Natural history of clinical outcomes and hepatic decompensation in metabolic dysfunction-associated steatotic liver disease.
Journal
Alimentary pharmacology & therapeutics
ISSN: 1365-2036
Titre abrégé: Aliment Pharmacol Ther
Pays: England
ID NLM: 8707234
Informations de publication
Date de publication:
03 Apr 2024
03 Apr 2024
Historique:
revised:
07
01
2024
received:
15
12
2023
accepted:
22
03
2024
medline:
4
4
2024
pubmed:
4
4
2024
entrez:
4
4
2024
Statut:
aheadofprint
Résumé
The natural progression of hepatic decompensation in metabolic dysfunction-associated steatotic liver disease (MASLD) is not well-characterised. We aimed to describe it by conducting a retrospective analysis. This longitudinal, retrospective analysis of well-characterised MASLD cohorts followed for hepatic decompensation and death. The sequence of liver-related events was evaluated, and the median time between hepatic decompensation episodes and death versus. transplantation was measured. Of the 2016 patients identified, 220 (11%) developed at least one episode of hepatic decompensation during a median follow-up of 3.2 years. Ascites was the most common first liver-related event [153 (69.5%)], followed by hepatic encephalopathy (HE) [55 (25%)] and variceal haemorrhage (VH) [30 (13.6%)]. Eighteen out of the 220 (8.1%) patients had more than one liver-related event as their first hepatic decompensation. Among the patients who had the first episode, 87 (39.5%) had a second episode [44 (50.5%) HE, 31 (35.6%) ascites, and 12 (13.7%) VH]. Eighteen out of 220 (8.1%) had a third episode [10 (55.5%) HE, 6 (33.3%) VH, and 2 (11.1%) ascites]. Seventy-three out of 220 (33.1%) died, and 31 (14%) received liver transplantation. The median time from the first episode to the second was 0.7 years and 1.3 years from the second episode to the third. The median survival time from the first episode to death or transplantation was 2.0 years. The most common first liver-related event in MASLD patients is ascites. The median survival from the first hepatic decompensation to either death or transplantation is 2 years.
Sections du résumé
BACKGROUND & AIMS
OBJECTIVE
The natural progression of hepatic decompensation in metabolic dysfunction-associated steatotic liver disease (MASLD) is not well-characterised. We aimed to describe it by conducting a retrospective analysis.
METHODS
METHODS
This longitudinal, retrospective analysis of well-characterised MASLD cohorts followed for hepatic decompensation and death. The sequence of liver-related events was evaluated, and the median time between hepatic decompensation episodes and death versus. transplantation was measured.
RESULTS
RESULTS
Of the 2016 patients identified, 220 (11%) developed at least one episode of hepatic decompensation during a median follow-up of 3.2 years. Ascites was the most common first liver-related event [153 (69.5%)], followed by hepatic encephalopathy (HE) [55 (25%)] and variceal haemorrhage (VH) [30 (13.6%)]. Eighteen out of the 220 (8.1%) patients had more than one liver-related event as their first hepatic decompensation. Among the patients who had the first episode, 87 (39.5%) had a second episode [44 (50.5%) HE, 31 (35.6%) ascites, and 12 (13.7%) VH]. Eighteen out of 220 (8.1%) had a third episode [10 (55.5%) HE, 6 (33.3%) VH, and 2 (11.1%) ascites]. Seventy-three out of 220 (33.1%) died, and 31 (14%) received liver transplantation. The median time from the first episode to the second was 0.7 years and 1.3 years from the second episode to the third. The median survival time from the first episode to death or transplantation was 2.0 years.
CONCLUSION
CONCLUSIONS
The most common first liver-related event in MASLD patients is ascites. The median survival from the first hepatic decompensation to either death or transplantation is 2 years.
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIDDK NIH HHS
ID : K23DK119460
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01DK061734
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01DK130190
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01DK106419
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01DK121378
Pays : United States
Organisme : NCATS NIH HHS
ID : 5UL1TR001442
Pays : United States
Organisme : NHLBI NIH HHS
ID : P01HL147835
Pays : United States
Informations de copyright
© 2024 John Wiley & Sons Ltd.
