Baveno VII has defined a clinically significant (, prognostically meaningful) decrease in liver stiffness measurement (LSM) in cACLD as a decrease of ≥20% associated with a final LSM <20 kPa or any decrease to <10 kPa. However, these rules have not yet been validated against direct clinical endpoints. We retrospectively analysed patients with cACLD (LSM ≥10 kPa) with paired liver stiffness measurement (LSM) before (BL) and after (FU) HCV cure by interferon-free therapies from 15 European centres. The cumulative incidence of hepatic decompensation was compared according to these criteria, considering hepatocellular carcinoma and non-liver-related death as competing risks. A total of 2,335 patients followed for a median of 6 years were analysed. Median BL-LSM was 16.6 kPa with 37.1% having ≥20 kPa. After HCV cure, FU-LSM decreased to a median of 10.9 kPa (<10 kPa: 1,002 [42.9%], ≥20 kPa: 465 [19.9%]) translating into a median LSM change of -5.3 (-8.8 to -2.4) kPa corresponding to -33.9 (-48.0 to -15.9) %. Patients achieving a clinically significant decrease (65.4%) had a significantly lower risk of hepatic decompensation (subdistribution hazard ratio: 0.12, 95% CI 0.04-0.35, <0.001). However, these risk differences were primarily driven by a negligible risk in patients with FU-LSM <10 kPa (5-year cumulative incidence: 0.3%) compared to a high risk in patients with FU-LSM ≥20 kPa (16.6%). Patients with FU-LSM 10-19.9 kPa (37.4%) also had a low risk of hepatic decompensation (5-year cumulative incidence: 1.7%), and importantly, the risk of hepatic decompensation did not differ between those with/without an LSM decrease of ≥20% ( = 0.550). FU-LSM is key for risk stratification after HCV cure and should guide clinical decision making. LSM dynamics do not hold significant prognostic information in patients with FU-LSM 10-19.9 kPa, and thus, their consideration is not of sufficient incremental value in the specific context of HCV cure. Liver stiffness measurement (LSM) is increasingly applied as a prognostic biomarker and commonly decreases in patients with compensated advanced chronic liver disease achieving HCV cure. Although Baveno VII proposed criteria for a clinically significant decrease, little is known about the prognostic utility of LSM dynamics (changes through antiviral therapy). Interestingly, in those with a post-treatment LSM of 10-19.9 kPa, LSM dynamics did not provide incremental information, arguing against the consideration of LSM dynamics as prognostic criteria. Thus, post-treatment LSM should guide the management of patients with compensated advanced chronic liver disease achieving HCV cure.

中文翻译：

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治疗后 LSM 而不是治疗期间的变化可预测 cACLD 患者 HCV 治愈后的失代偿

Baveno VII 将 cACLD 中肝脏硬度测量值 (LSM) 临床显着（具有预后意义）的降低定义为与最终 LSM <20 kPa 或任何降低至 <10 kPa 相关的≥20% 的降低。然而，这些规则尚未针对直接临床终点进行验证。我们回顾性分析了来自 15 个欧洲中心的 cACLD（LSM ≥ 10 kPa）患者，在 HCV 治疗前（BL）和治疗后（FU）进行了配对肝脏硬度测量（LSM）。根据这些标准比较肝功能失代偿的累积发生率，并将肝细胞癌和非肝脏相关死亡视为竞争风险。总共对 2,335 名患者进行了中位随访 6 年的分析。 BL-LSM 中位数为 16.6 kPa，其中 37.1% ≥20 kPa。 HCV 治愈后，FU-LSM 下降至中位 10.9 kPa（<10 kPa：1,002 [42.9%]，≥20 kPa：465 [19.9%]），转化为中位 LSM 变化为 -5.3（-8.8 至 -2.4） ) kPa 对应于-33.9（-48.0 至-15.9）%。实现临床显着降低的患者 (65.4%) 肝功能失代偿的风险显着降低（次分布风险比：0.12，95% CI 0.04-0.35，<0.001）。然而，这些风险差异主要是由于 FU-LSM <10 kPa 的患者风险可忽略不计（5 年累积发生率：0.3%），而 FU-LSM ≥20 kPa 的患者风险较高（16.6%）。 FU-LSM 10-19.9 kPa (37.4%) 的患者肝代偿失调的风险也较低（5 年累积发生率：1.7%），重要的是，有/无 LSM 的患者肝代偿失调的风险没有差异下降≥20% (= 0.550)。 FU-LSM 是 HCV 治愈后风险分层的关键，应指导临床决策。 LSM 动态对于 FU-LSM 10-19.9 kPa 的患者不具有重要的预后信息，因此，在 HCV 治愈的特定背景下，它们的考虑没有足够的增量价值。肝脏硬度测量 (LSM) 越来越多地用作预后生物标志物，并且在获得 HCV 治愈的代偿性晚期慢性肝病患者中通常会降低。尽管 Baveno VII 提出了临床上显着下降的标准，但人们对 LSM 动态（通过抗病毒治疗引起的变化）的预后效用知之甚少。有趣的是，对于那些治疗后 LSM 为 10-19.9 kPa 的患者，LSM 动力学没有提供增量信息，这反对将 LSM 动力学视为预后标准。因此，治疗后 LSM 应指导代偿性晚期慢性肝病患者的管理，以实现 HCV 治愈。