Department of Internal Medicine III, Division of Gastroenterology & Hepatology, Medical University of Vienna, Vienna, Austria.
Clin Gastroenterol Hepatol. 2011 Jul;9(7):602-8.e1. doi: 10.1016/j.cgh.2011.03.002. Epub 2011 Mar 10.
BACKGROUND & AIMS: There are limited data on the efficacy and safety of antiviral therapy in patients with hepatitis C virus (HCV)-related cirrhosis, particularly on the impact of portal hypertension.
We assessed hepatovenous pressure gradient (HVPG), liver stiffness (transient elastography), and interleukin (IL)-28B polymorphisms (rs12979860) in 90 cirrhotic patients with HCV infection (82% genotype 1 or 4) before antiviral therapy with pegylated interferon and ribavirin. Efficacy and safety were evaluated.
Rates of sustained virologic response were significantly lower among patients with clinically significant portal hypertension (CSPH; HVPG ≥ 10 mm Hg; n = 50) than among patients without CSPH (HVPG <10 mm Hg; n = 40): 14% vs 51% (P = .0007). Seventy-nine percent and 83% of patients with CSPH and without CSPH, respectively, received more than 80% of planned dose (P = .647). The predictive value of HVPG (area under the curve [AUC], 0.743) was greater than that of liver stiffness (AUC, 0.647) or of baseline HCV RNA levels (AUC, 0.620). The IL-28B polymorphism was not associated significantly with a sustained virologic response. Multivariate analysis revealed that HVPG (odds ratio [OR], 14.3; P = .009), baseline HCV RNA levels (OR, 5.3; P = .019), and HCV genotype (OR, 6.5; P = .046) were independent risk factors for treatment failure. A trend toward higher incidence of anemia and neutropenia was observed for patients with CSPH. The incidence and grade of thrombocytopenia were significantly higher among patients with than without CSPH (94% vs 75%; P = .006).
HVPG is an independent predictor of response to antiviral therapy, with better predictive value than liver stiffness, baseline HCV RNA levels, HCV genotype, or IL-28B polymorphism. The incidence and grade of thrombocytopenia during antiviral therapy are higher among patients with CSPH. In evaluating cirrhotic HCV patients for antiviral treatment, measurement of HVPG should be considered.
目前有关抗病毒治疗对丙型肝炎病毒（HCV）相关肝硬化患者的疗效和安全性的数据有限，尤其是对门静脉高压影响的数据。
我们评估了 90 例丙型肝炎病毒感染肝硬化患者（82%基因型 1 或 4）的肝静脉压力梯度（HVPG）、肝脏硬度（瞬时弹性成像）和白细胞介素（IL）-28B 多态性（rs12979860），这些患者均接受聚乙二醇干扰素和利巴韦林抗病毒治疗。评估了疗效和安全性。
与无临床显著门静脉高压（HVPG＜10mmHg；n=40）的患者相比，有临床显著门静脉高压（HVPG≥10mmHg；n=50）的患者持续病毒学应答率显著降低：14%比 51%（P=0.0007）。分别有 79%和 83%的有和无临床显著门静脉高压的患者接受了超过 80%的计划剂量（P=0.647）。HVPG（曲线下面积[AUC]，0.743）的预测价值大于肝脏硬度（AUC，0.647）或基线 HCV RNA 水平（AUC，0.620）。白细胞介素-28B 多态性与持续病毒学应答无显著相关性。多变量分析显示，HVPG（比值比[OR]，14.3；P=0.009）、基线 HCV RNA 水平（OR，5.3；P=0.019）和 HCV 基因型（OR，6.5；P=0.046）是治疗失败的独立危险因素。有临床显著门静脉高压的患者贫血和中性粒细胞减少症的发生率有升高趋势。有临床显著门静脉高压的患者血小板减少症的发生率和严重程度显著高于无临床显著门静脉高压的患者（94%比 75%；P=0.006）。
HVPG 是抗病毒治疗反应的独立预测因素，其预测价值优于肝脏硬度、基线 HCV RNA 水平、HCV 基因型或白细胞介素-28B 多态性。有临床显著门静脉高压的患者在接受抗病毒治疗期间血小板减少症的发生率和严重程度更高。在评估接受抗病毒治疗的丙型肝炎病毒肝硬化患者时，应考虑测量 HVPG。
