Idiopathic chronic hepatitis in dogs is defined as chronic periportal hepatitis with no identifiable cause.
Most affected animals are 5-6 yr old. There is no breed predilection and with males and females equally affected.
- Copper-associated hepatitis of Labrador Retrievers
- Acidophil hepatitis
- Chronic Hepatitis of Bedlington Terriers
- Chronic Hepatitis of West Highland White Terriers
- Idiopathic Chronic Hepatitis
- Chronic Hepatitis of Doberman Pinschers
- Chronic Hepatitis of Skye Terriers and Cocker Spaniels
- Lobular Dissecting Hepatitis
Clinical signs include those typical for chronic liver disease and include anorexia, vomiting, diarrhea, weight loss, jaundice, polyuria and polydipsia, ascites, depression, and weakness.
Common laboratory abnormalities include marked increases in ALT, moderate to marked increases of AP, bilirubinuria and hyperbilirubinemia, increased serum bile acids, and an abnormal ammonia tolerance test. Hypoalbuminemia, hyperglobulinemia, nonregenerative anemia, and abnormal coagulation profile are also reported. Radiographs may demonstrate a small liver, and nodular lesions may be detected on ultrasonographic studies. Definitive diagnosis is by liver biopsy. Histopathologic findings include lymphocytic-plasmacytic inflammation, piecemeal necrosis advancing to bridging necrosis, and in advanced cases, cirrhosis. Biopsy specimens should be submitted for both aerobic and anaerobic cultures.
Supportive care and use of specific therapy as indicated (eg, antibiotics if bacterial cultures are positive), along with choleretics, antifibrotic agents, and low-protein diets may be effective. Ursodeoxycholic acid is used if significant cholestasis is noted without biliary obstruction. The use of colchicine as an antifibrotic agent may be limited by side effects that include nausea, vomiting, and hemorrhagic diarrhea. Use of immunosuppressive drugs is controversial but recommended if there is no evidence of infectious disease, if there is strong evidence of immune-mediated disease, or if active disease is evident on biopsy. Prednisolone can be given at 1-2 mg/kg, divided bid until clinical remission, after which the dosage is slowly reduced. Complete remission is difficult to evaluate clinically and may require a followup biopsy. Prognosis depends on the amount of damage sustained by the liver and the degree of fibrosis but can be favorable if damage is mild to moderate and if initial therapy is effective.