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Copper Hepatopathy in Labradors

When there is an abnormal type of proteins that bind to copper
• there is an abnormality in the metabolism of bile
• in rare cases, zinc deficiency

Among the different breeds of dogs predisposed to Copper Hepatopathy, a higher incidence rate has been observed in Doberman females.

In order to better understand how any of these conditions lead to copper hepatopathy, there is a need to know the pathways that is undertaken by copper in the diet before being excreted. When copper is absorbed through the intestinal walls they become bound to liver proteins which facilitate appropriate excretion via the bile. If there is a defect in either the bile or the proteins, copper accumulates in the liver. Since copper is not a normal component in the liver, its continued presence and accumulation leads to a chronic inflammatory process in the liver known as chronic hepatitis. If the situation remains uncorrected, it leads to cirrhosis of the liver, a condition characterized by formation of scar tissue in the liver and eventually liver failure.

There are also instances when the accumulation of copper leads to the death of cells within the liver, a condition known as necrosis of the liver. When this happens, copper toxicity can occur leading to the extensive destruction of red blood cells.

There are three clinical syndromes of Copper Hepathopathy recognized in dogs—

The first syndrome is usually observed in young dogs and characterized by an acute onset of depression, vomiting, and anorexia. This syndrome is usually fatal and most dogs suffering from this syndrome die quickly.

The second syndrome has been observed to occur in middle-aged to geriatric dogs. This is a chronic type where symptoms usually come and go in a long span of time. Dogs with this form of the disease are lethargic and have very poor appetites. Increased water intake with increased urination, vomiting, and diarrhea may also be present. In the long run, patients develop jaundice, abnormalities in blood clotting, ascites (abdominal distension), and hepatic encephalopathy (a nervous disorder associated).

The third syndrome is classified as a subclinical case where affected dogs barely show clinical manifestations of the disease.

Diagnosis involves laboratory tests including CBC, blood chemistry, clotting times, liver biopsy, bile acid testing. Liver biopsy helps demonstrate the levels of copper in the liver. Radiographic tests such as x-rays may show an enlarged liver which is typical of an acute disease or a small liver which is usually characteristic of the late stages of the chronic form. There are also cases where x-rays do not reveal anything conclusive.

The screening tool used to demonstrate the amounts or levels of copper in the liver includes a stool test or fine needle aspiration of the liver.

Treatment for labradors or any dog depends on the form of the disease. Chronic and subclinical forms are often treated by a process called copper chelation where a drug is administered to bind the copper before it reaches the liver. This mode of treatment is often a lifelong effort to effectively manage the chronic and subclinical forms of copper hepatopathy.

Acute cases of copper hepatopathy are treated with antibiotics, fluid therapy, anti-nausea drugs and other symptomatic medications. When liver failure is already present, treatment seeks to rid the body of toxins which the liver fails to remove. Antibiotics help prevent or get rid of infections that the liver can no longer safeguard the body from.

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