This prospective cohort study (VICIS; n=464) evaluated stage-specific biomarkers — portal hypertension (HVPG), endothelial dysfunction (VWF), fibrogenesis (ELF), liver function (MELD/albumin/bile acids), systemic inflammation (CRP/IL-6/procalcitonin), and circulatory dysfunction (proBNP/copeptin) — for their ability to predict clinical transitions across compensated ACLD, decompensated cirrhosis, and further decompensation/ACLF, over a median 35-month follow-up.
In cACLD, 13% decompensated and 1.9% died from liver-related causes at 24 months; HVPG and albumin were independent prognostic markers. In decompensated cirrhosis, 19% progressed to further decompensation/ACLF and 6.1% died, with CRP as the key independent predictor. In further decompensation, 33% died at 12 months, with copeptin independently predictive.
Single-center prospective cohort limits generalizability; recompensation rates were low, reducing power to analyze that transition; patients were enrolled at HVPG measurement, potentially selecting a more severe or evaluated subgroup.
In compensated cirrhosis, prioritize reducing portal hypertension (e.g., target HVPG reduction) and optimizing albumin levels. Once decompensation occurs, shift focus to controlling systemic inflammation (CRP-guided) and, in further decompensation, address circulatory dysfunction (copeptin-guided).
Explore related topics
