Hepatotoxicity of phenobarbital in dogs: 18 cases (1985-1989)
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Summary
The medical records of 18 dogs that had hepatic disease and received phenobarbital as an anticonvulsant for 5 to 82 months were reviewed. Clinical signs included sedation and ataxia in all dogs, 5 dogs were also anorectic, 2 had coagulopathy, 3 were icteric, and 5 had ascites. Serum biochemical analysis revealed serum albumin concentration ≤ 2.2 g/dl in 12 dogs, serum alkaline phosphatase activity ≥ 169 U/L in 18 dogs, serum alanine transaminase activity ≥ 57 U/L in 15 dogs, and total bilirubin concentration ≥ 1 mg/dl (in the absence of lipemia) in 7 dogs.
Serum phenobarbital concentration was ≥ 40 μg/ml in 12 of 17 dogs. Sulfobromophthalein excretion was prolonged in 8 of 10 dogs. Preprandial serum bile acid concentrations were high in 8 of 10 dogs, and 2-hour postprandial serum bile acid concentrations were high in 9 of 10 dogs. Two of 4 dogs tested had resting plasma ammonia concentrations > 200 mg/dl. An ammonia tolerance test was performed on 2 other dogs; both had ammonia concentration ≥ 200 mg/dl in the plasma 30 minutes after receiving 100 mg of ammonium chloride/kg of body weight, po.
Nine dogs died, 1 was euthanatized, and necropsies were performed on these 10 dogs. Biopsies and necropsies of 6 dogs revealed chronic hepatic fibrosis with nodular regeneration (cirrhosis). One dog had hepatocellular carcinoma and mild cirrhosis. In 1 dog, after phenobarbital had been withheld, necropsy revealed complete recovery of the previously observed lesions.
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