Diagnosing and treating canine copper-associated hepatopathies - Veterinary Medicine
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Diagnosing and treating canine copper-associated hepatopathies
Whether from inflammatory hepatic disease or an inherited metabolic defect, copper accumulation can lead to hepatocellular damage and even cirrhosis. Treatment can successfully mitigate or even reverse copper-associated changes.


Rarely, severe acute hepatic necrosis may result in the release of stored copper into the blood. This release causes hemolysis, probably from direct oxidative damage to erythrocyte membranes. Affected dogs may present with pallor, jaundice, lethargy, inappetence, or pigmenturia. Hemolysis secondary to copper toxicosis has only been reported in Bedlington terriers.5,6


The most consistent laboratory finding is increased alanine transaminase (ALT) activity. Other liver enzyme activities may be increased concurrently, including alkaline phosphatase (ALP), aspartate transaminase (AST), and gamma-
glutamyltransferase (GGT). The relative increase in ALT activity is often much higher than the relative increase in ALP activity, suggesting predominantly hepatocellular rather than cholestatic liver disease. Even mild increases in ALT activity are important and merit more attention than changes in ALP activity. In addition, consider nonhepatic causes of increased ALP activity, particularly if it is the only abnormal parameter.

Hyperbilirubinemia, hypoalbuminemia, hypoglycemia, low blood urea nitrogen (BUN) concentration, or hypocholesterolemia suggests considerable compromise to hepatic function. Elevated bile acid concentrations, ammonia tolerance testing results, or ammonia concentrations can confirm liver dysfunction and may provide prognostic information. However, they do not obviate the need for liver biopsy.

Since copper accumulation in the liver occurs slowly, substantial increase of ALT or AST activity in a previously healthy patient is most suggestive of an acute injury by a noncopper hepatotoxin. Hepatoprotectants, supportive care, and periodic monitoring (every two weeks) of serum chemistry profile results are indicated before liver biopsy is pursued.

Other laboratory abnormalities may include anemia from chronic disease (nonregenerative) or gastrointestinal blood loss (regenerative or nonregenerative). Liver disease predisposes patients to gastrointestinal ulceration because of impaired mucosal blood flow, which is a result of dehydration and portal hypertension and decreased clearance of histamine and gastrin.6 Evidence of gastrointestinal bleeding may include melena, hematochezia, or an increased serum BUN to creatinine ratio. Urinalysis results may reveal bilirubinuria, dilute urine (isosthenuria), or glucosuria.


Figure 1. A laparoscopic photograph showing a nodular and discolored liver. (Photo courtesy of Dr. Mike Willard of Texas A&M University's College of Veterinary Medicine.)
Abdominal ultrasonography is indicated to rule out primary biliary tract disease, especially extrahepatic biliary obstruction, and can provide useful clues about the duration of a patient's liver disease. If the liver appears mottled (mixed echogenicity), small, cirrhotic, or nodular, the liver disease is probably chronic. If the liver appears unremarkable in terms of size and echogenicity in a patient with a one-time-only increase in liver enzyme activities, acute liver injury is more probable.


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