Journal of hepatology · 2025
Predicting hepatic decompensation using non-invasive tests in a contemporary multicentre cohort of patients with cACLD.
СтатьяМногоцентровое исследованиеНазвание и аннотация: Перевод в очереди
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Jachs Mathias, Thöne Paul, Odriozola Aitor, Turon Fanny, Moga Lucile, Téllez Luis, Fischer Petra, Saltini Dario, Kwanten Wilhelmus J, Grasso Maria, Llop Elba, Mendoza Yuly P, Armandi Angelo, Pardo Carlos, Colecchia Antonio, Ravaioli Federico, Maasoumy Benjamin, Laleman Wim, Presa José, Schattenberg Jörn M, Berzigotti Annalisa, Calleja José L, Calvaruso Vincenza, Vanwolleghem Thomas, Schepis Filippo, Procopet Bogdan, Albillos Agustín, Rautou Pierre-Emmanuel, Garcia-Pagan Juan C, Puente Ángela, Fortea José I, Reiberger Thomas, Mandorfer Mattias, SSM-100Hz/ACLD Study Group of the Baveno Cooperation: an EASL consortium
Аннотация
BACKGROUND & AIMS: The NICER (liver and spleen stiffness by vibration-controlled transient elastography, platelet count, and BMI) and the ANTICIPATE±NASH models predict clinically significant portal hypertension (CSPH) in compensated advanced chronic liver disease (cACLD). This study reports follow-up data from the NICER cohort, comparing the prognostic utility of non-invasive tests for CSPH (CSPH-NITs) and hepatic venous pressure gradient (HVPG).
METHODS: Patients with Child-Turcotte-Pugh A cACLD (liver stiffness ≥10 kPa and/or F3/4) from 16 European centres undergoing paired HVPG and CSPH-NIT assessment between 2020-2023 were included and followed until incident hepatic decompensation, hepatocellular carcinoma, death, or last visit.
RESULTS: Three hundred and fifty-eight patients with cACLD were included (MASLD: 40.7%; MetALD/ALD: 32.1%; viral: 16.2%), with a CSPH prevalence of 62.0%. The cumulative 1-year and 2-year incidences of decompensation were 7.3 (95% CI 5.9-8.7%) and 12.6 (10.3-14.9%). Albumin levels were a key predictor of decompensation (subdistribution hazard ratio [sHR] 0.836; 95% CI 0.779-0.897), alongside HVPG (albumin-adjusted SHR 1.126; 95% CI 1.059-1.198), NICER (albumin-adjusted SHR 1.207; 95% CI 1.043-1.397), or ANTICIPATE±NASH (albumin-adjusted SHR 1.174; 95% CI 1.003-1.374). Models incorporating albumin alongside HVPG or CSPH-NIT achieved high C-indices for decompensation (0.772-0.806). Stratifying patients by a predicted 1-year decompensation-free survival probability of ≥95% or <95% identified approximately 60% of patients as being at negligible 1-year risk (1.4-2.1%), while the remaining patients were at high risk of decompensation (14.3-16.0%).
CONCLUSION: In our multicentre study of contemporary European patients with cACLD, non-invasively estimated CSPH risk was as predictive for decompensation as HVPG. Models comprising indicators of portal hypertension and albumin discriminated between patients at negligible decompensation risk and those with a 1-year risk of approximately 15%, i.e. the potential target population for preventive strategies.
IMPACT AND IMPLICATIONS: Non-invasive tests (NITs) facilitate the early diagnosis and management of clinically significant portal hypertension in patients with compensated advanced chronic liver disease (cACLD). In our contemporary cohort of patients with cACLD, mainly steatotic liver disease, recruited at 16 European expert centres, the hepatic venous pressure gradient and NITs were similarly predictive of decompensation within 1 to 2 years of follow-up. Serum albumin levels were identified as the second main predictor of decompensation after hepatic venous pressure gradient or NITs for clinically significant portal hypertension. Novel models were developed that could accurately predict the risk of decompensation, thereby refining point-of-care risk stratification and informing clinical trial design for patients with CTP-A cACLD.
METHODS: Patients with Child-Turcotte-Pugh A cACLD (liver stiffness ≥10 kPa and/or F3/4) from 16 European centres undergoing paired HVPG and CSPH-NIT assessment between 2020-2023 were included and followed until incident hepatic decompensation, hepatocellular carcinoma, death, or last visit.
RESULTS: Three hundred and fifty-eight patients with cACLD were included (MASLD: 40.7%; MetALD/ALD: 32.1%; viral: 16.2%), with a CSPH prevalence of 62.0%. The cumulative 1-year and 2-year incidences of decompensation were 7.3 (95% CI 5.9-8.7%) and 12.6 (10.3-14.9%). Albumin levels were a key predictor of decompensation (subdistribution hazard ratio [sHR] 0.836; 95% CI 0.779-0.897), alongside HVPG (albumin-adjusted SHR 1.126; 95% CI 1.059-1.198), NICER (albumin-adjusted SHR 1.207; 95% CI 1.043-1.397), or ANTICIPATE±NASH (albumin-adjusted SHR 1.174; 95% CI 1.003-1.374). Models incorporating albumin alongside HVPG or CSPH-NIT achieved high C-indices for decompensation (0.772-0.806). Stratifying patients by a predicted 1-year decompensation-free survival probability of ≥95% or <95% identified approximately 60% of patients as being at negligible 1-year risk (1.4-2.1%), while the remaining patients were at high risk of decompensation (14.3-16.0%).
CONCLUSION: In our multicentre study of contemporary European patients with cACLD, non-invasively estimated CSPH risk was as predictive for decompensation as HVPG. Models comprising indicators of portal hypertension and albumin discriminated between patients at negligible decompensation risk and those with a 1-year risk of approximately 15%, i.e. the potential target population for preventive strategies.
IMPACT AND IMPLICATIONS: Non-invasive tests (NITs) facilitate the early diagnosis and management of clinically significant portal hypertension in patients with compensated advanced chronic liver disease (cACLD). In our contemporary cohort of patients with cACLD, mainly steatotic liver disease, recruited at 16 European expert centres, the hepatic venous pressure gradient and NITs were similarly predictive of decompensation within 1 to 2 years of follow-up. Serum albumin levels were identified as the second main predictor of decompensation after hepatic venous pressure gradient or NITs for clinically significant portal hypertension. Novel models were developed that could accurately predict the risk of decompensation, thereby refining point-of-care risk stratification and informing clinical trial design for patients with CTP-A cACLD.