Clinical, morphologic, and chemical studies on copper toxicosis of Bedlington Terriers
Twedt, D.C.; Sternlieb, I.; Gilbertson, S.R.
Journal of the American Veterinary Medical Association 175(3): 269-275
In a study of 90 Bedlington Terriers, 68 had a defect that resulted in the accumulation of toxic excesses of copper in the liver. Concentrations of copper were 5 to 50 times that of clinically normal mongrel dogs. The bulk of this excess copper was sequestered in lysosomes. When copper concentrations exceeded 2000 mu g/g dry liver, progressive signs of functional and morphological disturbance appeared as focal hepatitis, chronic active hepatitis, and ultimately cirrhosis. The disorder, which appears to be inherited, could only be diagnosed by liver biopsy. It was latent for many years in some dogs, but led early in life to acute or chronic hepatic disease and death in others.