Surgical attenuation of spontaneous congenital portosystemic shunts in dogs resolves hepatic encephalopathy but not hypermanganesemia.
Hypermanganesemia is commonly recognized in human patients with hepatic insufficiency and portosystemic shunting. Since manganese is neurotoxic, increases in brain manganese concentrations have been implicated in the development of hepatic encephalopathy although a direct causative role has yet to be demonstrated. Evaluate manganese concentrations in dogs with a naturally occurring congenital shunt before and after attenuation as well as longitudinally following the changes in hepatic encephalopathy grade. Our study demonstrated that attenuation of the shunt resolved encephalopathy, significantly reduced postprandial bile acids, yet a hypermanganasemic state persisted. This study demonstrates that resolution of hepatic encephalopathy can occur without the correction of hypermanganesemia, indicating that increased manganese concentrations alone do not play a causative role in encephalopathy. Our study further demonstrates the value of the canine congenital portosystemic shunt as a naturally occurring spontaneous model of human hepatic encephalopathy.
Division of Veterinary Clinical Studies, Easter Bush Veterinary Centre, Royal (Dick) School of Veterinary Studies, The Roslin Institute, The University of Edinburgh, Hospital for Small Animals, Roslin, Midlothian, EH25 9RG, UK, adam.gow@ed.ac.uk.
Adam G
AG
Gow
Polly E
PE
Frowde
Clive M
CM
Elwood
Carolyn A
CA
Burton
Roger M
RM
Powell
Simon W
SW
Tappin
Rob D
RD
Foale
Andrew
A
Duncan
Richard J
RJ
Mellanby
D000818:Animals; D004285:Dogs; D005260:Female; D006501:Hepatic Encephalopathy / Q000097:blood* / Q000175:diagnosis / Q000601:surgery*; D008274:Magnesium / Q000097:blood*; D008297:Male; D011170:Portasystemic Shunt, Surgical / Q000379:methods
D008274:Magnesium