Page 589 - Small Animal Internal Medicine, 6th Edition

CHAPTER 35
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Hepatobiliary Diseases

in the Cat

GENERAL CONSIDERATIONS loss of hepatocyte function, which is reversible if the fat can
be mobilized (Fig. 35.1). The reason for the differences in
The causes, clinical signs, and prognosis of hepatobiliary prevalence in different countries is unknown but intriguing.
tract diseases in cats are very different from those of dogs. Some researchers suggest environmental differences (e.g.,
Primary and secondary causes of liver disease in cats are differences in outdoor or indoor lifestyle or feeding habits),
outlined in Table 35.1. Cats typically have hepatobiliary genetic differences among cats, or both.
disease or acute hepatic lipidosis, but chronic parenchymal The pathogenesis of primary hepatic lipidosis remains
disease is uncommon in this species; in addition, feline liver incompletely understood, but it seems to involve a combina-
disease rarely progresses to cirrhosis, as is sometimes the tion of excessive peripheral lipid mobilization to the liver,
case in dogs. The clinical signs of hepatobiliary disease in deficiency of dietary proteins and other nutrients that would
cats are generally nonspecific and similar to the signs of usually allow fat metabolism and transport out of the liver,
inflammatory bowel disease (IBD) and pancreatitis; the and concurrent primary disturbances in appetite. Excessive
three conditions may coexist, further confusing diagnosis. mobilization of peripheral fat occurs particularly during
Hepatic lipidosis presents with more classic signs of liver periods of anorexia or stress in previously overweight cats.
disease, including jaundice and encephalopathy. The most Concurrently, anorexia results in deficiencies of dietary pro-
important differences between feline and canine hepatobili- teins and other nutrients; cats are particularly susceptible to
ary diseases are outlined in Table 35.2. these problems because of their high dietary requirements
The feline hepatopathies in this chapter are described (see Table 35.2). Some of these nutrients are important in fat
approximately in order of their frequency in clinical practice metabolism and mobilization, particularly methionine, car-
in the United States. Historically, hepatic lipidosis has been nitine, and taurine, so deficiencies in these nutrients are
most common in the United States and cholangitis most implicated as contributing to the pathogenesis of the disease.
common in Europe, but lipidosis is becoming increasingly Methionine is an important precursor in the synthesis of an
common in Europe, and cholangitis is now commonly rec- important hepatic antioxidant, glutathione, and hepatic con-
ognized in the United States. centrations of glutathione may decrease markedly in cats
with hepatic lipidosis. Relative arginine deficiency will con-
tribute to the resultant hepatic encephalopathy (HE) caused
HEPATIC LIPIDOSIS by decreased urea cycle activity. Concurrent primary appe-
tite disturbances result in persistent and marked anorexia,
Etiology and Pathogenesis which is likely caused by disturbances in the complex neu-
Feline hepatic lipidosis may be primary or secondary to rohormonal control of appetite. Recent studies have sug-
another disease, but in either case it is associated with a high gested that peripheral insulin resistance does not play a
mortality unless the cat is intensively fed. relevant role in the disease, unlike in human nonalcoholic
fatty liver disease.
PRIMARY HEPATIC LIPIDOSIS
Primary or idiopathic hepatic lipidosis usually affects obese SECONDARY HEPATIC LIPIDOSIS
cats and remains the most common hepatic disease of cats Secondary hepatic lipidosis is also common in cats; its
in North America; it is also now emerging as an increasingly pathogenesis is similar to that of the primary disease but is
common problem in Europe and Israel (Bayton et al., 2018; complicated by the more marked neuroendocrine responses
Kuzi et al., 2017). It is effectively an acute hepatopathy with to stress. Secondary lipidosis can therefore be seen in cats
a massive accumulation of fat in hepatocytes leading to acute that are less obese than those presenting with the primary

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