Copper is an essential trace element required by all living organisms. Even a mild copper deficiency impairs the ability of white blood cells to fight infections and production of hemoglobin. It is necessary for proper absorption of iron. Copper is involved in the neurotransmitter synthesis, connective tissue formation, pigmentation, and essential fatty acid and iron metabolism. However, as with all trace minerals, it is extremely toxic when present in excessive amounts inducing free radical production that results in cellular damage. In humans, excessive amounts of copper are hallmarks of three genetic disorders: Menkes disease, occipital horn syndrome, and Wilson's disease. The canine form is termed Copper associated hepatitis and most often affects the Bedlington Terrier, West Highland White Terrier, Skye Terrier, Doberman Pinscher, Dalmatian and, occasionally, Labrador Retriever. In addition, results from a large survey of liver copper concentrations in dogs (Thornburg et al. 1990) and results from a review on dogs diagnosed with primary hepatitis (Poldervaart et al. 2009) suggest that there may be more dog breeds in which high liver copper levels and copper-associated hepatitis are present.2
Copper toxicosis can be classified as primary when it results from an inherited metabolic defect, and as secondary when it is the consequence of an abnormally high intake, increased absorption, or reduced excretion of copper due to underlying pathologic processes. In Bedlington Terriers and Westies, there is an inherited defect of copper metabolism that allows toxic concentrations of copper to accumulate in the liver. Recently, a mutated MURR1 gene was discovered in Bedlington Terriers affected with the disease. Dobermans have been reported to have a very severe form of hepatitis and cirrhosis, which is seen almost exclusively in females and often has a fatal course within weeks or a few months after diagnosis. It is unclear in the Doberman and the Skye terrier whether high copper levels are the cause of the hepatitis or the result. As a rule, the higher the copper concentration, the more likely it is that the copper is the cause. Both sexes can be equally affected. At the early stage of the disease, affected dogs may have no signs, or show progressive liver disease characterized by failure to thrive, jaundice, and ascites. About half of the animals die within a week of the onset of jaundice. In Bedlington Terriers older than 1 year of age, there is a progressive increase in the accumulation of tissue copper until 8 years of age.
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Genetic testing for copper toxicosis is available. Blood tests, ultrasounds, and CT scans provide useful information, but the only definitive test is biopsy of the liver. The prognosis for recovery depends on how long the dog has been ill, the extent of liver damage, and whether the disease can be surgically cured or controlled with medications. Treatment of copper associated hepatitis varies with the breed. Medications can be given to move copper out of the liver into the circulation, where it can be excreted in the urine. The absorption of copper can be decreased by giving oral zinc and copper chelator products that bind copper in the gut. Early diagnosis and intervention are key to the successful treatment of dogs with hepatitis.
- Prescription for Nutritional Healing. Phyllis A. Balch
- Canine models of copper toxicosis for understanding mammalian copper metabolism
- Inherited Copper Transport Disorders: Biochemical Mechanisms, Diagnosis, and Treatment