Vacuolar hepatopathy (VH) is a common diagnosis in dogs. It describes a disorder in which hepatocytes become markedly distended with glycogen with or without discrete membrane bound lipid inclusions. VH characterized by cytosolic glycogen accumulation is associated with typical or atypical hyperadrenocorticism or endogenous release of corticosteroids in response to chronic stress, illness, inflammation, or neoplasia. Liver biopsy is often pursued in these patients because of unexplained increases in serum AP activity. Transaminase activity may only be modestly increased; GGT may or may not be increased. Intrahepatic extramedullary hematopoiesis is commonly observed.
Abdominal radiography may reveal hepatomegaly or changes associated with an underlying disease process. Metastatic disease or mineralized airways (chronic hyper-adrenocorticism) may be seen on thoracic radiography. Ultrasonography reveals subjective hepatomegaly and hypoechoic hepatic nodules against a hyperechoic parenchymal background; the so-called “Swiss cheese pattern,” cannot be differentiated from infiltrative mass lesions, hepatic fibrosis, nodular hyperplasia, regenerative nodules, or cirrhosis. In some cases, grossly evident hepatic nodules cannot be discerned by ultrasound examination. VH usually is the underlying hepatic lesion in dogs with idiopathic nodular hyperplasia and also is common in dogs with hepatic adenomas or biliary mucoceles. Progressive VH merges into the classic hepatic syndrome associated with the hepatocutaneous lesion (see Hepatic Disease in Small Animals: Hepatocutaneous Syndrome in Small Animals). Hepatic biopsy is needed for definitive diagnosis, because glycogen-vacuolated hepatocytes are also observed in necroinflammatory liver disorders.
It is critical to determine and treat any underlying disease process. Careful scrutiny for adverse drug reactions is also necessary, with a focus on drugs associated with “induction phenomenon.” These should be discontinued and replaced with an alternative therapy. Clinicians should investigate any use of holistic or herbal remedies that may deliver systemic glucocorticoid or ACTH effects.
Nutritional support is important and must be individualized. In most cases, a normal nitrogen intake is appropriate. VH in dogs with hyperlipidemia requires treatment with a fat-restricted diet (<2 g fat/100 kcal of diet). A protein-restricted diet should not be fed, unless indicated (eg, demonstration of HE). In fact, protein restriction may augment development of this liver lesion, especially if it is associated with hypoaminoacidemia as in the hepatocutaneous syndrome. A supplementary water-soluble vitamin is recommended for all dogs. Antioxidants should be provided, and ursodeoxycholic acid is recommended if TSBA concentrations are increased.
Last full review/revision March 2012 by Sharon A. Center, DVM, DACVIM