Using liver stiffness to predict and monitor the risk of decompensation and mortality in patients with alcohol-related liver disease

失代偿 医学 肝病 疾病 内科学 心脏病学 胃肠病学 生物 生物化学
作者
Katrine Thorhauge,Georg Semmler,Stine Johansen,Katrine Prier Lindvig,Maria Kjærgaard,Johanne Kragh Hansen,Nikolaj Torp,Camilla Dalby Hansen,Peter Andersen,Benedikt Hofer,Wen Gu,Mads Israelsen,Mattias Mandorfer,Thomas Reiberger,Jonel Trebicka,Maja Thiele,Aleksander Krag
出处
期刊:Journal of Hepatology [Elsevier BV]
卷期号:81 (1): 23-32 被引量:15
标识
DOI:10.1016/j.jhep.2024.02.019
摘要

Background & Aims Liver stiffness measurements (LSM) are recommended for disease prognostication and monitoring. We evaluated if LSM, using transient elastography, and LSM changes predict decompensation and mortality in patients with alcohol-related liver disease (ALD). Methods Observational cohort study of compensated patients at risk of ALD from Denmark and Austria. We evaluated the risk of decompensation and all-cause mortality, stratified for compensated advanced chronic liver disease (cACLD: Baseline LSM ≥10 kPa) and LSM changes after a median of 2 years. In patients with cACLD, we defined LSM changes as (A) LSM increase ≥20% ("cACLD increasers") and (B) follow-up LSM <10 kPa or <20 kPa with LSM decrease ≥20% ("cACLD decreasers"). In patients without cACLD, we defined follow-up LSM ≥10 kPa as a LSM increase ("No cACLD increasers"). Remaining patients were considered LSM stable. Results We followed 536 patients for 3,008 patient-years, median age 57 years (IQR 49–63), baseline LSM 8.1 kPa (IQR 4.9-21.7). 371 patients (69%) had follow-up LSM after a median of 25 months (IQR 17–38), 41 subsequently decompensated and 55 died. Of 125 with cACLD at baseline, 14% were "cACLD increasers" and 43% "cACLD decreasers", while 13% of patients without cACLD were "No cACLD increasers" (n=33/246). Baseline LSM, follow-up LSM and LSM changes accurately predicted decompensation (C-index: Baseline LSM 0.85; Follow-up LSM 0.89; LSM changes 0.85) and mortality (C-index: Baseline LSM 0.74; Follow-up LSM 0.74; LSM changes 0.70). When compared to "cACLD decreasers", "cACLD increasers" had significantly lower decompensation-free survival and higher risks of decompensation (SHR=4.39, P=0.004) and mortality (HR=3.22, P=0.01). Conclusion Liver stiffness by transient elastography predicts decompensation and all-cause mortality in patients with compensated alcohol-related liver disease both at diagnosis and when used for monitoring.
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