Lobular dissecting hepatitis is a unique hepatic reaction pattern rather than a unique hepatic syndrome. The histologic features are typified by liver injury associated with intrasinusoidal nonsuppurative inflammatory infiltrates leading to panlobular sinusoidal fibrosis.
Although more commonly described in juvenile to young adult dogs and in a small group of related Standard Poodles, lobular dissecting hepatitis seemingly has no breed, sex, or age predilection. Weight loss and ascites, with or without jaundice, are common clinical features.
Laboratory abnormalities include hypoalbuminemia, hypocholesterolemia, low BUN, and increased total serum bile acid concentrations in nonjaundiced dogs. Liver enzymes may be normal or mildly or markedly increased. Acquired portosystemic shunts develop due to acquired intrahepatic sinusoidal portal hypertension. Hepatic copper concentrations are not consistently increased. The syndrome commonly progresses to cirrhosis.
Supportive treatment is recommended for hepatic encephalopathy, ascites, and control of fibroplasia and inflammation. Colchicine (0.03 mg/kg, PO, every 24 to 48 hours) has been used to control fibrosis and sinusoidal inflammation in some dogs. Other dogs have been managed with more conventional immunomodulatory protocols with polyunsaturated phosphatidylcholine with 52% dilinoleoylphosphatidylcholine, 25–50 mg/kg, PO, every 24 hours, used as an antifibrotic with fewer adverse affects.
This is a poorly understood and characterized syndrome and in some cases may reflect hepatotoxin exposure.
