Gastroenterology and Multivisceral Transplant Unit, Azienda Ospedale - Università Padova, Padova, Italy.
Department of Surgery, Oncology and Gastroenterology, University of Padova, Padova, Italy.
United European Gastroenterol J. 2023 Nov;11(9):815-824. doi: 10.1002/ueg2.12472. Epub 2023 Oct 4.
The clinical course of acutely decompensated cirrhosis (AD) is heterogeneous. Presepsin (PSP) is a plasmatic biomarker that reflects Toll-like receptor activity and systemic inflammation. We conducted a prospective study to: (1) measure PSP in AD and (2) assess whether PSP in AD can predict the development of acute-on-chronic liver failure (ACLF).
Patients with AD were prospectively recruited at admission and underwent determination of PSP. In study part 1, we compared PSP in AD versus controls (stable decompensated and compensated cirrhosis). In study part 2, we prospectively followed patients with AD for 1 year and evaluated predictors of ACLF.
One hundred and seventy three patients with AD were included (median MELD: 18; CLIF-C AD score: 54). Compared with controls, patients with AD had higher levels of PSP (674 ng/L vs. 310 ng/L vs. 157 ng/L; p < 0.001). In patients with AD, Child-Pugh C and acute kidney injury were associated with higher levels of PSP. During the follow-up, 52 patients developed ACLF (median time from recruitment: 66 days). PSP, CLIF-C AD score, and Child-Pugh stage were independently associated with ACLF. A predictive model combining these variables (Padua model 2.0) accurately identified patients at higher risk of ACLF (AUROC 0.864; 95% CI 0.780-0.947; sensitivity 82.9%, specificity 76.7%). In patients at lower risk of ACLF based on a CLIF-C AD <50, a PSP >674 ng/L could discriminate between two groups at significantly different risk of ACLF. Finally, in patients who did not develop ACLF, baseline PSP was significantly higher in those who progressed toward unstable versus stable decompensated cirrhosis.
The Padua model 2.0 can be used to identify patients with AD at high risk of ACLF. If these results are validated by external cohorts, PSP could become a new biomarker to improve risk stratification in AD.
急性失代偿性肝硬化（AD）的临床病程具有异质性。Presepsin（PSP）是一种反映 Toll 样受体活性和全身炎症的血浆生物标志物。我们进行了一项前瞻性研究：（1）测量 AD 中的 PSP；（2）评估 AD 中的 PSP 是否可以预测慢加急性肝衰竭（ACLF）的发生。
前瞻性招募 AD 患者入院，并测定 PSP。在研究部分 1 中，我们比较了 AD 患者与对照组（稳定失代偿和代偿性肝硬化）之间的 PSP。在研究部分 2 中，我们前瞻性随访 AD 患者 1 年，并评估了 ACLF 的预测因素。
共纳入 173 例 AD 患者（中位 MELD：18；CLIF-C AD 评分：54）。与对照组相比，AD 患者的 PSP 水平更高（674ng/L 比 310ng/L 比 157ng/L；p<0.001）。在 AD 患者中，Child-Pugh C 级和急性肾损伤与更高的 PSP 水平相关。在随访期间，52 例患者发生 ACLF（招募后中位时间：66 天）。PSP、CLIF-C AD 评分和 Child-Pugh 分期与 ACLF 独立相关。将这些变量结合起来的预测模型（Padua 模型 2.0）能准确识别出 ACLF 风险较高的患者（AUROC 0.864；95%CI 0.780-0.947；敏感性 82.9%，特异性 76.7%）。在基于 CLIF-C AD<50 风险较低的患者中，PSP>674ng/L 可以区分 ACLF 风险显著不同的两组患者。最后，在未发生 ACLF 的患者中，进展为不稳定失代偿性肝硬化的患者其基线 PSP 明显更高。
Padua 模型 2.0 可用于识别 AD 患者 ACLF 风险较高的患者。如果这些结果在外部队列中得到验证，PSP 可能成为 AD 中改善风险分层的新生物标志物。
