1. Acute-on-Chronic Liver Failure, Human Serum Albumin, and Immune Modulation: The Beginning of an Exciting Adventure 
Vicente Arroyo 
Clinical Gastroenterology and Hepatology 
Volume 16, Issue 5, Pages (May 2018)
DOI: /j.cgh
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2. Figure 1
(A) Decompensation of cirrhosis is characterized by the development of specific complication and the impairment in the function of extrahepatic organs or systems, which may be moderate (dysfunction) or severe (failure). Several pathophysiological events (steps) contribute to cirrhosis decompensation. Step 1 consists in an increased intestinal translocation of viable bacteria and pathogen-associated molecular patterns (PAMPs). At the early phase of cirrhosis, inflammation is predominantly located at the lamina propia, where it induces arterial vasodilation. However, as the disease progresses, inflammation extends systemically affecting also the extrasplanchnic organs. Systemic inflammation may also develop by the release of damage-associated molecular patterns from the diseased liver (eg, in the case of acute liver injury superimposed to cirrhosis). Organ hypoperfusion related to circulatory dysfunction and direct deleterious effects of inflammatory mediators on tissue homeostasis are the two predominant mechanisms or multiorgan dysfunction/failure in cirrhosis. (B) Time course of systemic inflammation, acute decompensation, and acute-on-chronic liver failure (ACLF) development in cirrhosis. Systemic inflammation that is absent or moderate in compensated cirrhosis, rises rapidly during the transition to decompensated cirrhosis and then follows a relatively steady course. ACLF develops in the setting of a burst of systemic inflammation (represented as yellow figures) promoted by a precipitating event (PE). Three inflammatory bursts are represented in compensated and decompensated cirrhosis. There are thresholds for systemic inflammation for ACLF development. Please note that the magnitude of the systemic inflammatory reaction (inverted red triangles) required for ACLF development is greater in patients with compensated cirrhosis than in those with decompensated cirrhosis. If the inflammatory reaction promoted by a PE is insufficient to reach the threshold level, no ACLF develops.
Clinical Gastroenterology and Hepatology  , DOI: ( /j.cgh )
Copyright © 2018 AGA Institute Terms and Conditions