DogMatchUp
Health Condition

Copper Toxicosis

Copper toxicosis is a hereditary liver disorder characterized by abnormal accumulation of copper in the liver, leading to progressive liver damage and potentially fatal liver failure.

Detailed Description

Copper toxicosis is caused by a mutation in the COMMD1 gene, which impairs copper excretion from liver cells. Over time, copper accumulates to toxic levels, resulting in chronic hepatitis, cirrhosis, and liver failure. Clinical signs often appear after significant hepatic damage has occurred, and the disease is most commonly seen in Bedlington Terriers.

Common Symptoms

  • Lethargy
  • Anorexia
  • Vomiting
  • Jaundice
  • Ascites
  • Weight loss
  • Polyuria
  • Polydipsia
  • Neurological signs in advanced cases

Management Options

  • Copper-chelating agents (D-penicillamine, trientine)
  • Low-copper diet
  • Zinc supplementation
  • Supportive care for liver failure

Frequently Asked Questions

Can copper toxicosis be prevented?

Yes, through genetic testing and selective breeding to avoid producing affected puppies.

Is copper toxicosis curable?

No, but it can be managed with medication and diet if caught early.

What is the best screening method?

DNA testing for the COMMD1 mutation is the gold standard.

Are all Bedlington Terriers at risk?

All should be considered at risk unless proven clear by genetic testing.

How often should liver function be checked?

Annually, or more frequently in at-risk dogs.

Condition Details

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Typical Age of Onset

2-6 years

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Testing Available

Yes

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Diagnosing Methods

Bloodwork (ALT, AST, ALP, bilirubin); Liver biopsy (histopathology and copper quantification); Genetic testing

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Preventative Measures

Genetic testing and responsible breeding; Early screening of puppies from at-risk lines

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Related Conditions

Chronic hepatitis, Wilson’s disease in humans

Affected Breeds

Bedlington Terrier

Prevalence: 5% Severity: 5/5

Bedlington Terriers have the highest known risk for copper toxicosis due to a breed-specific COMMD1 gene mutation. Up to 25% are carriers and 5-10% develop clinical disease.
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