Risk of further decompensation/mortality in patients with cirrhosis and ascites as the first single decompensation event.

ACLF, acute-on-chronic liver failure Acute kidney injury Baveno CI, confidence interval CPS, Child–Pugh score HCC, hepatocellular carcinoma HE, hepatic encephalopathy HRS-AKI, hepatorenal syndrome–acute kidney injury Hepatic decompensation ICA, International Club of Ascites INR, international normalised ratio IQR, interquartile range LT, liver transplantation MELD, model for end-stage liver disease NAFLD, non-alcoholic fatty liver disease NASH, non-alcoholic steatohepatitis PVT, portal vein thrombosis Portal hypertension RA, refractory ascites SBP, spontaneous bacterial peritonitis SHR, subdistribution hazard ratio Spontaneous bacterial peritonitis TFS, transplant-free survival TIPS, transjugular intrahepatic portosystemic shunt UNOS MELD (2016), United Network for Organ Sharing model for end-stage liver disease (2016) VB, variceal bleeding aSHR, adjusted subdistribution hazard ratio

Journal

JHEP reports : innovation in hepatology
ISSN: 2589-5559
Titre abrégé: JHEP Rep
Pays: Netherlands
ID NLM: 101761237

Informations de publication

Date de publication:
Aug 2022
Historique:
received: 15 05 2022
accepted: 19 05 2022
entrez: 18 7 2022
pubmed: 19 7 2022
medline: 19 7 2022
Statut: epublish

Résumé

Although ascites is the most frequent first decompensating event in cirrhosis, the clinical course after ascites as the A total of 622 patients with cirrhosis presenting with grade 2/3 ascites as the The mean age was 57 ± 11 years, and most patients were male (n = 423, 68%) with alcohol-related (n = 366, 59%) and viral (n = 200,32%) liver disease as the main aetiologies. In total, 323 (52%) patients presented with grade 2 and 299 (48%) with grade 3 ascites. The median Child-Pugh score at presentation was 8 (IQR 7-9), and the mean model for end-stage liver disease (MELD) was 15 ± 6. During a median follow-up period of 49 months, 350 (56%) patients experienced further decompensation: refractory ascites (n = 130, 21%), hepatic encephalopathy (n = 112, 18%), spontaneous bacterial peritonitis (n = 32, 5%), hepatorenal syndrome-acute kidney injury (n = 29, 5%). Variceal bleeding as an isolated further decompensation event was rare (n = 18, 3%), whereas non-bleeding further decompensation (n = 161, 26%) and ≥2 concomitant further decompensation events (n = 171, 27%) were frequent. Transjugular intrahepatic portosystemic shunt was used in only 81 (13%) patients. In patients presenting with grade 2 ascites, MELD ≥15 indicated a considerable risk for further decompensation (subdistribution hazard ratio [SHR] 2.18; Further decompensation is frequent in patients with ascites as a Decompensation (the development of symptoms as a result of worsening liver function) marks a turning point in the disease course for patients with cirrhosis. Ascites (

Sections du résumé

Background & Aims UNASSIGNED
Although ascites is the most frequent first decompensating event in cirrhosis, the clinical course after ascites as the
Methods UNASSIGNED
A total of 622 patients with cirrhosis presenting with grade 2/3 ascites as the
Results UNASSIGNED
The mean age was 57 ± 11 years, and most patients were male (n = 423, 68%) with alcohol-related (n = 366, 59%) and viral (n = 200,32%) liver disease as the main aetiologies. In total, 323 (52%) patients presented with grade 2 and 299 (48%) with grade 3 ascites. The median Child-Pugh score at presentation was 8 (IQR 7-9), and the mean model for end-stage liver disease (MELD) was 15 ± 6. During a median follow-up period of 49 months, 350 (56%) patients experienced further decompensation: refractory ascites (n = 130, 21%), hepatic encephalopathy (n = 112, 18%), spontaneous bacterial peritonitis (n = 32, 5%), hepatorenal syndrome-acute kidney injury (n = 29, 5%). Variceal bleeding as an isolated further decompensation event was rare (n = 18, 3%), whereas non-bleeding further decompensation (n = 161, 26%) and ≥2 concomitant further decompensation events (n = 171, 27%) were frequent. Transjugular intrahepatic portosystemic shunt was used in only 81 (13%) patients. In patients presenting with grade 2 ascites, MELD ≥15 indicated a considerable risk for further decompensation (subdistribution hazard ratio [SHR] 2.18;
Conclusions UNASSIGNED
Further decompensation is frequent in patients with ascites as a
Lay summary UNASSIGNED
Decompensation (the development of symptoms as a result of worsening liver function) marks a turning point in the disease course for patients with cirrhosis. Ascites (

