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Background and objective: Non-acute decompensation (NAD) has emerged as an intermediate, outpatient phenotype on the cirrhosis continuum, yet prospective prognostic data remain limited. We evaluated predictors of (i) acute decompensation (AD) and (ii) death or liver transplantation (Death/LTx) in a well-phenotyped cohort.

Method: In this single-centre prospective study, adults with cirrhosis underwent standardized clinical assessment, laboratory testing and ultrasound quantification of ascites at baseline and 3 months, then were followed for 12 months. Patients were categorized as compensated cirrhosis(CC) or NAD. Outcomes were incident AD and Death/LTx. Variable selection and robustness, we used Elastic Net(ENet)–penalized Cox models with 10-fold-cross-validation (1-SE rule).

Result: Among 325 patients, 122(37.5%) had NAD at baseline. Over follow-up, AD occurred in 50/321(15.6%) overall—27/120(22.5%) NAD vs 23/201(11.4%) CC—and Death/LTx in 50/323(15.5%). Within NAD, the clearest predictors for future AD were more perihepatic ascites on ultrasound and higher creatinine. A small, contribution came from higher IL-6. Classic liver markers and MELD-Na did not showed a predictive value. For the composite of death or liver transplantation, bilirubin was the most consistent predictor. When MELD-Na was considered, it became the dominant predictor for Death/LTx.

Summary: NAD marks a clinically relevant risk state with higher AD incidence and reduced transplant-free survival versus CC. Progression to AD is chiefly signaled by ascites and renal dysfunction, with a smaller, contribution from IL-6, while traditional liver indices and MELD-Na add little for AD. For Death/LTx, bilirubin/MELD-Na dominates prognostication. Findings support routine ultrasound-based ascites quantification and inflammatory profiling to refine risk in NAD.