Hepatoportal fibrosis in three young dogs

Abstract

Three young dogs with a history of apathy, anorexia and weight loss were presented with severe ascites. Abnormal laboratory findings include hypoalbuminaemia and increased activities of alkaline phosphatase, serum aspartate amino-transferase, serum glutamic pyruvic transaminase and gamma-glutamyl transferase. Ammonia tolerance was also abnormal. At autopsy ascites and peripheral portosystemic collaterals were found. The livers were abnormally small and firm and their surfaces were irregular. Histologically, there was marked periportal fibrosis, increased numbers of bile ductules and arteriolae in the portal areas and an absence of normal portal vein tributaries. No inflammatory changes were found. These lesions are discussed in relation to the various causes of hepatic fibrosis.

Congenital Intrahepatic Arteriovenous Fistulae in a Young Beagle Dog

“…The etiologies of AVF include trauma, rupture of hepatic artery aneurysms, congenital defects (vascular hamartoma), hepatic vein obstruction, and cirrhosis with extreme portal hypertension (4,6,12,13,15,17,19 (1,4,8,10,(20)(21)(22). Moreover, AVF, portosystemic shunt, and microvascular portal dysplasia often coexist in the same cases (4,17,19).…”

“…Hepatic vascular anomalies have been described as arteriovenous fistulae (6,13,17,19) and vascular hamartomas (12,15), as well as portosystemic shunts (1,4,8,10,(20)(21)(22)(23). These vascular lesions tend to be congenital in young dogs, and the animals often reveal clinical hepatic hypofunction and encephalopathy (1,3,4,21).…”

Chronic hepatitis in man and in dog: a comparative update

“…As described by some authors (25), fibrosing hepatitis results from a progression of piecemeal necrosis and consists in dissection of the lobular parenchyma by reticulin and fine collagen fibers with minimal portal inflammation (26). Two other conditions, histologically characterized by noninflammatory fibrosis, which varied from diffuse to zonal reticulofibrosis, have also been reported (27,28) and named noninflammatory primary hepatic fibrosis (27) and idiopathic hepatic fibrosis (28). In the latter condition, the young age of the patients and overrepresentation of German shepherds suggested a genetic component (28).…”

Ascites

“…38 Posthepatic portal hypertension is uncommon in cats. 6,47,48 End-stage acquired hepatic disease, and congenital portosystemic shunting both cause substantially decreased albumin production. The most common cause of sinusoidal or postsinusoidal portal hypertension is diffuse parenchymal disease such as cirrhosis (an end-stage disease in breed-specific hepatopathies), drug-related hepatopathies, fibrosis, diffuse neoplasia, chronic diffuse hepatitis, and chronic cholangiohepatitis.…”