Identifiants

pubmed: 35845294
doi: 10.1016/j.jhepr.2022.100513
pii: S2589-5559(22)00085-4
pmc: PMC9284386
doi:

Types de publication

Journal Article

Langues

eng

Pagination

100513

Informations de copyright

© 2022 The Author(s).

Déclaration de conflit d'intérêts

The authors have nothing to disclose regarding the work under consideration for publication. The following authors disclose conflicts of interests outside the submitted work: LB, MTo, GS, VC, LH, SI, MJ, BSH, CGC, AA, AB, and SP have nothing to disclose. DB received travel support from AbbVie and Gilead and speaker fees from AbbVie and Siemens, as well as grant support form Gilead and Siemens. MTr received grant support from Albireo, Alnylam, Cymabay, Falk, Gilead, Intercept, MSD, Takeda, and UltraGenyx; honouraria for consulting from Albireo, Boehringer Ingelheim, BiomX, Falk, Genfit, Gilead, Intercept, Janssen, MSD, Novartis, Phenex, Pliant, Regulus, and Shire; speaker fees from Bristol-Myers Squibb, Falk, Gilead, Intercept, and MSD; and travel support from AbbVie, Falk, Gilead, and Intercept. MM served as a speaker and/or consultant and/or advisory board member for AbbVie, Collective Acumen, Gilead, and W.L. Gore & Associates and received travel support from AbbVie and Gilead. TR received grant support from AbbVie, Boehringer-Ingelheim, Gilead, Intercept, MSD, Myr Pharmaceuticals, Philips Healthcare, Pliant, Siemens, and W.L. Gore & Associates; speaking honoraria from AbbVie, Gilead, Gore, Intercept, Roche, and MSD; consulting/advisory board fees from AbbVie, Bayer, Boehringer-Ingelheim, Gilead, Intercept, MSD, and Siemens; and travel support from AbbVie, Boehringer-Ingelheim, Gilead, and Roche. Please refer to the accompanying ICMJE disclosure forms for further details.

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Auteurs

Lorenz Balcar (L)

Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Vienna Hepatic Hemodynamic Lab, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Marta Tonon (M)

Unit of Internal Medicine and Hepatology, Department of Medicine, University of Padova, Padua, Italy.

Georg Semmler (G)

Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Vienna Hepatic Hemodynamic Lab, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Valeria Calvino (V)

Unit of Internal Medicine and Hepatology, Department of Medicine, University of Padova, Padua, Italy.

Lukas Hartl (L)

Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Vienna Hepatic Hemodynamic Lab, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Simone Incicco (S)

Unit of Internal Medicine and Hepatology, Department of Medicine, University of Padova, Padua, Italy.

Mathias Jachs (M)

Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Vienna Hepatic Hemodynamic Lab, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

David Bauer (D)

Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Vienna Hepatic Hemodynamic Lab, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Benedikt Silvester Hofer (BS)

Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Vienna Hepatic Hemodynamic Lab, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Christian-Doppler Laboratory for Portal Hypertension and Liver Fibrosis, Medical University of Vienna, Vienna, Austria.

Carmine Gabriele Gambino (CG)

Unit of Internal Medicine and Hepatology, Department of Medicine, University of Padova, Padua, Italy.

Antonio Accetta (A)

Unit of Internal Medicine and Hepatology, Department of Medicine, University of Padova, Padua, Italy.

Alessandra Brocca (A)

Unit of Internal Medicine and Hepatology, Department of Medicine, University of Padova, Padua, Italy.

Michael Trauner (M)

Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Mattias Mandorfer (M)

Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Vienna Hepatic Hemodynamic Lab, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.

Salvatore Piano (S)

Unit of Internal Medicine and Hepatology, Department of Medicine, University of Padova, Padua, Italy.

Thomas Reiberger (T)

Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Vienna Hepatic Hemodynamic Lab, Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Christian-Doppler Laboratory for Portal Hypertension and Liver Fibrosis, Medical University of Vienna, Vienna, Austria.

Classifications MeSH