Références
Younossi ZM, Koenig AB, Abdelatif D, Fazel Y, Henry L, Wymer M. Global epidemiology of nonalcoholic fatty liver disease—meta‐analytic assessment of prevalence, incidence, and outcomes. Hepatology. 2016;64:73–84.
Riazi K, Azhari H, Charette JH, Underwood FE, King JA, Afshar EE, et al. The prevalence and incidence of NAFLD worldwide: a systematic review and meta‐analysis. Lancet Gastroenterol Hepatol. 2022;7:851–861.
Le MH, Devaki P, Ha NB, Jun DW, Te HS, Cheung RC, et al. Prevalence of non‐alcoholic fatty liver disease and risk factors for advanced fibrosis and mortality in the United States. PLoS One. 2017;12:e0173499.
Rinella ME, Lazarus JV, Ratziu V, Francque SM, Sanyal AJ, Kanwal F, et al. A multi‐society Delphi consensus statement on new fatty liver disease nomenclature. Ann Hepatol. 2023;101133:E93–E94.
Loomba R, Friedman SL, Shulman GI. Mechanisms and disease consequences of nonalcoholic fatty liver disease. Cell. 2021;184:2537–2564.
Paik JM, Golabi P, Younossi Y, Mishra A, Younossi ZM. Changes in the global burden of chronic liver diseases from 2012 to 2017: the growing impact of NAFLD. Hepatology. 2020;72:1605–1616.
Rinella ME, Neuschwander‐Tetri BA, Siddiqui MS, Abdelmalek MF, Caldwell S, Barb D, et al. AASLD practice guidance on the clinical assessment and management of nonalcoholic fatty liver disease. Hepatology. 2023;1097:10–1835.
Noureddin M, Vipani A, Bresee C, Todo T, Kim IK, Alkhouri N, et al. NASH leading cause of liver transplant in women: updated analysis of indications for liver transplant and ethnic and gender variances. Am J Gastroenterol. 2018;113:1649–1659.
Tapper EB, Ufere NN, Huang DQ, Loomba R. Current and emerging therapies for the management of cirrhosis and its complications. Aliment Pharmacol Ther. 2022;55:1099–1115.
Singh S, Allen AM, Wang Z, Prokop LJ, Murad MH, Loomba R. Fibrosis progression in nonalcoholic fatty liver vs nonalcoholic steatohepatitis: a systematic review and meta‐analysis of paired‐biopsy studies. Clin Gastroenterol Hepatol. 2015;13:643–654.e9.
Tan DJH, Setiawan VW, Ng CH, Lim WH, Muthiah MD, Tan EX, et al. Global burden of liver cancer in males and females: changing etiological basis and the growing contribution of NASH. Hepatology. 2022;77:1150–1163.
Taylor RS, Taylor RJ, Bayliss S, Hagström H, Nasr P, Schattenberg JM, et al. Association between fibrosis stage and outcomes of patients with nonalcoholic fatty liver disease: a systematic review and meta‐analysis. Gastroenterology. 2020;158:1611–1625.e12.
Dulai PS, Singh S, Patel J, Soni M, Prokop LJ, Younossi Z, et al. Increased risk of mortality by fibrosis stage in nonalcoholic fatty liver disease: systematic review and meta‐analysis. Hepatology. 2017;65:1557–1565.
Simon TG, Roelstraete B, Khalili H, Hagström H, Ludvigsson JF. Mortality in biopsy‐confirmed nonalcoholic fatty liver disease: results from a nationwide cohort. Gut. 2021;70:1375–1382.
Ekstedt M, Hagström H, Nasr P, Fredrikson M, Stål P, Kechagias S, et al. Fibrosis stage is the strongest predictor for disease‐specific mortality in NAFLD after up to 33 years of follow‐up. Hepatology. 2015;61:1547–1554.
