recent review of the role of albumin in cirrhosis (see HEPATOLOGY 2013;58:1836-1846), which strays a bit from the primary care focus of the vast majority of these blog posts, but i always find it interesting when new data significantly changes the way we look at how the body works. in this case, albumin therapy was always presented as a plasma volume expander, but it turns out that there are many other roles it plays (and who knows which is the most important physiologically???). basically, its biological roles (in patients with cirrhosis) include:
–plasma volume expansion (provides 75% of the plasma oncotic pressure) and is >50% of total plasma proteins
–binds to diverse array of molecules (bile acids, hormones, metals, long-chain fatty acids, nitric oxide, endotoxins….): solubilizes , transports them
–the thiol group on albumen is the most important extracellular antioxidant (80% of the thiol groups are on albumin)
–by binding to endotoxins, in vitro studies show that albumin decreases endotoxin activity
–albumin inhibits TNF-a upregulation of vascular adhesion molecules.
–albumin binds to nitric oxide and can lead to vasodilation and inhibit platelet aggregation
–endothelial stabilization, perhaps related to albumin’s ability to modulate inflammation, reduces oxidative damage and interferes in neutrophil adhesion
–in cirrhosis, double effect of decreased albumin quantity as well as dysfunction as above
–clinically, albumin is useful in pts with cirrhosis and spontaneous bacterial peritonitis, hepatorenal syndrome, paracentesis-induced circulatory dysfunction.
–in those without cirrhosis, some data suggests efficacy in women with ovarian hyperstimulation syndrome and in pts with malaria, burns, and possibly has protective role in those with ischemic stroke and Alzheimer’s.
so, seems to be more than just a volume expander…. (and again shows that our models of physiologic function are often rather primitive. and need to be continually challenged)
geoff