Background & Aims

Non-invasive tests (NITs) for clinically significant portal hypertension (CSPH; hepatic venous pressure gradient [HVPG] ≥10 mmHg) have predominantly been studied in patients with active HCV infection. Investigations after HCV cure are limited and have yielded conflicting results. We conducted a pooled analysis to determine the diagnostic/prognostic utility of liver stiffness measurement (LSM)/platelet count (PLT) in this setting.

Methods

A total of 418 patients with pre-treatment HVPG ≥6 mmHg who achieved sustained virological response (SVR) and underwent post-treatment HVPG measurement were assessed, of whom 324 (HVPG/NIT-cohort) also had paired data on pre-/post-treatment LSM/PLT. The derived LSM/PLT criteria were then validated against the direct endpoint decompensation in 755 patients with compensated advanced chronic liver disease (cACLD) with SVR (cACLD-validation-cohort).

Results

HVPG/NIT-cohort: Among patients with cACLD, the pre-/post-treatment prevalence of CSPH was 80%/54%. The correlation between LSM/HVPG increased from pre- to post-treatment (r = 0.45 vs. 0.60), while that of PLT/HVPG remained unchanged. For given LSM/PLT values, HVPG tended to be lower post- vs. pre-treatment, indicating the need for dedicated algorithms. Combining post-treatment LSM/PLT yielded a high diagnostic accuracy for post-treatment CSPH in cACLD (AUC 0.884; 95% CI 0.843–0.926). Post-treatment LSM <12 kPa & PLT >150 G/L excluded CSPH (sensitivity: 99.2%), while LSM ≥25 kPa was highly specific for CSPH (93.6%). cACLD-validation-cohort: the 3-year decompensation risk was 0% in the 42.5% of patients who met the LSM <12 kPa & PLT >150 G/L criteria. In patients with post-treatment LSM ≥25 kPa (prevalence: 16.8%), the 3-year decompensation risk was 9.6%, while it was 1.3% in those meeting none of the above criteria (prevalence: 40.7%).

Conclusions

NITs can estimate the probability of CSPH after HCV cure and predict clinical outcomes. Patients with cACLD but LSM <12 kPa & PLT>150 G/L may be discharged from portal hypertension surveillance if no co-factors are present, while patients with LSM ≥25 kPa require surveillance/treatment.

Lay summary

Measurement of liver stiffness by a specific ultrasound device and platelet count (a simple blood test) are broadly used for the non-invasive diagnosis of increased blood pressure in the veins leading to the liver, which drives the development of complications in patients with advanced liver disease. The results of our pooled analysis refute previous concerns that these tests are less accurate after the cure of hepatitis C virus (HCV) infection. We have developed diagnostic criteria that facilitate personalized management after HCV cure and allow for a de-escalation of care in a high proportion of patients, thereby decreasing disease burden.

中文翻译：

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HCV 治愈后临床显着门静脉高压症的无创检测

背景与目标

临床显着门静脉高压症（CSPH；肝静脉压力梯度 [HVPG] ≥10 mmHg）的非侵入性检测 (NIT)主要在活动性 HCV 感染患者中进行了研究。HCV 治愈后的调查是有限的，并产生了相互矛盾的结果。我们进行了一项汇总分析，以确定肝脏硬度测量 (LSM)/血小板计数 (PLT) 在这种情况下的诊断/预后效用。

方法

共评估了 418 名治疗前 HVPG ≥ 6 mmHg 并获得持续病毒学应答 (SVR) 并接受治疗后 HVPG 测量的患者，其中 324 名（HVPG/NIT-队列）也有治疗前/治疗后的配对数据-治疗 LSM/PLT。然后，针对 755 名具有 SVR 的代偿性晚期慢性肝病 (cACLD) 患者（cACLD 验证队列）中的直接终点失代偿对衍生的 LSM/PLT 标准进行了验证。

结果

HVPG/NIT 队列：在 cACLD 患者中，CSPH 的治疗前/治疗后患病率为 80%/54%。LSM/HVPG 之间的相关性从治疗前到治疗后增加（r = 0.45对0.60），而 PLT/HVPG 的相关性保持不变。对于给定的 LSM/PLT 值， HVPG往往在治疗后低于治疗后。预处理，表明需要专门的算法。结合治疗后 LSM/PLT 对 cACLD 中治疗后 CSPH 产生了很高的诊断准确性（AUC 0.884；95% CI 0.843–0.926）。治疗后 LSM <12 kPa 和 PLT >150 G/L 排除 CSPH（敏感性：99.2%），而 LSM ≥25 kPa 对 CSPH 具有高度特异性（93.6%）。cACLD 验证队列：在符合 LSM <12 kPa 和 PLT >150 G/L 标准的 42.5% 患者中，3 年失代偿风险为 0%。在治疗后 LSM ≥ 25 kPa 的患者中（患病率：16.8%），3 年失代偿风险为 9.6%，而在不符合上述标准的患者中为 1.3%（患病率：40.7%）。

结论

NIT 可以估计 HCV 治愈后 CSPH 的概率并预测临床结果。cACLD 但 LSM <12 kPa 和 PLT > 150 G/L 的患者如果不存在辅助因素，可以解除门脉高压监测，而 LSM ≥25 kPa 的患者需要监测/治疗。

外行总结

通过特定的超声设备测量肝脏硬度和血小板计数（一种简单的血液测试）被广泛用于无创诊断通往肝脏的静脉血压升高，这会导致晚期肝病患者出现并发症疾病。我们的汇总分析结果驳斥了先前的担忧，即这些测试在丙型肝炎病毒 (HCV) 感染治愈后准确性较低。我们制定了诊断标准，以促进 HCV 治愈后的个性化管理，并允许对大部分患者进行降级护理，从而减轻疾病负担。