Journal of clinical and experimental hepatology · 2026
Predicting Recompensation in Alcohol, HBV and HCV-associated Decompensated Cirrhosis.
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Arora Umang, Goyal Ritik, Gupta Ishan, Garg Sanil, Vadodaria Vishwa, Boparai Gurasis, Jha Rosemary, Mehta Shubham, Narayan Hari, Vaishnav Manas, Biswas Sagnik, Aggarwal Arnav, Sheikh Sabreena, Agarwal Ayush, Gamanagatti Shivanand, Sharma Raju, Shalimar
Аннотация
BACKGROUND: Recompensation of cirrhosis represents sustained clinical improvement in decompensated cirrhosis following effective etiological treatment. Baseline predictors can help prognostication in hepatology practice.
METHODS: We conducted a retrospective study of patients with decompensated cirrhosis due to alcohol-associated (ALD) or viral (HBV or HCV) cirrhosis who received etiology-specific treatment following decompensation. Demographic details, laboratory parameters, and liver stiffness measurement (LSM) parameters were recorded at index decompensation, presentation, and follow-up. Recompensation was defined per Baveno-VII criteria. CT-derived sarcopenia (L3) and vertebral bone density (L1) were obtained when scans were available within 2 years of decompensation. Fine-Gray competing risk regression accounted for death, hepatocellular carcinoma (HCC), and liver transplantation as competing events.
RESULTS: Of 244 patients (median age 43 (35-50) years; 78.7% males) with ALD (n = 104), HBV (n = 81), or HCV (n = 59) decompensated cirrhosis, 70 (28.7%) achieved recompensation over a median follow-up of 38 months (IQR 18.5-69). Recompensation was more frequent in HBV(42%) and HCV(35.6%) cirrhosis vs ALD (14.4%, P < 0.001). Recompensated patients had lower MELD score (10.1 vs 14.7, P < 0.001), bilirubin (1.5 vs 2.2 mg/dL, P = 0.006), and INR (1.3 vs 1.5, P = 0.002) at baseline. Univariate competing-risk analysis showed stepwise reduction in recompensation likelihood with increasing MELD category (MELD 10-15: sHR 0.56, MELD >15: sHR 0.34, vs MELD <10). On multivariable analysis, higher platelet count, absence of jaundice at baseline, and HBV etiology were independently associated with recompensation. LSM (n = 145) was numerically lower in recompensated patients (29.3 vs 36.9 kPa, P = 0.1), with greater median decline at follow-up (-20.7% vs 0%, P = 0.007). CT-based measurements (n = 69) showed recompensated patients had lower prevalence of sarcopenia (27.3% vs 59.6%, P = 0.01), higher vertebral bone density (243.1 ± 50.5 vs 196.2 ± 62.8 HU, P = 0.003), and no osteopenia (L1 vertebral body density <150 HU, 0% vs 31.9%, P = 0.003). Three (4.3%) recompensated patients developed HCC.
CONCLUSION: Recompensation occurs in one-fourth of patients with decompensated cirrhosis and is more frequent in viral than alcohol-associated etiologies. Higher platelet count and absence of jaundice at baseline independently predicted recompensation.
METHODS: We conducted a retrospective study of patients with decompensated cirrhosis due to alcohol-associated (ALD) or viral (HBV or HCV) cirrhosis who received etiology-specific treatment following decompensation. Demographic details, laboratory parameters, and liver stiffness measurement (LSM) parameters were recorded at index decompensation, presentation, and follow-up. Recompensation was defined per Baveno-VII criteria. CT-derived sarcopenia (L3) and vertebral bone density (L1) were obtained when scans were available within 2 years of decompensation. Fine-Gray competing risk regression accounted for death, hepatocellular carcinoma (HCC), and liver transplantation as competing events.
RESULTS: Of 244 patients (median age 43 (35-50) years; 78.7% males) with ALD (n = 104), HBV (n = 81), or HCV (n = 59) decompensated cirrhosis, 70 (28.7%) achieved recompensation over a median follow-up of 38 months (IQR 18.5-69). Recompensation was more frequent in HBV(42%) and HCV(35.6%) cirrhosis vs ALD (14.4%, P < 0.001). Recompensated patients had lower MELD score (10.1 vs 14.7, P < 0.001), bilirubin (1.5 vs 2.2 mg/dL, P = 0.006), and INR (1.3 vs 1.5, P = 0.002) at baseline. Univariate competing-risk analysis showed stepwise reduction in recompensation likelihood with increasing MELD category (MELD 10-15: sHR 0.56, MELD >15: sHR 0.34, vs MELD <10). On multivariable analysis, higher platelet count, absence of jaundice at baseline, and HBV etiology were independently associated with recompensation. LSM (n = 145) was numerically lower in recompensated patients (29.3 vs 36.9 kPa, P = 0.1), with greater median decline at follow-up (-20.7% vs 0%, P = 0.007). CT-based measurements (n = 69) showed recompensated patients had lower prevalence of sarcopenia (27.3% vs 59.6%, P = 0.01), higher vertebral bone density (243.1 ± 50.5 vs 196.2 ± 62.8 HU, P = 0.003), and no osteopenia (L1 vertebral body density <150 HU, 0% vs 31.9%, P = 0.003). Three (4.3%) recompensated patients developed HCC.
CONCLUSION: Recompensation occurs in one-fourth of patients with decompensated cirrhosis and is more frequent in viral than alcohol-associated etiologies. Higher platelet count and absence of jaundice at baseline independently predicted recompensation.