Does hepatitis C virus co-infection accelerate clinical and immunological evolution of HIV-infected patients?
Does hepatitis C virus co-infection accelerate clinical and immunological evolution of HIV-infected patients?
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DOI：
10.1097/00002030-199804000-00006
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发表时间：
1998-02-01
期刊：
影响因子：
3.8
通讯作者：
Chavanet, P
中科院分区：
文献类型：
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作者：
Piroth, L;Duong, M;Chavanet, P
目的：研究丙型肝炎病毒（HCV）合并感染对HIV感染患者临床和免疫学演变的影响。设计：对第戎戎大学医院传染病科确定的有或无HCV感染的HIV感染者进行纵向研究，并纳入历史队列。119例合并HCV感染的HIV感染者和119例单独感染HIV的匹配个体被纳入队列（中位参与时间3年;范围，2个月至11.5年）。临床进展定义为以下一项或多项：Karnofsky指数下降30%;体重减轻20%; AIDS定义疾病（非AIDS患者）;死亡（意外、自杀或药物过量除外）。免疫学进展定义为初始CD 4 T细胞计数下降50%（对于初始计数> 100 x 10（6）个细胞/l的患者）。使用Kaplan-Meier生存分析评估HCV合并感染的影响，并使用单变量（对数秩和Peto检验）和多变量方法（考克斯模型）。在单因素分析中，HCV阳性组和HCV阴性组的免疫学进展无统计学差异，而HCV阳性患者的临床进展明显更快（P < 0.005，对数秩检验）。在多变量考克斯模型中，临床进展与HCV感染显著相关[风险比（HR），1.64; 95%可信区间（CI），1.06-2.55; P < 0.05]。分层多变量分析保留HCV作为临床进展的重要预后因素（HR，10.9; 95% CI，1.09-109.3; P < 0.05）和免疫学进展（HR，2.31; 95% CI，1.16-4.62; P < 0.02）对于初始CD 4计数高于600 × 10（6）个细胞/l的患者。HIV-HCV合并感染患者的临床进展比未感染HCV的HIV血清阳性患者更快。在HIV感染的早期阶段，HCV感染对临床和免疫学进展的预后价值是显著的。这些发现可能会为在合并感染的个体中积极管理丙型肝炎感染提出论据，特别是对于CD 4计数高于600 x 10（6）个细胞/l的无症状患者，以预测和预防HCV和HIV疾病的加速进展。(C)1998 Rapid Science Ltd.
Objective: To study the influence of hepatitis C virus (HCV) co-infection on clinical and immunological evolution of HIV-infected patients.Design: A longitudinal study of HIV-infected individuals with or without HCV infection, identified at the Infectious Diseases Department of Dijon University Hospital and enrolled in a historical cohort, was performed.Methods: One hundred and nineteen HIV-infected people co-infected with HCV and 119 matched individuals infected with HIV alone were included in the cohort (median participation time 3 years; range, 2 months to 11.5 years). Clinical progression was defined as one or more of the following: a 30% decrease in the Karnofsky index; a 20% loss of body weight; an AIDS-defining illness (for non-AIDS patients); death (except by accident, suicide or overdose). Immunological progression was defined as a 50% decrease in the initial CD4 T-cell count (for patients with an initial count > 100 x 10(6) cells/l). Effects of HCV co-infection were evaluated using Kaplan-Meier survival analysis and significance was tested using univariate (log-rank and Peto's tests) and multivariate methods (Cox's model).Results: In univariate analysis, immunological progression was not statistically different between the HCV-positive group and the HCV-negative group, whereas clinical progression was significantly faster in HCV-positive patients (P < 0.005, log-rank test). In a multivariate Cox model, clinical progression remained significantly associated with infection by HCV [hazard ratio (HR), 1.64; 95% confidence interval (CI), 1.06-2.55; P < 0.05]. Stratified multivariable analysis retained HCV as a significant prognostic factor of clinical progression (HR, 10.9; 95% CI, 1.09-109.3; P < 0.05) and immunological progression (HR, 2.31; 95% CI, 1.16-4.62; P < 0.02) for patients with an initial CD4 count above 600 x 10(6) cells/l.Conclusions: Clinical progression is more rapid in HIV-HCV co-infected patients than in HIV-seropositive patients are not infected by HCV. The prognostic value of HCV infection for both clinical and immunological progression is significant at early stages of HIV infection. These findings may argue for active management of hepatitis C infection in co-infected individuals, especially for asymptomatic patients whose CD4 count is above 600 x 10(6) cells/l, to predict and prevent accelerated progression of HCV and HIV diseases. (C) 1998 Rapid Science Ltd.