Impaired hepatic removal of galectin–3 and association with worse liver function in patients with alcoholic liver cirrhosis

Objective: Galectin–3 eliminates advanced glycation end products (AGE) and thereby protects from their cytotoxic effects. Recently, we demonstrated higher galectin-3 in portal venous serum (PVS) compared to hepatic venous serum (HVS) in patients with normal liver function, suggesting that the liver removes galectin–3. Galectin–3 is induced in cirrhotic liver but so far it has not been analysed whether hepatic galectin–3 synthesis is associated with an elevated hepatic release of galectin–3 and/or worse liver function in humans. Methods: Serum galectin-3 was measured by ELISA in PVS, HVS and SVS of 33 patients with alcoholic liver cirrhosis and compared to galectin-3 levels of 4 patients with normal liver function. Results: In liver cirrhosis, galectin-3 was either similarly concentrated or higher in HVS than PVS indicating that it is not removed by the cirrhotic liver. Galectin-3 was significantly 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 in all blood compartments positively correlated with serum creatinine, and this association was still significant after adjusting for age and body mass index (BMI). Conclusion: Systemic, portal and hepatic levels of galectin-3 are negatively associated with liver function in patients with alcoholic liver cirrhosis and this may in part be related to impaired hepatic removal.

hepatic vein - liver cirrhosis - portal vein