Manganese (Mn) is an essential mineral that is a cofactor for many enzymes required in the synthesis of proteins, carbohydrates, and lipids. Because hepatic clearance is essential in Mn homeostasis, conditions in humans resulting in hepatic insufficiency including cirrhosis and both acquired and congenital portosystemic shunting have been reported to result in increased blood Mn concentrations and increased Mn content in the central nervous system. Because Mn toxicity causes neurologic disturbances, increased Mn concentrations have been implicated in the pathogenesis of hepatic encephalopathy.
Dogs with congenital portosystemic shunts (cPSS) have significantly higher whole blood Mn concentrations than do healthy dogs or those with nonhepatic illnesses.
Eighteen dogs with cPSS, 26 dogs with nonhepatic illnesses, and 14 healthy dogs.
Whole blood Mn was measured by graphite furnace atomic absorption spectrometry. The diagnosis of cPSS was made by ultrasonography or during celiotomy either by visual inspection of a shunting vessel or portovenography.
Dogs with a cPSS had significantly higher whole blood Mn concentrations than did healthy dogs and dogs with nonhepatic illnesses. Whole blood Mn concentrations were not significantly different between healthy dogs and dogs with nonhepatic illnesses.
Conclusion and Clinical Importance
Dogs with a cPSS have significantly increased whole blood Mn concentrations. Additional studies are warranted to investigate the role of Mn in cPSS-associated hepatic encephalopathy.