RESEARCH COMMUNICATIONS OF THE 28th ECVIM-CA CONGRESS

Hepatic encephalopathy (HE) is a syndrome of neurologic dysfunction present in several liver diseases and an important contributor to patient morbidity. Canine HE is most commonly reported in association with congenial portosystemic shunting (cPSS). Although not completely characterised, several factors are known to influence the pathogenesis of HE, namely increased ammonia, inflammation and manganese, as well as alkalosis, hyponatraemia and hypokalaemia. Melatonin is a hormone secreted by the pineal gland in the brain and by the enterochromaffin‐like cells in the gastric mucosa, with actions linked with regulation of the circadian rhythm, enterocyte integrity, and free oxygen radical scavenging, amongst others. The majority of melatonin is metabolised in the liver and recently, melatonin levels were noted to be significantly increased in human alcohol‐induced liver cirrhosis, correlating with both disease severity and with the severity of HE, hence hypothesised as a potential contributor to the development of the latter. To the authors’ knowledge, melatonin homeostasis in canine liver disease is currently unknown. The aim of this study was to investigate whether melatonin concentrations could be altered in dogs with cPSS, with the hypothesis that higher levels would be present when compared to healthy controls.