Lobular dissecting hepatitis
A characteristic feature of histopathology of this disease is disruption of the hepatic architecture by complete fibrotic dissection of the lobular parenchyma into individual and small groups of hepatocytes with subsequent portal hypertension.
Secondary portosystemic shunts and cirrhosis may develop secondary to advanced hepatic failure.
Supportive treatment is recommended (eg, antibiotics if bacterial cultures are positive), along with choleretics, antifibrotic agents, low-protein diet and ursodeoxycholic acid.
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.
However, the prognosis is less favorable than dogs with idiopathic or copper-associated hepatitis.
- Mekonnen GA et al (2007) Tenascin-C in chronic canine hepatitis: immunohistochemical localization and correlation with necro-inflammatory activity, fibrotic stage, and expression of alpha-smooth muscle actin, cytokeratin 7, and CD3+ cells. Vet Pathol 44(6):803-813
- Jensen AL & Nielsen OL (1981) Chronic hepatitis in three young standard poodles. Zentralbl Veterinarmed A 38(3):194-197
- Mizooku H et al (2012) Histological and Immunohistochemical Evaluation of Lobular Dissecting Hepatitis in American Cocker Spaniel Dogs. J Vet Med Sci Dec 28
- van den Ingh TS & Rothuizen J (1994) Lobular dissecting hepatitis in juvenile and young adult dogs. J Vet Intern Med 8(3):217-220
- Merck Veterinary Manual
- Poldervaart JH et al (2009) Primary hepatitis in dogs: a retrospective review (2002-2006). J Vet Intern Med 23(1):72-80