The influence of human immunodeficiency virus coinfection on chronic hepatitis C in injection drug users: A long-term retrospective cohort study
The influence of human immunodeficiency virus coinfection on chronic hepatitis C in injection drug users: A long-term retrospective cohort study
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DOI：
10.1053/jhep.2001.29201
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发表时间：
2001-12-01
期刊：
影响因子：
13.5
通讯作者：
Marcellin, P
中科院分区：
文献类型：
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作者：
Di Martino, V;Rufat, P;Marcellin, P
在这项研究中，我们分析了人类免疫缺陷病毒（HIV）感染对慢性丙型肝炎病程的影响，通过多变量分析，包括年龄，饮酒，免疫状态，丙型肝炎病毒（HCV）相关的病毒学因素。根据年龄、性别和HCV感染持续时间，对1980年至1995年期间80例HIV阳性和80例HIV阴性注射吸毒者进行匹配，并随访52个月。肝硬化的进展是主要的结局指标。HIV对HCV-RNA载量、组织学活性指数、干扰素治疗反应和肝脏相关死亡的影响也被考虑。在HIV阳性患者中，慢性丙型肝炎的特征是血清HCV-RNA水平较高（P = 0.012），总Knodell评分较高（P = 0.011），对干扰素治疗的持续应答较差（P = 0.009）。高血清HCV-RNA水平与低CD 4-淋巴细胞计数相关（P = 0.001）。HIV阳性患者的坏死性炎症评分较高（P = 0.023），与CD 4淋巴细胞计数无关，而纤维化增加与CD 4淋巴细胞计数降低有关（P = 0.011）。HIV阳性患者CD 4细胞计数低（RR 4.06，P = 0.024）和未接受干扰素治疗的患者（RR 4.76，P = 0.001）肝硬化进展加速，与HCV感染时的年龄无关（P = 0.001）。5例HIV阳性患者因肝硬化死亡。重度饮酒者（RR = 10.8，P = 0.001）和CD 4细胞计数低于200/mm 3的HIV阳性患者（RR = 11.9，P = 0.007）与肝硬化相关的死亡风险增加。在这项回顾性队列研究中，HIV合并感染恶化了慢性丙型肝炎的预后，增加了血清HCV-RNA水平和肝损伤，降低了对干扰素治疗的持续应答。年龄和饮酒是与肝硬化和死亡率相关的辅助因素。干扰素治疗对HCV相关肝硬化有保护作用，无论患者的HIV状态如何。
In this study we analyzed the influence of human immunodeficiency virus (HIV) infection on the course of chronic hepatitis C through multivariate analysis including age, alcohol consumption, immune status, and hepatitis C virus (HCV)-related virologic factors. Eighty HIV-positive and 80 HIV-negative injection drug users included between 1980 and 1995 were matched according to age, gender, and duration of HCV infection and followed-up during 52 months. The progression to cirrhosis was the primary outcome measure. The impact of HIV on HCV-RNA load, histologic activity index, response to interferon therapy, and liver-related death was also considered. In HIV-positive patients, chronic hepatitis C was characterized by higher serum HCV-RNA levels (P =.012), higher total Knodell score (P =.011), and poorer sustained response to interferon therapy (P =.009). High serum HCV-RNA level was associated with low CD4-lymphocyte count (P =.001). Necroinflamatory score was higher in HIV-positive patients (P =.023) independently of the CD4-lymphocyte count, whereas increased fibrosis was related to decreased CD4-lymphocyte count (P =.011). The progression to cirrhosis was accelerated in HIV-positive patients with low CD4 cell count (RR 4.06, P =.024) and in interferon-untreated patients (RR 4.76, P =.001), independently of age at HCV infection (P =.001). Cirrhosis caused death in 5 HIV-positive patients. The risk of death related to cirrhosis was increased in heavy drinkers (RR = 10.8, P =.001) and in HIV-positive patients with CD4 cell count less than 200/mm(3) (RR = 11.9, P =.007). In this retrospective cohort study, HIV coinfection worsened the outcome of chronic hepatitis C, increasing both serum HCV-RNA level and liver damage and decreasing sustained response to interferon therapy. Age and alcohol were cofactors associated with cirrhosis and mortality. Interferon therapy had a protective effect against HCV-related cirrhosis no matter what the patient's HIV status was.