Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; Vienna Hepatic Hemodynamic Laboratory, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Department of Biostatistics, Erasmus University Medical Center, Rotterdam, Zuid-Holland, The Netherlands.
Gastroenterology. 2023 Oct;165(4):1041-1052. doi: 10.1053/j.gastro.2023.06.030. Epub 2023 Jul 11.
BACKGROUND & AIMS: Liver stiffness measurements (LSMs) provide an opportunity to monitor liver disease progression and regression noninvasively. We aimed to determine the prognostic relevance of LSM dynamics over time for liver-related events and death in patients with chronic liver disease.
Patients with chronic liver disease undergoing 2 or more reliable LSMs at least 180 days apart were included in this retrospective cohort study and stratified at baseline (BL) as nonadvanced chronic liver disease (non-ACLD, BL-LSM < 10 kPa), compensated ACLD (cACLD; BL-LSM ≥ 10 kPa), and decompensated ACLD. Data on all consecutive LSMs and clinical outcomes were collected.
There were 2508 patients with 8561 reliable LSMs (3 per patient; interquartile range, 2-4) included: 1647 (65.7%) with non-ACLD, 757 (30.2%) with cACLD, and 104 (4.1%) with decompensated ACLD. Seven non-ACLD patients (0.4%) and 83 patients with cACLD (10.9%) developed hepatic decompensation (median follow-up, 71 months). A 20% increase in LSM at any time was associated with an approximately 50% increased risk of hepatic decompensation (hazard ratio, 1.58; 95% CI, 1.41-1.79; P < .001) and liver-related death (hazard ratio, 1.45; 95% CI, 1.28-1.68; P < .001) in patients with cACLD. LSM dynamics yielded a high accuracy to predict hepatic decompensation in the following 12 months (area under the receiver operating characteristics curve = 0.933). The performance of LSM dynamics was numerically better than dynamics in Fibrosis-4 score (0.873), Model for End-Stage Liver Disease (0.835), and single time-point LSM (BL-LSM: 0.846; second LSM: 0.880). Any LSM decrease to <20 kPa identified patients with cACLD with a substantially lower risk of hepatic decompensation (hazard ratio, 0.13; 95% CI, 0.07-0.24). If reliable, LSM also confers prognostic information in decompensated ACLD.
Repeating LSM enables an individual and updated risk assessment for decompensation and liver-related mortality in ACLD.
肝脏硬度测量（LSM）提供了一种机会，可以非侵入性地监测肝脏疾病的进展和逆转。我们旨在确定慢性肝病患者中随时间推移的 LSM 动态变化对肝脏相关事件和死亡的预后相关性。
本回顾性队列研究纳入了至少相隔 180 天进行了 2 次或更多次可靠 LSM 的慢性肝病患者，并在基线（BL）时分层为非进展性慢性肝病（非 ACLD，BL-LSM < 10 kPa）、代偿性 ACLD（cACLD；BL-LSM ≥ 10 kPa）和失代偿性 ACLD。收集了所有连续的 LSM 和临床结局数据。
共纳入了 2508 例患者的 8561 次可靠 LSM（每位患者 3 次；中位数，2-4）：1647 例（65.7%）为非 ACLD，757 例（30.2%）为 cACLD，104 例（4.1%）为失代偿性 ACLD。7 例非 ACLD 患者（0.4%）和 83 例 cACLD 患者（10.9%）发生肝失代偿（中位随访时间为 71 个月）。任何时候 LSM 增加 20%，肝失代偿的风险约增加 50%（风险比，1.58；95%CI，1.41-1.79；P <.001）和与肝脏相关的死亡（风险比，1.45；95%CI，1.28-1.68；P <.001）在 cACLD 患者中。LSM 动态变化在预测接下来 12 个月内肝失代偿方面具有很高的准确性（接受者操作特征曲线下面积=0.933）。LSM 动态变化的性能在数值上优于 Fibrosis-4 评分（0.873）、终末期肝病模型（0.835）和单次时间点 LSM（BL-LSM：0.846；第二次 LSM：0.880）。任何 LSM 下降至<20 kPa 均可识别出 cACLD 患者肝失代偿的风险显著降低（风险比，0.13；95%CI，0.07-0.24）。如果可靠，LSM 也可以在失代偿性 ACLD 中提供预后信息。
重复 LSM 可以对 ACLD 患者的失代偿和与肝脏相关的死亡率进行个体化和更新的风险评估。
