Elsevier

Journal of Hepatology

Volume 61, Issue 2, August 2014, Pages 396-407
Journal of Hepatology

Review
Human serum albumin, systemic inflammation, and cirrhosis

https://doi.org/10.1016/j.jhep.2014.04.012Get rights and content
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open access

Summary

Human serum albumin (HSA) is one of the most frequent treatments in patients with decompensated cirrhosis. Prevention of paracentesis-induced circulatory dysfunction, prevention of type-1 HRS associated with bacterial infections, and treatment of type-1 hepatorenal syndrome are the main indications. In these indications treatment with HSA is associated with improvement in survival. Albumin is a stable and very flexible molecule with a heart shape, 585 residues, and three domains of similar size, each one containing two sub-domains. Many of the physiological functions of HSA rely on its ability to bind an extremely wide range of endogenous and exogenous ligands, to increase their solubility in plasma, to transport them to specific tissues and organs, or to dispose of them when they are toxic. The chemical structure of albumin can be altered by some specific processes (oxidation, glycation) leading to rapid clearance and catabolism. An outstanding feature of HSA is its capacity to bind lipopolysaccharide and other bacterial products (lipoteichoic acid and peptidoglycan), reactive oxygen species, nitric oxide and other nitrogen reactive species, and prostaglandins. Binding to NO and prostaglandins are reversible, so they can be transferred to other molecules at different sites from their synthesis. Through these functions, HSA modulates the inflammatory reaction. Decompensated cirrhosis is a disease associated systemic inflammation, which plays an important role in the pathogenesis of organ or system dysfunction/failure. Although, the beneficial effects of HAS have been traditionally attributed to plasma volume expansion, they could also relate to its effects modulating systemic and organ inflammation.

Abbreviations

HSA
human serum albumin
HRS
hepatorenal
PICD
paracentesis-induced circulatory dysfunction
SBP
spontaneous bacterial peritonitis
RCT
randomized controlled trial
LPS
lipopolisaccharide
TLR4
Toll-like receptor 4
PAMPs
pathogen-associated molecular paterns
DAMPs
damaged-associated molecular paterns
ROS
reactive oxygen species
RNS
reactive nitrogen species
HMA
human-mercapto-albumin
NMA
non-mercapto-albumin
NO
nitric oxide
CRP
c-reactive protein
RAS
renin-angiotensin system
SNS
sympathetic nervous system
ADH
antidiuretic hormone
PGs
prostaglandins
BDK
bradikinin
ACLF
acute-on-chronic liver failure
TNFα
tumor necrosis factor α

Keywords

Cirrhosis
Human serum albumin
Paracentesis-induced circulatory dysfunction
Spontaneous bacterial peritonitis
Hepatorenal syndrome
Systemic inflammation
Organ inflammation
Oxidative stress
Decompensated cirrhosis
Acute-on-chronic liver failure

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