目的:BavenoVII定义了一种临床上有意义的(即,具有预后意义的)cACLD中肝脏硬度测量值(LSM)的降低与最终LSM<20kPa或任何降低至<10kPa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.
方法:我们回顾性分析了来自15个欧洲中心的cACLD(LSM≥10kPa)患者在无干扰素治疗HCV治愈之前(BL)和之后(FU)进行配对肝硬度测量(LSM)。根据这些标准比较肝失代偿的累积发生率,将肝细胞癌和非肝脏相关死亡视为竞争风险。
结果:总共分析了2,335名患者的中位随访时间为6年。BL-LSM中位数为16.6kPa,37.1%≥20kPa。HCV治愈后,FU-LSM降至10.9kPa的中值(<10kPa:1,002[42.9%],≥20kPa:465[19.9%])转换为-5.3(-8.8至-2.4)kPa的中位数LSM变化,对应于-33.9(-48.0至-15.9)%。达到临床显着下降(65.4%)的患者肝功能失代偿的风险显着降低(亚分布风险比:0.12,95%CI0.04-0.35,p<0.001)。然而,这些风险差异主要是由于FU-LSM<10kPa患者的风险可忽略不计(5年累积发生率:0.3%),而FU-LSM≥20kPa患者的风险较高(16.6%).FU-LSM10-19.9kPa(37.4%)的患者也有肝脏失代偿的低风险(5年累积发生率:1.7%),而且重要的是,肝代偿失调的风险在LSM降低≥20%的患者之间没有差异(p=0.550).
结论:FU-LSM是HCV治愈后危险分层的关键,应指导临床决策。LSM动力学在FU-LSM10-19.9kPa患者中不具有重要的预后信息,因此,他们的考虑在HCV治愈的特定背景下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,并且通常在代偿性晚期慢性肝病患者中减少实现HCV治愈。尽管BavenoVII提出了临床显着下降的标准,关于LSM动力学(通过抗病毒治疗的变化)的预后效用知之甚少。有趣的是,在治疗后LSM为10-19.9kPa的患者中,LSM动态没有提供增量信息,反对将LSM动力学作为预后标准。因此,治疗后LSM应指导获得HCV治愈的代偿性晚期慢性肝病患者的管理。
OBJECTIVE: Baveno VII has defined a clinically significant (i.e., 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.
METHODS: 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.
RESULTS: 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, p <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% (p = 0.550).
CONCLUSIONS: 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.
UNASSIGNED: 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.