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Tijdschr Diergeneeskd. 2012 May 1;137(5):310-4.

Copper-associated hepatic cirrhosis in a Friesian horse.

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DVM, Utrecht University, Faculty of Veterinary Medicine, Department of Pathobiology, Yalelaan 1, 3584 CL Utrecht, The Netherlands.


A 6-year-old Friesian stallion was examined because of signs of exercise intolerance, stiff gait and symmetrical hind weakness, and increased serum liver enzymes. On presentation, the horse showed muscle atrophy of the hindquarters. Neurological investigation showed no abnormalities. Laboratory findings revealed a prolonged prothrombin time and increased levels of alkaline phosphatase (AF), aspartate aminotransferase (ASAT), gamma-glutamyl-transferase (GGT), lactate dehydrogenase (LDH), and bile acids. Histological evaluation of the liver revealed severe cirrhosis and intracytoplasmic greyish brown granules in almost all hepatocytes, sinusoidal Kuppfer cells, and macrophages. These granules stained strongly for copper. Treatment to slow hepatic fibrosis was advised and included oral prednisolone administration for at least 1 month. A diet to support liver function was formulated by a nutritional specialist, and vitamin E was advised as dietary supplement to support neuromuscular function. Soon after diagnosis, the animal showed signs of intravascular haemolysis, with the presence of Heinz bodies in peripheral blood smears, and haemoglobinuria. On the basis of this haemolytic crisis and the poor prognosis of the chronic hepatic disease, the horse was euthanized at the owners' request. Although we could not establish the cause of the hepatic copper accumulation, this case report highlights that excessive copper in the liver should be considered in the differential diagnosis of hepatic cirrhosis and Heinz body anaemia in the horse.

[Indexed for MEDLINE]

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