Systemic Inflammation and Acute-on-Chronic Liver Failure: Too Much, Not Enough

Wim Laleman, Joan Claria, Schalk Van der Merwe, Richard Moreau, Jonel Trebicka

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Resumé

ACLF is a specific, but complex and multifactorial form of acute decompensation of cirrhosis and is characterized by an extraordinary dynamic natural course, rapidly evolving organ failure, and high short-term mortality. Dysbalanced immune function is central to its pathogenesis and outcome with an initial excessive systemic inflammatory response that drives organ failure and mortality. Later in its course, immuno-exhaustion/immunoparalysis prevails predisposing the patient to secondary infectious events and reescalation in end-organ dysfunction and mortality. The management of patients with ACLF is still poorly defined. However, as its pathophysiology is gradually being unravelled, potential therapeutic targets emerge that warrant further study such as restoring or substituting albumin via plasma exchange or via albumin dialysis and evaluating usefulness of TLR4 antagonists, modulators of gut dysbiosis (pre- or probiotics), and FXR-agonists.

OriginalsprogEngelsk
Artikelnummer1027152
TidsskriftCanadian Journal of Gastroenterology and Hepatology
Vol/bind2018
Antal sider10
ISSN2291-2789
DOI
StatusUdgivet - 1. jan. 2018

Fingeraftryk

Albumins
Prebiotics
Plasma Exchange
Probiotics
Acute-On-Chronic Liver Failure

Citer dette

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abstract = "ACLF is a specific, but complex and multifactorial form of acute decompensation of cirrhosis and is characterized by an extraordinary dynamic natural course, rapidly evolving organ failure, and high short-term mortality. Dysbalanced immune function is central to its pathogenesis and outcome with an initial excessive systemic inflammatory response that drives organ failure and mortality. Later in its course, immuno-exhaustion/immunoparalysis prevails predisposing the patient to secondary infectious events and reescalation in end-organ dysfunction and mortality. The management of patients with ACLF is still poorly defined. However, as its pathophysiology is gradually being unravelled, potential therapeutic targets emerge that warrant further study such as restoring or substituting albumin via plasma exchange or via albumin dialysis and evaluating usefulness of TLR4 antagonists, modulators of gut dysbiosis (pre- or probiotics), and FXR-agonists.",
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Systemic Inflammation and Acute-on-Chronic Liver Failure : Too Much, Not Enough. / Laleman, Wim; Claria, Joan; Van der Merwe, Schalk; Moreau, Richard; Trebicka, Jonel.

I: Canadian Journal of Gastroenterology and Hepatology, Bind 2018, 1027152, 01.01.2018.

Publikation: Bidrag til tidsskriftReviewForskningpeer review

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T1 - Systemic Inflammation and Acute-on-Chronic Liver Failure

T2 - Too Much, Not Enough

AU - Laleman, Wim

AU - Claria, Joan

AU - Van der Merwe, Schalk

AU - Moreau, Richard

AU - Trebicka, Jonel

PY - 2018/1/1

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N2 - ACLF is a specific, but complex and multifactorial form of acute decompensation of cirrhosis and is characterized by an extraordinary dynamic natural course, rapidly evolving organ failure, and high short-term mortality. Dysbalanced immune function is central to its pathogenesis and outcome with an initial excessive systemic inflammatory response that drives organ failure and mortality. Later in its course, immuno-exhaustion/immunoparalysis prevails predisposing the patient to secondary infectious events and reescalation in end-organ dysfunction and mortality. The management of patients with ACLF is still poorly defined. However, as its pathophysiology is gradually being unravelled, potential therapeutic targets emerge that warrant further study such as restoring or substituting albumin via plasma exchange or via albumin dialysis and evaluating usefulness of TLR4 antagonists, modulators of gut dysbiosis (pre- or probiotics), and FXR-agonists.

AB - ACLF is a specific, but complex and multifactorial form of acute decompensation of cirrhosis and is characterized by an extraordinary dynamic natural course, rapidly evolving organ failure, and high short-term mortality. Dysbalanced immune function is central to its pathogenesis and outcome with an initial excessive systemic inflammatory response that drives organ failure and mortality. Later in its course, immuno-exhaustion/immunoparalysis prevails predisposing the patient to secondary infectious events and reescalation in end-organ dysfunction and mortality. The management of patients with ACLF is still poorly defined. However, as its pathophysiology is gradually being unravelled, potential therapeutic targets emerge that warrant further study such as restoring or substituting albumin via plasma exchange or via albumin dialysis and evaluating usefulness of TLR4 antagonists, modulators of gut dysbiosis (pre- or probiotics), and FXR-agonists.

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