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Abstract Details
Pathophysiology of decompensated cirrhosis: Portal hypertension, circulatory dysfunction, inflammation, metabolism and mitochondrial dysfunction
Cornelius Engelmann1, Joan Clària2, Gyongyi Szabo3, Jaume Bosch4, Mauro Bernardi5
Author information
1Department of Hepatology and Gastroenterology, Charité Universitätsmedizin Berlin, Berlin, Germany; Institute for Liver and Digestive Health, University College London, London, United Kingdom; Section Hepatology, Clinic for Gastroenterology and Rheumatology, University Hospital Leipzig, Leipzig, Germany; Berlin Institute of Health (BIH), Berlin, Germany. Electronic address: cornelius.engelmann@charite.de.
2European Foundation for the Study of Chronic Liver Failure (EF-Clif) and Grifols Chair, Barcelona, Spain; Biochemistry and Molecular Genetics Service, Hospital Clínic-IDIBAPS and CIBERehd, Spain; Department of Biomedical Sciences, University of Barcelona, Barcelona, Spain.
3Department of Medicine, Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, USA.
4IDIBAPS and CIBERehd, University of Barcelona, Barcelona, Spain; Department for Biomedical Research (DBMR), Bern University, Bern, Switzerland.
5Department of Medical and Surgical Sciences; Alma Mater Studiorum - University of Bologna; Italy.
Abstract
Patients with acutely decompensated cirrhosis have a dismal prognosis and frequently progress to acute-on-chronic liver failure, which is characterised by hepatic and extrahepatic organ failure(s). The pathomechanisms involved in decompensation and disease progression are still not well understood, and as specific disease-modifying treatments do not exist, research to identify novel therapeutic targets is of the utmost importance. This review amalgamates the latest knowledge on disease mechanisms that lead to tissue injury and extrahepatic organ failure - such as systemic inflammation, mitochondrial dysfunction, oxidative stress and metabolic changes - and marries these with the classical paradigms of acute decompensation to form a single paradigm. With this detailed breakdown of pathomechanisms, we identify areas for future research. Novel disease-modifying strategies that break the vicious cycle are urgently required to improve patient outcomes.
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