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Copper Toxicosis (Accumulating)
ATP7B
- Liver
This condition affects the liver’s ability to remove excess copper. Over time, copper can build up in the liver and damage liver cells. Both genetic and environmental factors play a role in how the condition develops.
Signs typically develop in adults.
Talk to your vet about your dog’s copper toxicosis result so you can discuss if dietary management or monitoring is indicated.
Copper is an essential nutrient, but amounts can vary widely among commercial diets, so your vet may recommend a specific food or periodic testing to maintain safe levels.
Many dogs with this result never develop clinical disease. Watch for signs that may indicate high copper levels, such as decreased appetite, vomiting, lethargy, or jaundice.
Learn more about how the three variants for Copper Toxicosis are inherited and, if applicable, how results can be used in a breeding program here.
This mutation was first described in the Labrador Retriever. Further studies have indicated that it may play a role in Doberman Pinscher copper-associated liver disease.
Penetrance: This mutation is inherited in an autosomal incomplete dominant manner, meaning that one or two copies of this gene can cause the disorder. However, it is incompletely penetrant, meaning that not all dogs with one or two copies of the mutation will actually develop the disease. Dogs with two copies of the mutation are at greater risk of developing this disease than dogs with one copy of the mutation.
- Gene
- ATP7B
- Inheritance type
- incomplete dominance
- Clinical category
- Hepatic
Citations
English Labrador Retriever
Labrador Retriever
Doberman Pinscher
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