Recompensation after acute decompensation in alcohol-related cirrhosis is rare and likely unrelated to platelet-poor plasma thrombin generation and fibrinolysis

Background: Hemostasis may be involved in cirrhosis progression. However, its potential involvement in hepatic recompensation is unknown. Objective: We investigated predictors of recompensation, including coagulation and fibrinolysis, in acutely decompensated, alcohol-related cirrhosis. Methods: Clinical and laboratory data were collected at hospitalization. Coagulation was assessed via factor VIII, natural anticoagulants, and thrombin generation assay. Fibrinolysis was assessed via pro and anti-fibrinolytic factors and plasmin-antiplasmin complexes. Patients were prospectively followed up for recompensation according to Baveno VII criteria. Results: We included 224 patients (Child-Pugh B/C 46/54 %). Cumulative rate of recompensation was 5.4 % (median follow-up: 450 days). Patients who achieved recompensation had lower MELD (12 vs. 17, p = 0.02), Child-Pugh C (25 % vs 56 %, p = 0.04), and higher platelet count (106 × 109/L vs. 83 × 109/L) than those who did not, without differences in coagulation and fibrinolysis. In Cox-regression analysis, Child-Pugh was the only predictor of recompensation (HR: 0.26; p = 0.02). Same results were observed with the "expanded" Baveno VII criteria for recompensation. A competing risk analysis considering ACLF/liver-related death, transplantation, and TIPS as competing risks showed comparable results. Conclusion: In acutely decompensated, alcohol-related cirrhosis, recompensation is rare and linked to the baseline severity of liver disease. Coagulation and fibrinolysis seem not to be involved in cirrhosis recompensation.