Hepatopatia crônica associada ao acúmulo de cobre em um cão da raça American Pitbull Terrier

Background: The liver plays a variety of essential biochemical functions such as the metabolism of carbohydrates, proteins, lipids and vitamins, the maintenance of blood glucose and bile acids synthesis. Hepatic insuffi ciency occurs when 70 to 80% of the functional liver mass is committed the liver is unable to metabolize substances on the circulation. In some cases, chronic liver disease may be associated with copper accumulation, which may occur by increased dietary intake, faults in hepatic copper metabolism or liver diseases that cause colestase. The purpose of this paper is to report a case of chronic liver disease associated with copper accumulation in a 8-month-old American Pit Bull Terrier. Case: An American Pitbull Terrier was referred to the Veterinary Teaching Hospital of the Federal University of Rio Grande do Sul with a history of abdominal distension, decreased appetite, vomiting, diarrhea, weight loss and exhaustion. On physical examination the animal presented ascites and dehydration and laboratory tests were suggestive of active liver disease. Supportive care was provided. The patient was prescribed ranitidine (2 mg/kg) VO BID for 7 days, metoclopramide (0.3 mg/kg) VO BID also for 7 days and furosemide (1 mg/kg) PO BID until further instructions while awaiting for test results. The next appointment was scheduled for ten days later but the owner came back for consultation only 60 days after the fi rst visit. The patient had then a history of abdominal distension, dullness and polydipsia. During physical examination, it was possible to notice pale mucous membranes, dehydration, cachexia, hypothermia and ascites. The animal was then hospitalized for additional tests, abdominocentesis, support treatment and further observation. Laboratory fi ndings showed liver failure. The patient died after two days. Necropsy revealed macroscopic alterations compatible with liver cirrhosis. On microscopic examination, it was observed marked diffuse proliferation of fi brous connective tissue and epithelial cells of the bile ducts, besides moderate multifocal histiocytic infi ltrate with granular intracytoplasmic brownish pigment. Copper determination on hepatic fragment was performed. The examination found 1320 mg/g on dry weight of copper in the body. The necropsy report was liver cirrhosis associated with copper accumulation. Discussion: Liver disease associated with copper accumulation has been reported in West Highland Terriers, Skye Terriers and Bedlington Terriers. There are not, however, reports of this disease in American Pitbull Terriers. Laboratory fi ndings of this case are consistent with liver failure, also reported by previous studies. Based on laboratory fi ndings supportive care was established since the patient was in an irreversible condition. A biopsy was not performed, despite being the defi nitive diagnostic method for cirrhosis, since the patient had alterations in the coagulation tests, preventing the procedure. The acquired portosystemic shunt observed on necropsy was due to increased intrahepatic resistance, caused by fi brosis and is a common fi nding in cases of cirrhosis. The copper concentration found in the liver was three times greater than the value considered normal for the canine species. However, it was not possible to determine whether the copper accumulation was the cirrhosis’ cause or consequence. Chronic liver disease is common in veterinary care, but it is often diffi cult to identify the cause of injury. The copper accumulation should be considered as a liver failure cause in same breeds as predisposed but yet unreported, especially in young patients.