Hagström H, Nasr P, Ekstedt M, Hammar U, Stål P, Hultcrantz R, et al. Fibrosis stage but not NASH predicts mortality and time to development of severe liver disease in biopsy‐proven NAFLD. J Hepatol. 2017;67:1265–1273.
Huang DQ, Wilson LA, Behling C, Kleiner DE, Kowdley KV, Dasarathy S, et al. Fibrosis progression rate in biopsy‐proven nonalcoholic fatty liver disease among people with diabetes versus people without diabetes: a multicenter study. Gastroenterology. 2023;165:463–472.e5.
Loomba R, Lim JK, Patton H, El‐Serag HB. AGA clinical practice update on screening and surveillance for hepatocellular carcinoma in patients with nonalcoholic fatty liver disease: expert review. Gastroenterology. 2020;158:1822–1830.
Loomba R, Sanyal AJ. The global NAFLD epidemic. Nat Rev Gastroenterol Hepatol. 2013;10:686–690.
Tan DJH, Ng CH, Lin SY, Pan XH, Tay P, Lim WH, et al. Clinical characteristics, surveillance, treatment allocation, and outcomes of non‐alcoholic fatty liver disease‐related hepatocellular carcinoma: a systematic review and meta‐analysis. Lancet Oncol. 2022;23:521–530.
Huang DQ, Singal AG, Kono Y, Tan DJ, El‐Serag HB, Loomba R. Changing global epidemiology of liver cancer from 2010 to 2019: NASH is the fastest growing cause of liver cancer. Cell Metab. 2022;34:969–977.e2.
Angulo P, Kleiner DE, Dam‐Larsen S, Adams LA, Bjornsson ES, Charatcharoenwitthaya P, et al. Liver fibrosis, but no other histologic features, is associated with long‐term outcomes of patients with nonalcoholic fatty liver disease. Gastroenterology. 2015;149:389–397.e10.
Estes C, Razavi H, Loomba R, Younossi Z, Sanyal AJ. Modeling the epidemic of nonalcoholic fatty liver disease demonstrates an exponential increase in burden of disease. Hepatology. 2018;67:123–133.
Chalasani N, Younossi Z, Lavine JE, Charlton M, Cusi K, Rinella M, et al. The diagnosis and management of nonalcoholic fatty liver disease: practice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2018;67:328–357.
Vilstrup H, Amodio P, Bajaj J, Cordoba J, Ferenci P, Mullen KD, et al. Hepatic encephalopathy in chronic liver disease: 2014 practice guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the liver. Hepatology. 2014;60:715–735.
Garcia‐Tsao G, Sanyal AJ, Grace ND, Carey W. Practice guidelines Committee of the American Association for the study of liver diseases tPPCotACoG. Prevention and management of gastroesophageal varices and variceal hemorrhage in cirrhosis. Hepatology. 2007;46:922–938.
Sanyal AJ, Van Natta ML, Clark J, Neuschwander‐Tetri BA, Diehl A, Dasarathy S, et al. Prospective study of outcomes in adults with nonalcoholic fatty liver disease. N Engl J Med. 2021;385:1559–1569.
Allen AM, Therneau TM, Ahmed OT, Gidener T, Mara KC, Larson JJ, et al. Clinical course of non‐alcoholic fatty liver disease and the implications for clinical trial design. J Hepatol. 2022;77:1237–1245.
Bassegoda O, Rivera‐Esteban J, Serra I, Morillas R, Broquetas T, Vergara M, et al. High frequency of acute decompensation and cancer in patients with compensated cirrhosis due to nonalcoholic fatty liver disease: a retrospective cohort study. Hepatol Commun. 2022;6:3212–3222.
Balcar L, Tonon M, Semmler G, Calvino V, Hartl L, Incicco S, et al. Risk of further decompensation/mortality in patients with cirrhosis and ascites as the first single decompensation event. JHEP Reports. 2022;4:100513.
Sanyal AJ, Anstee QM, Trauner M, Lawitz EJ, Abdelmalek MF, Ding D, et al. Cirrhosis regression is associated with improved clinical outcomes in patients with nonalcoholic steatohepatitis. Hepatology. 2020;72:67–68.