Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/175350
Title: The Systemic Inflammation Hypothesis: Towards a New Paradigm of Acute Decompensation and Multiorgan Failure in Cirrhosis
Author: Arroyo, Vicente
Angeli, Paolo
Moreau, Richard
Jalan, Rajiv
Clària i Enrich, Joan
Trebicka, Jonel
Fernández Gómez, Javier
Gustot, Thierry
Caraceni, Paolo
Bernardi, Mauro
Keywords: Cirrosi hepàtica
Inflamació
Hepatic cirrhosis
Inflammation
Issue Date: 7-Dec-2020
Publisher: Elsevier
Abstract: Acute decompensation (AD) of cirrhosis is defined by the development of ascites, hepatic encephalopathy and/or variceal bleeding. Ascites is traditionally attributed to splanchnic arterial vasodilation and left ventricular dysfunction, hepatic encephalopathy to hyperammonaemia, and variceal haemorrhage to portal hypertension. Recent large-scale European observational studies have shown that systemic inflammation is a hallmark of AD. Here we present a working hypothesis, the systemic inflammation hypothesis, suggesting that systemic inflammation through an impairment of the functions of one or more of the major organ systems may be a common theme and act synergistically with the traditional mechanisms involved in the development of AD. Systemic inflammation may impair organ system function through mechanisms which are not mutually exclusive. The first mechanism is a nitric oxide-mediated accentuation of the preexisting splanchnic vasodilation, resulting in the overactivation of the endogenous vasoconstrictor systems which elicit intense vasoconstriction and hypoperfusion in certain vascular beds, in particular the renal circulation. Second, systemic inflammation may cause immune-mediated tissue damage, a process called immunopathology. Finally, systemic inflammation may induce important metabolic changes. Indeed, systemic inflammatory responses are energetically expensive processes, requiring reallocation of nutrients (glucose, amino acids and lipids) to fuel immune activation. Systemic inflammation also inhibits nutrient consumption in peripheral (non-immune) organs, an effect that may provide one mechanism of reallocation and prioritisation of metabolic fuels for inflammatory responses. However, the decrease in nutrient consumption in peripheral organs may result in decreased mitochondrial production of ATP (energy) and subsequently impaired organ function.
Note: Reproducció del document publicat a: https://doi.org/10.1016/j.jhep.2020.11.048
It is part of: Journal of Hepatology, 2021, vol. 74, num. 3, p. 670-685
URI: http://hdl.handle.net/2445/175350
Related resource: https://doi.org/10.1016/j.jhep.2020.11.048
ISSN: 0168-8278
Appears in Collections:Articles publicats en revistes (Biomedicina)

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