Canis ISSN: 2398-2942

Copper toxicosis (Bedlington Terrier)

Contributor(s): Kyle Braund

Introduction

  • Excessive storage of copper in liver.
  • Cause: autosomal recessive.
  • Signs: liver failure (acute or chronic), rarely hemolytic crisis.
  • Diagnosis: liver biopsy.
  • Treatment: supportive, eg diet; copper chelating agents, eg D-penicillinamine.
  • Prognosis: reasonable, some → cirrhosis.
  • See also: Acute liver disease Liver: acute disease.

Pathogenesis

Etiology

  • Autosomal recessive.

Pathophysiology

  • An inherited metabolic defect in biliary copper excretion caused by abnormal binding of copper with metalothionein in the liver.
  • The hepatic injury involves oxidant damage to hepatic mitochondria.
  • Genetic trait → hepatocytes accumulate copper (massive liver copper accumulation) → hepatocytes die → hepatocytes replaced by fibrosis → hepatic failure. Hepatitic damage does not consistently occur until copper concentrations exceed 2000 ug/g.
  • Rare: lysis of large numbers of hepatocytes → massive hemolysis.

Timecourse

  • Variable.
  • Affected dogs can be symptomatic or show signs of acute hepatic necrosis, chronic hepatitis or cirrhosis.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Holems N G et al (1998) DNA marker C04107 for copper toxicosis in a population of Bedlinton Terriers in the United Kingdom. Vet Rec 142 (14), 351-352 PubMed.
  • Yuzbagiyan-Gurkan V et al (1997) Linkage of a microsatellite marker to the canine copper toxicosis locus in Bedlington Terriers. Am J Vet Res 58 (1), 23-27 PubMed.

Other sources of information

  • Johnson S E (2000)Chronic hepatic disorders.In:Textbook of Veterinary Internal Medicine. 5th edn. Eds: S J Ettinger & E C Feldman. Philadelphia: W B Saunders. pp 1298-1325.


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