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。