Page 1115 - Small Animal Clinical Nutrition 5th Edition

Hepatobiliary Disease 1161

es the diagnostic accuracy of the histologic diagnosis
VetBooks.ir (Rothuizen et al, 2006). One study showed a poor histologic
correlation when only two 18-gauge needle biopsy specimens
were compared to a wedge biopsy (Cole et al, 2002).
The advantage of fine-needle aspiration cytology (Figure
68-5) is decreased risk of complications or bleeding. However,
a representative sample might not be obtained with this tech-
nique because of the very small amount of tissue that is ob-
tained and the fact that liver architecture is not left intact dur-
ing fine-needle aspiration procedures. Interpretation of hepatic
cytology should be used in light of all clinical findings because
hepatic cytology does not always correlate with histopathology.
Ideally, liver tissue should be submitted for histopathologic and
cytologic evaluation, aerobic and anaerobic bacterial cultures
and copper quantification when copper toxicosis or chronic
hepatitis is suspected. Specific stains for collagen, lipid, copper,
iron and infectious agents may be required in some cases
(Figure 68-6).
Abnormal concentrations of copper can occur from either a
primary metabolic defect in copper metabolism reported to
occur in certain dog breeds or secondarily as a result of chronic
Figure 68-5. A cytologic specimen obtained by fine-needle aspira-
cholestatic liver disease. Abnormal copper levels damage hepa- tion of the liver from a cat with hepatic lipidosis. Note the lipid-laden
tocytes. Hepatic copper content can be determined using either hepatocytes. (Photograph courtesy Dr. Joseph Taboada, Louisiana
fresh or formalin-fixed liver tissue (Meyer, 1996; Thornburg et State University, Baton Rouge.)
al, 1985). Most laboratories require one gram or less of tissue for
analysis (Center, 1996a; Thornburg et al, 1990, 1996, 1985a).
Normal canine hepatic copper concentrations should be 400
µg/g dry weight (DW) or less. Concentrations ranging from
750 to 2,000 µg/g DW may result from primary or secondary
causes. The disease most likely results from a breed-associated
copper accumulation disorder when hepatic copper concentra-
tions exceed 2,000 µg/g DW. Hepatic copper concentrations
can also be subjectively estimated using a histochemical copper
stain grading system. Copper grading ranges tends to correlate
with quantitative copper analysis (Teske et al, 1992).
Fine-needle aspiration of the liver using special copper stain-
ing correlates with histochemical grading but the extent of liver
pathology cannot be adequately determined (Stockhaus et al,
2004). Genetic markers have been made available for testing
Bedlington terriers (Yuzbasiyan-Gurkan et al, 1997).
Figure 68-6. Photomicrograph of a liver biopsy specimen from a
Common Hepatobiliary Diseases Doberman pinscher with chronic hepatitis. Note the accumulation of
Feline Hepatic Lipidosis copper (arrows) as detected with rubeanic acid stain. In such cases,
Hepatic lipidosis in cats is a well-recognized syndrome charac- the hepatic copper content should be determined by quantitative
methods.
terized by accumulation of excess triglycerides in hepatocytes
with resulting cholestasis and hepatic dysfunction (Figures 68- deficiency, excessive peripheral lipolysis, excessive lipogenesis,
7 and 68-8) (Biourge et al, 1990, 1993; Center et al, 1993; inhibition of lipid oxidation and inhibition of the synthesis and
Cornelius and Jacobs, 1989; Dimski and Taboada, 1995). Lip- secretion of very low-density lipoproteins.The prognosis for this
idosis can occur secondary to diabetes mellitus, diseases result- life-threatening disorder has improved dramatically during the
ing in anorexia and weight loss (such as pancreatitis or inflam- past several years as a result of long-term enteral feeding (i.e.,
matory bowel disease) or as an idiopathic disorder of unknown three to eight weeks or longer) (Biourge et al, 1990, 1994a;
etiology. Cats with idiopathic hepatic lipidosis often present Dimski and Taboada, 1995). Hepatic lipidosis is a reversible
with a history of prolonged anorexia after a stressful event. The process but resolution of hepatic lipidosis secondary to pancre-
biochemical mechanisms responsible for inducing hepatic lipi- atitis, infection or other causes depends on the success of treat-
dosis during fasting are not completely understood (Biourge et ing the underlying disorder (Cornelius and Jacobs, 1989) and
al, 1990, 1994; Center, 1996c). Potential causes include protein providing appropriate nutritional support.