Hepatology international · 2022
Liver stiffness can predict decompensation and need for beta-blockers in compensated cirrhosis: a step beyond Baveno-VI criteria.
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Jindal Ankur, Sharma Sanchit, Agarwal Samagra, Kumar Manoj, Saraya Anoop, Sarin Shiv Kumar
Аннотация
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.
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.