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

Hemostasis may be involved in cirrhosis progression. However, its potential involvement in hepatic recompensation is unknown. We investigated predictors of recompensation, including coagulation and fibrinolysis, in acutely decompensated, alcohol-related cirrhosis. 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. 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. 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.