Ankur Jindal1, Sanchit Sharma2, Samagra Agarwal1, Manoj Kumar1, Anoop Saraya3, Shiv Kumar Sarin4. 1. Department of Hepatology and Liver Transplantation, Institute of Liver and Biliary Sciences, New Delhi, 110070, India. 2. Department of Gastroenterology and Human Nutrition Unit, All India Institute of Medical Sciences, New Delhi, 110029, India. 3. Department of Gastroenterology and Human Nutrition Unit, All India Institute of Medical Sciences, New Delhi, 110029, India. ansaraya@yahoo.com. 4. Department of Hepatology and Liver Transplantation, Institute of Liver and Biliary Sciences, New Delhi, 110070, India. shivsarin@gmail.com.
Abstract
BACKGROUND AND AIMS: Liver stiffness measurement (LSM) alone or its combination with platelet counts [Baveno-VI criteria (B6C)] is an important non-invasive tool to predict risk of clinical decompensation in patients with advanced compensated cirrhosis. We compared its utility to decide need for beta-blockers in this regard compared with hepatic venous pressure gradient (HVPG) estimation. METHODS: Patients with compensated cirrhosis with available baseline HVPG and LSM were followed up over a median follow-up of 26 (IQR 7-55) months to determine onset of clinical decompensations. Optimal cut-off for LSM for predicting decompensations was identified and compared with HVPG of 10 mmHg and B6C. Feasibility of initiating beta-blockers based on these strategies was assessed using decision curve analysis (DCA) at different threshold probabilities of rates of clinical decompensation. RESULTS: 626 patients (mean age: 50.8 ± 12.4 years, 72.4% males) related to alcohol (30.3%), non-alcoholic steatohepatitis (26.4%), hepatitis C (16.6%), hepatitis B (10.2%) were included. Altogether, 132 (21.0%) patients developed clinical decompensation. The time-dependant area under curve over 5 years for HVPG and LSM for predicting clinical decompensation was 0.716-0.742 and 0.709-0.784, respectively. A LSM of 22 kPa (Sensitivity-88.6%/Specificity-51.8%) had a similar negative predictive value but a higher positive predictive value [37.9% (LSM) vs.30.9% (HVPG)vs.30.6% (B6C), p = 0.026 at 3 years] for incident decompensations. On DCA, LSM-based strategy emerged superior for deciding beta-blocker initiation with 150, 47, and 18 additional patients meriting treatment identified over and above B6C and HVPG based strategy at 5%, 10%, 20% annual rates of clinical decompensation, respectively. CONCLUSION: Measurement of liver stiffness alone can be a useful alternative to B6C and HVPG in deciding need for beta-blockers to prevent decompensations in compensated cirrhosis.
BACKGROUND AND AIMS: Liver stiffness measurement (LSM) alone or its combination with platelet counts [Baveno-VI criteria (B6C)] is an important non-invasive tool to predict risk of clinical decompensation in patients with advanced compensated cirrhosis. We compared its utility to decide need for beta-blockers in this regard compared with hepatic venous pressure gradient (HVPG) estimation. METHODS: Patients with compensated cirrhosis with available baseline HVPG and LSM were followed up over a median follow-up of 26 (IQR 7-55) months to determine onset of clinical decompensations. Optimal cut-off for LSM for predicting decompensations was identified and compared with HVPG of 10 mmHg and B6C. Feasibility of initiating beta-blockers based on these strategies was assessed using decision curve analysis (DCA) at different threshold probabilities of rates of clinical decompensation. RESULTS: 626 patients (mean age: 50.8 ± 12.4 years, 72.4% males) related to alcohol (30.3%), non-alcoholic steatohepatitis (26.4%), hepatitis C (16.6%), hepatitis B (10.2%) were included. Altogether, 132 (21.0%) patients developed clinical decompensation. The time-dependant area under curve over 5 years for HVPG and LSM for predicting clinical decompensation was 0.716-0.742 and 0.709-0.784, respectively. A LSM of 22 kPa (Sensitivity-88.6%/Specificity-51.8%) had a similar negative predictive value but a higher positive predictive value [37.9% (LSM) vs.30.9% (HVPG)vs.30.6% (B6C), p = 0.026 at 3 years] for incident decompensations. On DCA, LSM-based strategy emerged superior for deciding beta-blocker initiation with 150, 47, and 18 additional patients meriting treatment identified over and above B6C and HVPG based strategy at 5%, 10%, 20% annual rates of clinical decompensation, respectively. CONCLUSION: Measurement of liver stiffness alone can be a useful alternative to B6C and HVPG in deciding need for beta-blockers to prevent decompensations in compensated cirrhosis.
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