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.
Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
J Hepatol. 2016 Oct;65(4):692-699. doi: 10.1016/j.jhep.2016.05.027. Epub 2016 May 27.
BACKGROUND & AIMS: We aimed to investigate the impact of sustained virologic response (SVR) to interferon (IFN)-free therapies on portal hypertension in patients with paired hepatic venous pressure gradient (HVPG) measurements.
One hundred and four patients with portal hypertension (HVPG ⩾6mmHg) who underwent HVPG and liver stiffness measurement before IFN-free therapy (baseline [BL]) were retrospectively studied. Among 100 patients who achieved SVR, 60 patients underwent HVPG and transient elastography (TE) after antiviral therapy (follow-up [FU]).
SVR to IFN-free therapies significantly decreased HVPG across all BL HVPG strata: 6-9mmHg (BL: 7.37±0.28 vs. FU: 5.11±0.38mmHg; -2.26±0.42mmHg; p<0.001), 10-15mmHg (BL: 12.2±0.4 vs. FU: 8.91±0.62mmHg; -3.29±0.59mmHg; p<0.001) and ⩾16mmHg (BL: 19.4±0.73 vs. FU: 17.1±1.21mmHg; -2.3±0.89mmHg; p=0.018). In the subgroup of patients with BL HVPG of 6-9mmHg, HVPG normalized (<6mmHg) in 63% (12/19) of patients, while no patient progressed to ⩾10mmHg. Among patients with BL HVPG ⩾10mmHg, a clinically relevant HVPG decrease ⩾10% was observed in 63% (26/41); 24% (10/41) had a FU HVPG <10mmHg. Patients with Child-Pugh stage B were less likely to have a HVPG decrease (hazard ratio [HR]: 0.103; 95% confidence interval [CI]: 0.02-0.514; p=0.006), when compared to Child-Pugh A patients. In the subgroup of patients with BL CSPH, the relative change in liver stiffness (per %; HR: 0.972; 95% CI: 0.945-0.999; p=0.044) was a predictor of a HVPG decrease ⩾10%. The area under the receiver operating characteristic curve for the diagnosis of FU CSPH by FU liver stiffness was 0.931 (95% CI: 0.865-0.997).
SVR to IFN-free therapies might ameliorate portal hypertension across all BL HVPG strata. However, changes in HVPG seemed to be more heterogeneous among patients with BL HVPG of ⩾16mmHg and a HVPG decrease was less likely in patients with more advanced liver dysfunction. TE might be useful for the non-invasive evaluation of portal hypertension after SVR.
We investigated the impact of curing hepatitis C using novel interferon-free treatments on portal hypertension, which drives the development of liver-related complications and mortality. Cure of hepatitis C decreased portal pressure, but a decrease was less likely among patients with more pronounced hepatic dysfunction. Transient elastography, which is commonly used for the non-invasive staging of liver disease, might identify patients without clinically significant portal hypertension after successful treatment.
我们旨在研究无干扰素治疗的持续病毒学应答(SVR)对经配对肝静脉压力梯度(HVPG)测量的门静脉高压的影响。
回顾性研究了 104 例门静脉高压(HVPG ⩾6mmHg)患者,这些患者在无干扰素治疗前(基线[BL])进行了 HVPG 和肝脏硬度测量。在 100 例达到 SVR 的患者中,60 例在抗病毒治疗后(随访[FU])进行了 HVPG 和瞬时弹性成像(TE)。
无干扰素治疗的 SVR 显著降低了所有 BL HVPG 分层的 HVPG:6-9mmHg(BL:7.37±0.28 与 FU:5.11±0.38mmHg;-2.26±0.42mmHg;p<0.001),10-15mmHg(BL:12.2±0.4 与 FU:8.91±0.62mmHg;-3.29±0.59mmHg;p<0.001)和 ⩾16mmHg(BL:19.4±0.73 与 FU:17.1±1.21mmHg;-2.3±0.89mmHg;p=0.018)。在 BL HVPG 为 6-9mmHg 的亚组中,63%(12/19)的患者 HVPG 正常化(<6mmHg),而没有患者进展为 ⩾10mmHg。在 BL HVPG ⩾10mmHg 的患者中,63%(26/41)观察到 HVPG 有临床意义的下降 ⩾10%;24%(10/41)FU HVPG <10mmHg。与 Child-Pugh A 患者相比,Child-Pugh B 患者的 HVPG 下降可能性更小(风险比[HR]:0.103;95%置信区间[CI]:0.02-0.514;p=0.006)。在 BL CSPH 患者亚组中,肝脏硬度的相对变化(每%;HR:0.972;95%CI:0.945-0.999;p=0.044)是 HVPG 下降 ⩾10%的预测因素。FU 肝脏硬度诊断 FU CSPH 的受试者工作特征曲线下面积为 0.931(95%CI:0.865-0.997)。
无干扰素治疗的 SVR 可能改善所有 BL HVPG 分层的门静脉高压。然而,BL HVPG ⩾16mmHg 的患者中 HVPG 的变化似乎更为复杂,肝功能更严重的患者 HVPG 下降的可能性较小。TE 可能有助于 SVR 后门静脉高压的非侵入性评估。