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Using liver stiffness to predict and monitor the risk of decompensation and mortality in patients with alcohol-related liver disease.
Thorhauge, Katrine Holtz; Semmler, Georg; Johansen, Stine; Lindvig, Katrine Prier; Kjærgaard, Maria; Hansen, Johanne Kragh; Torp, Nikolaj; Hansen, Camilla Dalby; Andersen, Peter; Hofer, Benedikt Silvester; Gu, Wenyi; Israelsen, Mads; Mandorfer, Mattias; Reiberger, Thomas; Trebicka, Jonel; Thiele, Maja; Krag, Aleksander.
Afiliación
  • Thorhauge KH; Fibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark; Department of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark.
  • Semmler G; Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Spitalgasse 23 A-1090 Vienna, Austria.
  • Johansen S; Fibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark; Department of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark.
  • Lindvig KP; Fibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark; Department of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark.
  • Kjærgaard M; Fibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark; Department of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark.
  • Hansen JK; Fibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark; Department of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark.
  • Torp N; Fibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark; Department of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark.
  • Hansen CD; Fibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark; Department of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark.
  • Andersen P; Fibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark.
  • Hofer BS; Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Spitalgasse 23 A-1090 Vienna, Austria.
  • Gu W; Department of Internal Medicine B, Münster University Hospital, University of Münster, Münster, Germany.
  • Israelsen M; Fibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark; Department of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark.
  • Mandorfer M; Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Spitalgasse 23 A-1090 Vienna, Austria.
  • Reiberger T; Division of Gastroenterology and Hepatology, Department of Internal Medicine III, Medical University of Vienna, Spitalgasse 23 A-1090 Vienna, Austria.
  • Trebicka J; Department of Internal Medicine B, Münster University Hospital, University of Münster, Münster, Germany.
  • Thiele M; Fibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark; Department of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark. Electronic address: maja
  • Krag A; Fibrosis, Fatty Liver and Steatohepatitis Research Center Odense (FLASH), Department of Gastroenterology and Hepatology, Odense University Hospital, Odense, Denmark; Department of Clinical Research, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark.
J Hepatol ; 81(1): 23-32, 2024 Jul.
Article en En | MEDLINE | ID: mdl-38428644
ABSTRACT
BACKGROUND &

AIMS:

Liver stiffness measurement (LSM) is recommended for disease prognostication and monitoring. We evaluated if LSM, using transient elastography, and LSM changes predict decompensation and mortality in patients with alcohol-related liver disease (ALD).

METHODS:

We performed an observational cohort study of compensated patients at risk of ALD from Denmark and Austria. We evaluated the risk of decompensation and all-cause mortality, stratified for compensated advanced chronic liver disease (cACLD baseline LSM ≥10 kPa) and LSM changes after a median of 2 years. In patients with cACLD, we defined LSM changes as (A) LSM increase ≥20% ("cACLD increasers") and (B) follow-up LSM <10 kPa or <20 kPa with LSM decrease ≥20% ("cACLD decreasers"). In patients without cACLD, we defined follow-up LSM ≥10 kPa as an LSM increase ("No cACLD increasers"). The remaining patients were considered LSM stable.

RESULTS:

We followed 536 patients for 3,008 patient-years-median age 57 years (IQR 49-63), baseline LSM 8.1 kPa (IQR 4.9-21.7)-371 patients (69%) had follow-up LSM after a median of 25 months (IQR 17-38), 41 subsequently decompensated and 55 died. Of 125 with cACLD at baseline, 14% were "cACLD increasers" and 43% "cACLD decreasers", while 13% of patients without cACLD were "No cACLD increasers" (n = 33/246). Baseline LSM, follow-up LSM and LSM changes accurately predicted decompensation (C-index baseline LSM 0.85; follow-up LSM 0.89; LSM changes 0.85) and mortality (C-index baseline LSM 0.74; follow-up LSM 0.74; LSM changes 0.70). When compared to "cACLD decreasers", "cACLD increasers" had significantly lower decompensation-free survival and higher risks of decompensation (subdistribution hazard ratio 4.39, p = 0.004) and mortality (hazard ratio 3.22, p = 0.01).

CONCLUSION:

LSM by transient elastography predicts decompensation and all-cause mortality in patients with compensated ALD both at diagnosis and when used for monitoring. IMPACT AND IMPLICATIONS Patients at risk of alcohol-related liver disease (ALD) are at significant risk of progressive disease and adverse outcomes. Monitoring is essential for optimal disease surveillance and patient guidance, but non-invasive monitoring tools are lacking. In this study we demonstrate that liver stiffness measurement (LSM), using transient elastography, and LSM changes after a median of 2 years, can predict decompensation and all-cause mortality in patients at risk of ALD with and without compensated advanced chronic liver disease. These findings are in line with results from non-alcoholic fatty liver disease, hepatitis C and primary sclerosing cholangitis, and support the clinical utility of LSM, using transient elastography, for disease prognostication and monitoring in chronic liver diseases including ALD, as recommended by the Baveno VII.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Diagnóstico por Imagen de Elasticidad / Hepatopatías Alcohólicas Límite: Female / Humans / Male / Middle aged País/Región como asunto: Europa Idioma: En Revista: J Hepatol Asunto de la revista: GASTROENTEROLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Dinamarca

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Diagnóstico por Imagen de Elasticidad / Hepatopatías Alcohólicas Límite: Female / Humans / Male / Middle aged País/Región como asunto: Europa Idioma: En Revista: J Hepatol Asunto de la revista: GASTROENTEROLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Dinamarca