On guard for hepatobiliary diseases in dogs - DVM
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On guard for hepatobiliary diseases in dogs


DVM360 MAGAZINE


Portal-vein hypoplasia

Portal-vein hypoplasia, also referred to as microvascular dysplasia (MVD), is a confusing syndrome associated with abnormal microscopic hepatic portal circulation. Initially, the condition has been referred to as hepatic microvascular dysplasia. Hepatic portal-vein hypoplasia has been suggested as better terminology that may better reflect the cause of this condition. It is believed that the primary defect in affected dogs is the result of hypoplastic small intrahepatic portal veins.

This condition is thought to be a defect in embryologic development of the portal veins. With paucity in size or presence of portal veins, there is a resultant increased arterial blood flow in attempt to maintain hepatic sinusoidal blood flow. The hepatic arteries become torturous and abundant in the triad. Sinusoidal hypertension occurs under this high-pressure system. Lymphatic and venous dilation results with opening up of embryologic sinusoidal vessels and, thus, acquired shunts develop to transport some of the blood to the central vein, bypassing the sinusoidal hepatocytes.

This results in abnormal hepatic parenchymal perfusion and lack of normal trophic factors bathing the sinusoids, causing hepatic atrophy. With portal shunting of blood, increased iron uptake occurs that results in hepatic iron granuloma formation. Ascites or portal hypertension generally does not occur in this condition. Angiography or transcolonic portal scintigraphy fails to demonstrate macroscopic shunting in this condition.

Often a needle biopsy is not sufficient to provide enough portal areas to make the diagnosis, and consequently a wedge or laparoscopic biopsy may be necessary. All dogs have abnormal serum bile acid concentrations (usually moderate elevations) and variable serum liver enzymes. Therapy is symptomatic and includes management of hepatic encephalopathy. Evidence of oxidative damage to livers of shunt dogs provides evidence for antioxidant supplementation. The long-term prognosis is uncertain because of lack of experience with this relatively new disease.

Portal-vein hypoplasia and secondary portal hypertension

Portal vein hypoplasia with portal hypertension (also known as idiopathic noncirrhotic portal hypertension or congenital hepatic fibrosis) and ascites occurs as a fibrosis variant. It is generally accepted that dogs having congenital portosystemic vascular anomalies with a single intrahepatic or extrahepatic shunting vessel have signs associated with hepatic encephalopathy but do not have portal hypertension or ascites. However, there is a subgroup of dogs with portal-vein hypoplasia that have moderate to marked fibrosis of the portal tracts, sometimes resulting in portal to portal fibrosis and a varying proliferation of arterioles and bile ductules, particularly at the periphery of the portal area.

Ascites, portal hypertension and secondary acquired portosystemic shunts occur. The hepatic pathology is void of inflammatory infiltrates. There are increased amounts of hepatic iron deposited in the liver. The fibrosis and bile-duct replication may be a non-specific reaction from increased growth factors promoting arterial proliferation. This condition is observed in dogs under 2.5 years of age and there is no breed prevalence; however, Doberman Pinschers, Cocker Spaniels and Rottweilers may be over-represented. The clinical presentation is similar to dogs having either congenital intrahepatic or extrahepatic shunts except most dogs have ascites. The serum liver enzymes generally are increased with a hypoalbuminemia and very high serum bile acid concentrations. Work-up of these dogs fails to identify a single shunting vessel, but rather these cases have marked portal hypertension associated with multiple acquired portosystemic shunts. These dogs present with ascites and signs of hepatic encephalopathy. Ultrasound study often is helpful, showing microhepatica, hepatofugal portal blood flow and multiple abnormal extrahepatic collateral shunts. Portal contrast studies indicate acquired portal shunts and pressure measurements document portal hypertension. The prognosis for this condition generally is guarded, but some dogs are reported to have a prolonged survival using anti-fibrotic agents and hepatic encephalopathy therapy.

Hepatic vacuolar hepatopathies

Diffuse vacuolar hepatopathies can be very frustrating in determining the underlying cause. When hepatocytes become injured, one response is for them to swell and become vacuolated. Hepatocellular vacuoles distending the cytosolic compartment may contain fat, glycogen, intracellular water (edema), or other metabolic wastes or intermediates. Vacuolar hepatopathies may occur in conjunction with hydropic degeneration in which there is cytosolic swelling but the hepatocytes are devoid of distinct vacuoles. A number of conditions can be responsible for vacuolar hepatopathies.

Glucocorticoid (steroid) hepatopathies

Glucocorticoid (steroid) hepatopathies occur in the dog secondary to exogenous or endogenous glucocorticoids. The vacuolar lesions contain glycogen that is not easily differentiated from other vacuolar contents without specialized histopathologic processing. The development of steroid hepatopathies is linked with marked increases in serum ALP. The glucocorticoid-associated ALP (G-ALP) is unique to the dog and dogs having steroid hepatopathies are associated with a large component of G-ALP.


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