Abstract

Background:
Excess hepatic copper can be either a cause or a consequence of chronic liver inflammation. The main mechanisms involved in copper accumulation include primary defects in hepatic copper metabolism, cholestasis leading to impaired biliary excretion, and excessive dietary copper intake. Copper overload may result in acute hepatic necrosis, often associated with hemolytic anemia. The aim of this study was to report a case of copper-associated hepatitis (CAH).

Case Description:
A 13-year-old mixed-breed spayed female dog was evaluated due to a progressive increase in serum liver enzyme activities and ultrasonographic liver abnormalities, with a clinical course of six months. Based on the initial diagnostic findings, a liver histopathological examination was performed, revealing hepatocellular hyperplasia associated with mild fibrosis and moderate diffuse vacuolar degeneration. Rhodanine staining demonstrated copper accumulation within hepatocytes, confirming hepatic copper accumulation consistent with copper-associated hepatitis. Medical treatment and dietary management were instituted. Approximately one year and six months after diagnosis, the patient returned with recurrent emesis, food selectivity, residual head tilt, and ultrasonographic alterations involving the liver, gallbladder, and pancreas. Due to clinical deterioration, euthanasia was elected.

Conclusion:
This case report contributes to the limited literature on CAH in mixed-breed dogs, emphasizing the importance of histopathology and specific copper staining for definitive diagnosis, as well as the chronic and progressive nature of the disease despite therapeutic management.

Key words: Canine; Copper; Hepatopathy; Inflammation; Liver.