Department of Gastroenterology & Hepatology, Medical University of Vienna, Vienna, Austria.
J Viral Hepat. 2010 Jun;17(6):400-9. doi: 10.1111/j.1365-2893.2009.01197.x. Epub 2009 Sep 15.
Patients co-infected with the human immunodeficiency virus (HIV) and the hepatitis C virus (HCV) are fraught with a rapid fibrosis progression rate and with complications of portal hypertension (PHT) We aimed to assess the influence of immune function [Centers of Disease Control and Prevention (CDC) stage] on development of PHT and disease progression in HIV-HCV co-infection. Data of 74 interferon-naïve HIV-HCV co-infected patients undergoing liver biopsy, measurement of portal pressure and of liver stiffness and routine laboratory tests (including CD4+ cell count, HIV and HCV viral load) were analysed. Time of initial exposure (risk behaviour) was used to assess fibrosis progression. Fibrosis progression, time to cirrhosis and portal pressure were correlated with HIV status (CDC stage). HIV-HCV patients had rapid progression of fibrosis [0.201 +/- 0.088 METAVIR fibrosis units/year (FU/y)] and accelerated time to cirrhosis (24 +/- 13 years), high HCV viral loads (4.83 x 10(6) IU/mL) and a mean HVPG at the upper limit of normal (5 mmHg). With moderate or severe immunodeficiency, fibrosis progression was even higher (CDC-2 = 0.177 FU/y; CDC-3 = 0.248 FU/y) compared with patients with higher CD4+ nadirs (CDC-1 = 0.120 FU/y; P = 0.0001). An indirect correlation between CD4+ cell count and rate of fibrosis progression (R = -0.6654; P < 0.001) could be demonstrated. Hepatic venous pressure gradient (HVPG) showed early elevation of portal pressure with median values of 4, 8 and 12 mmHg after 10, 15 and 20 years of HCV infection for CDC-3 patients. Patients treated with highly active anti-retroviral therapy (HAART) had similar rates of progression and portal pressure values than patients without HAART. Progression of HCV disease is accelerated in HIV-HCV co-infection, being more pronounced in patients with low CD4+ cell count. A history of a CD4+ cell nadir <200/microL is a risk factor for rapid development of cirrhosis and PHT. Thus, HCV treatment should be considered early in patients with HIV-HCV co-infection and largely preserved CD4+ cell counts.
患者同时感染人类免疫缺陷病毒（HIV）和丙型肝炎病毒（HCV），其肝纤维化进展迅速，并伴有门静脉高压（PHT）的并发症。我们旨在评估免疫功能（疾病预防控制中心 [CDC] 分期）对 HIV-HCV 合并感染患者 PHT 发展和疾病进展的影响。分析了 74 例接受肝活检、门静脉压力和肝硬度测量以及常规实验室检查（包括 CD4+细胞计数、HIV 和 HCV 病毒载量）的干扰素初治 HIV-HCV 合并感染患者的数据。初始暴露（风险行为）时间用于评估纤维化进展。纤维化进展、肝硬化时间和门静脉压力与 HIV 状态（CDC 分期）相关。HIV-HCV 患者的纤维化进展迅速[0.201 +/- 0.088 METAVIR 纤维化单位/年（FU/y）]，肝硬化时间提前（24 +/- 13 年），HCV 病毒载量高（4.83 x 10(6) IU/mL），平均 HVPG 处于正常值上限（5 mmHg）。免疫功能中度或重度缺陷的患者，纤维化进展更高（CDC-2 = 0.177 FU/y；CDC-3 = 0.248 FU/y），与 CD4+细胞计数较低的患者相比（CDC-1 = 0.120 FU/y；P = 0.0001）。可以证明 CD4+细胞计数与纤维化进展率之间存在间接相关性（R = -0.6654；P < 0.001）。肝静脉压力梯度（HVPG）显示，在感染 HCV 10、15 和 20 年后，CDC-3 患者的门静脉压力中位值分别为 4、8 和 12 mmHg，出现早期升高。接受高效抗逆转录病毒治疗（HAART）的患者与未接受 HAART 的患者相比，进展率和门静脉压力值相似。在 HIV-HCV 合并感染中，HCV 疾病的进展加快，CD4+细胞计数较低的患者更为明显。CD4+细胞计数最低点<200/μL 的病史是肝硬化和 PHT 快速发展的危险因素。因此，在 HIV-HCV 合并感染患者中应尽早考虑 HCV 治疗，并尽量保留 CD4+细胞计数。
