Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Vienna Hepatic Hemodynamic Lab, Medical University of Vienna, Vienna, Austria.
Hepatology. 2020 Mar;71(3):1023-1036. doi: 10.1002/hep.30885. Epub 2019 Oct 14.
Sustained virologic response (SVR) to interferon (IFN)-free therapies ameliorates portal hypertension (PH); however, it remains unclear whether a decrease in hepatic venous pressure gradient (HVPG) after cure of hepatitis C translates into a clinical benefit. We assessed the impact of pretreatment HVPG, changes in HVPG, and posttreatment HVPG on the development of hepatic decompensation in patients with PH who achieved SVR to IFN-free therapy. Moreover, we evaluated transient elastography (TE) and von Willebrand factor to platelet count ratio (VITRO) as noninvasive methods for monitoring the evolution of PH.
The study comprised 90 patients with HVPG ≥ 6 mm Hg who underwent paired HVPG, TE, and VITRO assessments before (baseline [BL]) and after (follow-up [FU]) IFN-free therapy. FU HVPG but not BL HVPG predicted hepatic decompensation (per mm Hg, hazard ratio, 1.18; 95% confidence interval, 1.08-1.28; P < 0.001). Patients with BL HVPG ≤ 9 mm Hg or patients who resolved clinically significant PH (CSPH) were protected from hepatic decompensation. In patients with CSPH, an HVPG decrease ≥ 10% was similarly protective (36 months, 2.5% vs. 40.5%; P < 0.001) but was observed in a substantially higher proportion of patients (60% vs. 24%; P < 0.001). Importantly, the performance of noninvasive methods such as TE/VITRO for diagnosing an HVPG reduction ≥ 10% was inadequate for clinical use (area under the receiver operating characteristic curve [AUROC], < 0.8), emphasizing the need for HVPG measurements. However, TE/VITRO were able to rule in or rule out FU CSPH (AUROC, 0.86-0.92) in most patients, especially if assessed in a sequential manner.
Reassessment of HVPG after SVR improved prognostication in patients with pretreatment CSPH. An "immediate" HVPG decrease ≥ 10% was observed in the majority of these patients and was associated with a clinical benefit, as it prevented hepatic decompensation. These results support the use of HVPG as a surrogate endpoint for interventions that lower portal pressure by decreasing intrahepatic resistance.
无干扰素治疗的持续病毒学应答（SVR）可改善门静脉高压（PH）；然而，丙型肝炎治愈后肝静脉压力梯度（HVPG）的下降是否能转化为临床获益尚不清楚。我们评估了达到无干扰素治疗 SVR 的 PH 患者的 HVPG 治疗前、治疗中及治疗后对肝失代偿发展的影响。此外，我们还评估了瞬时弹性成像（TE）和血管性血友病因子至血小板比值（VITRO）作为监测 PH 演变的非侵入性方法。
该研究纳入了 90 例 HVPG≥6mmHg 的患者，这些患者在无干扰素治疗前（基线[BL]）和治疗后（随访[FU]）接受了配对的 HVPG、TE 和 VITRO 评估。FU HVPG 而非 BL HVPG 预测肝失代偿（每毫米汞柱，危险比，1.18；95%置信区间，1.08-1.28；P<0.001）。BL HVPG≤9mmHg 的患者或临床显著 PH（CSPH）得到解决的患者可免于肝失代偿。在 CSPH 患者中，HVPG 下降≥10%同样具有保护作用（36 个月时，2.5%比 40.5%；P<0.001），但观察到的患者比例更高（60%比 24%；P<0.001）。重要的是，TE/VITRO 等非侵入性方法诊断 HVPG 下降≥10%的性能不足（接受者操作特征曲线下面积[AUROC]，<0.8），强调需要进行 HVPG 测量。然而，TE/VITRO 能够在大多数患者中确定或排除 FU CSPH（AUROC，0.86-0.92），尤其是在以连续方式评估时。
SVR 后 HVPG 的重新评估改善了治疗前 CSPH 患者的预后。在这些患者中，大多数患者观察到 HVPG 的“即刻”下降≥10%，与临床获益相关，因为它可预防肝失代偿。这些结果支持将 HVPG 作为降低肝内阻力以降低门静脉压力的干预措施的替代终点。
