xi’an Mental Health Center, 710061 Xi’an, China
Abstract:ObjectiveTo investigate the risk factors of hepatotoxicity during treatment for Mycobacterium tuberculosis in patients with human immunodeficiency virus infection/acquired immune deficiency syndrome (HIV/AIDS). MethodsThe blood samples and clinical data of 321 HIV/AIDS cases complicated with Mycobacterium tuberculosis were collected in the Eighth Hospital of Xi’an from August 2011 to May 2015. Patients were followed up for 4 months after anti-Mycobacterium tuberculosis treatment. N-acetyltransferase 2 (NAT2) genotypes were detected. The risk factors of hepatotoxicity during anti-Mycobacterium tuberculous therapy were analyzed by Logistic regression. ResultsTotal of 96 patients were lost in the follow-up, while 73 cases (32.4%) had drug-induced hepatotoxicity (hepatotoxicity group), and 152 cases (67.6%) without hepatotoxicity (no-hepatotoxicity group) among the other 225 cases. Body mass index (BMI) (χ2 = 0.830, P = 0.003), N-acetytransferase 2 (NAT2) genotypes (χ2 = 7.361, P = 0.025), CD4 cell count (χ2 = 4.380, P = 0.036) and cases with fluconazole treatment (χ2 = 9.924, P = 0.002) in two groups were all with significant differences. BMI, NAT2 genotype and fluconazole treatment were independent risk factors of hepatotoxicity associated with anti-Mycobacterium tuberculosis treatment of patients with HIV/AIDS (all P < 0.05). ConclusionsLow BMI and slow acetyl NAT2 genetypes of HIV/AIDS patients complicated with tuberculosis were susceptible to hepatotoxicity by anti-Mycobacterium tuberculosis therapy, and both the use of anti-Mycobacterium tuberculosis drugs and fluconazole should be carefully recommended.
Keywords:Human immunodeficiency virus infection/acquired immune deficiency syndrome  Tuberculosis  Anti-Mycobacterium tuberculosis therapy  Hepatotoxicity  Risk factor  
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