Reiberger Thomas, Payer Berit A, Ferlitsch Arnulf, Sieghart Wolfgang, Breitenecker Florian, Aichelburg Maximilian C, Schmied Brigitte, Rieger Armin, Trauner Michael, Peck-Radosavljevic Markus
Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Antivir Ther. 2012;17(7):1327-34. doi: 10.3851/IMP2349. Epub 2012 Sep 5.
Patients coinfected with HIV and HCV are at risk for developing portal hypertension (PHT), hyperdynamic circulation and pulmonary arterial hypertension (PAH). Data on the influence of antiviral therapy with pegylated interferon-α (PEG-IFN-α) and ribavirin (RBV) are limited.
Haemodynamic parameters, including hepatic venous pressure gradient (HVPG), pulmonary arterial pressure (PAP(mean)), cardiac output (CO) and systemic vascular resistance (SysVR), were prospectively evaluated before and after PEG-IFN-α+RBV therapy in 80 HIV-HCV-coinfected patients.
Baseline evaluation showed a mean HVPG of 4.7 mmHg, CO of 6.15 l/min and PAP(mean) of 14.8 mmHg. PHT was present in 26% of patients, hyperdynamic circulation in 5% and PAH in 4%. Patients with advanced fibrosis (METAVIR stage F3/F4; n=32) had significantly higher CO (P=0.008), lower SysVR (P=0.035), higher PAP(mean) (P=0.018) and higher pulmonary vascular resistance (P=0.022) than patients with stage F0-F2 fibrosis (n=48). Both hyperdynamic circulation and PAH were significantly associated with liver stiffness, fibrosis stage and portal pressure; a non-significant trend was found for CD4(+) T-cell counts and HIV RNA levels. No significant changes in PAP(mean), CO and SysVR were observed after PEG-IFN-α+RBV treatment, although a significant decrease in HVPG was noted in patients with HCV eradication (P=0.013).
The overall prevalence of hyperdynamic circulation and PAH in HIV-HCV coinfection is low. Advanced fibrosis, increased liver stiffness, elevated portal pressure and probably CD4(+) T-cell count and HIV viraemia represent risk factors for hyperdynamic circulation and PAH. PHT is present in 26% of HIV-HCV-coinfected patients evaluated for antiviral therapy. Successful HCV eradication significantly decreases HVPG.
合并感染人类免疫缺陷病毒（HIV）和丙型肝炎病毒（HCV）的患者有发生门静脉高压（PHT）、高动力循环和肺动脉高压（PAH）的风险。关于聚乙二醇化干扰素-α（PEG-IFN-α）和利巴韦林（RBV）抗病毒治疗影响的数据有限。
对80例HIV-HCV合并感染患者在接受PEG-IFN-α+RBV治疗前后，前瞻性评估血流动力学参数，包括肝静脉压力梯度（HVPG）、肺动脉压（PAP（平均））、心输出量（CO）和全身血管阻力（SysVR）。
基线评估显示平均HVPG为4.7 mmHg，CO为6.15 l/min，PAP（平均）为14.8 mmHg。26%的患者存在PHT，5%的患者存在高动力循环，4%的患者存在PAH。与F0-F2纤维化阶段（n=48）的患者相比，晚期纤维化（METAVIR分期F3/F4；n=32）的患者CO显著更高（P=0.008），SysVR更低（P=0.035），PAP（平均）更高（P=0.018），肺血管阻力更高（P=0.022）。高动力循环和PAH均与肝硬度、纤维化阶段和门静脉压力显著相关；CD4(+)T细胞计数和HIV RNA水平存在无显著意义的趋势。PEG-IFN-α+RBV治疗后，PAP（平均）、CO和SysVR未观察到显著变化，尽管HCV根除的患者HVPG显著降低（P=0.013）。
HIV-HCV合并感染中高动力循环和PAH的总体患病率较低。晚期纤维化、肝硬度增加、门静脉压力升高以及可能的CD4(+)T细胞计数和HIV病毒血症是高动力循环和PAH的危险因素。接受抗病毒治疗评估的HIV-HCV合并感染患者中26%存在PHT。成功根除HCV可显著降低HVPG。
