Liver stiffness measurement (LSM) is 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). We performed an 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 an LSM increase (“No cACLD increasers”). The remaining patients were considered LSM stable. 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 (subdistribution hazard ratio 4.39, 0.004) and mortality (hazard ratio 3.22, 0.01). LSM by transient elastography predicts decompensation and all-cause mortality in patients with compensated ALD both at diagnosis and when used for monitoring. Patients at risk of alcohol-related liver disease (ALD) are at significant risk of progressive disease and adverse outcomes. Monitoring is essential for optimal disease surveillance and patient guidance, but non-invasive monitoring tools are lacking. In this study we demonstrate that liver stiffness measurement (LSM), using transient elastography, and LSM changes after a median of 2 years, can predict decompensation and all-cause mortality in patients at risk of ALD with and without compensated advanced chronic liver disease. These findings are in line with results from non-alcoholic fatty liver disease, hepatitis C and primary sclerosing cholangitis, and support the clinical utility of LSM, using transient elastography, for disease prognostication and monitoring in chronic liver diseases including ALD, as recommended by the Baveno VII.

中文翻译：

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利用肝脏硬度来预测和监测酒精相关性肝病患者的失代偿和死亡风险

建议使用肝脏硬度测量（LSM）进行疾病预测和监测。我们使用瞬时弹性成像评估了 LSM 和 LSM 变化是否可以预测酒精相关性肝病 (ALD) 患者的失代偿和死亡率。我们对来自丹麦和奥地利的有 ALD 风险的代偿患者进行了一项观察性队列研究。我们评估了失代偿和全因死亡率的风险，针对代偿性晚期慢性肝病（cACLD：基线 LSM ≥10 kPa）和中位 2 年后 LSM 变化进行分层。在 cACLD 患者中，我们将 LSM 变化定义为 (A) LSM 增加 ≥20%（“cACLD 增加者”）和 (B) 随访 LSM <10 kPa 或 <20 kPa，且 LSM 降低 ≥20%（“cACLD 减少者”） ）。对于无 cACLD 的患者，我们将随访 LSM ≥10 kPa 定义为 LSM 增加（“无 cACLD 增加者”）。其余患者被认为 LSM 稳定。我们对 536 名患者进行了 3,008 患者年的随访，中位年龄 57 岁（IQR 49-63），基线 LSM 8.1 kPa（IQR 4.9-21.7）。 371 名患者 (69%) 在中位 25 个月 (IQR 17-38) 后进行了 LSM 随访，41 名患者随后失代偿，55 名死亡。在 125 名基线患有 cACLD 的患者中，14% 为“cACLD 增加者”，43% 为“cACLD 减少者”，而无 cACLD 的患者中有 13% 为“无 cACLD 增加者”(n = 33/246)。基线 LSM、随访 LSM 和 LSM 变化准确预测了失代偿（C 指数：基线 LSM 0.85；随访 LSM 0.89；LSM 变化 0.85）和死亡率（C 指数：基线 LSM 0.74；随访 LSM 0.74；LSM）变化 0.70)。与“cACLD 减少者”相比，“cACLD 增加者”的无失代偿生存率显着较低，失代偿风险较高（次分布风险比 4.39，0.004）和死亡率（风险比 3.22，0.01）。通过瞬时弹性成像的 LSM 可预测代偿性 ALD 患者在诊断时和用于监测时的失代偿和全因死亡率。有酒精相关性肝病 (ALD) 风险的患者面临疾病进展和不良后果的显着风险。监测对于最佳疾病监测和患者指导至关重要，但缺乏非侵入性监测工具。在这项研究中，我们证明，使用瞬时弹性成像的肝脏硬度测量 (LSM) 以及中位 2 年后 LSM 的变化，可以预测有或没有代偿性晚期慢性肝病的 ALD 风险患者的失代偿和全因死亡率。这些发现与非酒精性脂肪性肝病、丙型肝炎和原发性硬化性胆管炎的结果一致，并支持 LSM 的临床实用性，使用瞬时弹性成像，对包括 ALD 在内的慢性肝病进行疾病预测和监测，正如巴韦诺七世。