title: Systemic and hepatic vein galectin-3 are increased in patients with alcoholic liver cirrhosis and negatively correlate with liver function.
abstract: Recently we demonstrated higher galectin-3 in portal venous serum (PVS) compared to hepatic venous serum (HVS) in a small cohort of patients with normal liver function suggesting hepatic removal of galectin-3. Here, galectin-3 was measured by ELISA in PVS, HVS and systemic venous blood (SVS) of 33 patients with alcoholic liver cirrhosis and a larger cohort of 11 patients with normal liver function. Galectin-3 was cleared by the healthy but not the cirrhotic liver, and subsequently HVS and SVS galectin-3 levels were significantly increased in the patients with liver cirrhosis compared to controls. In healthy liver galectin-3 was produced by cholangiocytes and synthesis by hepatocytes was only observed in cirrhotic liver. Hepatic venous pressure gradient did not correlate with galectin-3 levels excluding hepatic shunting as the principal cause of higher SVS galectin-3. Galectin-3 was elevated in all blood compartments of patients with CHILD-PUGH stage C compared to patients with CHILD-PUGH stage A, and was higher in patients with ascites than patients without this complication. Galectin-3 was negatively associated with antithrombin-3 whose synthesis is reduced with worse liver function. Galectin-3 positively correlated with urea and creatinine, and PVS galectin-3 showed a negative association with creatinine clearance as an accepted measure of kidney function. To summarize in the current study systemic, portal and hepatic levels of galectin-3 were found to be negatively associated with liver function in patients with alcoholic liver cirrhosis and this may in part be related to impaired hepatic removal and/or increased synthesis in cirrhotic liver.
authors.affiliation: Department of Internal Medicine I, Regensburg University Hospital, D-93042 Regensburg, Germany.
authors.forename: Josef
authors.initials: J
authors.lastname: Wanninger
authors.forename: Johanna
authors.initials: J
authors.lastname: Weigert
authors.forename: Reiner
authors.initials: R
authors.lastname: Wiest
authors.forename: Sabrina
authors.initials: S
authors.lastname: Bauer
authors.forename: Thomas
authors.initials: T
authors.lastname: Karrasch
authors.forename: Stefan
authors.initials: S
authors.lastname: Farkas
authors.forename: Marcus N
authors.initials: MN
authors.lastname: Scherer
authors.forename: Roland
authors.initials: R
authors.lastname: Walter
authors.forename: Thomas S
authors.initials: TS
authors.lastname: Weiss
authors.forename: Claus
authors.initials: C
authors.lastname: Hellerbrand
authors.forename: Markus
authors.initials: M
authors.lastname: Neumeier
authors.forename: Andreas
authors.initials: A
authors.lastname: Schäffler
authors.forename: Christa
authors.initials: C
authors.lastname: Buechler
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000991:Antithrombins / Q000097:blood; D001201:Ascites / Q000378:metabolism / Q000473:pathology; D003404:Creatinine / Q000097:blood; D005260:Female; D037502:Galectin 3 / Q000096:biosynthesis* / Q000097:blood*; D006503:Hepatic Veins / Q000503:physiopathology; D022781:Hepatocytes / Q000378:metabolism; D006801:Humans; D015151:Immunoblotting; D007668:Kidney / Q000378:metabolism; D008103:Liver Cirrhosis / Q000097:blood / Q000503:physiopathology; D008104:Liver Cirrhosis, Alcoholic / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D014508:Urea / Q000097:blood
chemical_list: D000991:Antithrombins; D037502:Galectin 3; D014508:Urea; D003404:Creatinine