Page 1113 - Small Animal Clinical Nutrition 5th Edition

Hepatobiliary Disease 1159

bodies (cats) and microcytosis are erythrocytic abnormalities
VetBooks.ir seen in animals with liver disease (Center, 1995, 1996e; Dial,
1995). Erythrocyte microcytosis is associated with acquired
and congenital portosystemic vascular shunts in dogs.
Measurement of plasma enzyme activities (usually but not
entirely correctly called “liver enzymes”) is based on the concept
that certain enzymes are released and enter the bloodstream
when changes occur in the liver or bile ducts.The most impor-
tant enzymes for dogs and cats are discussed below.

Alkaline Phosphatase
Alkaline phosphatase (AP) is found in almost all organs but
primarily in bone, liver, kidney, small bowel mucosa, placenta
and bile duct epithelium. The plasma half-life of intestinal,
renal and placental AP is only a few minutes; their contribution
to total serum AP is negligible. In dogs, measurable serum AP
arises from bone, liver or corticosteroid induction.
The half-life of AP from liver and bone in dogs is about 70
hours. Bone AP increases from osteoblastic activity in young
growing dogs or occasionally from osteoblastic bone tumors.
AP increases from cholestatic disorders resulting in induction
of a liver AP and subsequent enzyme solublization and elu-
tion from damaged membranes into the blood (Gary and Figure 68-3. A miniature schnauzer with head pressing due to hepat-
ic encephalopathy as a result of chronic hepatitis and cirrhosis.
Twedt, 2009). Abnormal bile acid concentrations may play a
role in AP production and release. Thus,
significant extrahepatic cholestasis usually
causes very high plasma AP activity.
Finally, in dogs but not cats, corticos-
teroids, either endogenous or exogenous,
can induce specific corticosteroid AP
isoenzyme produced in the liver, leading
to higher AP activity. The corticosteroid
fraction of AP can be determined by heat-
ing plasma to 65°C (149°F) for two min-
utes, which inactivates AP of liver and
bone origin, but not that induced by cor-
ticosteroids. Clinically determining the
percent fraction arising from corticos-
teroids is generally not helpful in deter-
mining hyperadrenocorticism from other
diseases.
In cats, AP is of less diagnostic impor- Figure 68-4. Algorithm for the diagnosis of hepatobiliary disease. (Adapted from Rothuizen
tance because the half-life is very short (i.e., J, Meyer HP . History, physical examination, and signs of liver disease. In: Ettinger SJ,
5.8 hours); thus, it is only elevated in severe Feldman EC, eds. Textbook of Veterinary Internal Medicine: Diseases of the Dog and Cat,
5th ed. Philadelphia, PA: WB Saunders Co, 2000; 1272-1277.)
hepatobiliary diseases. In addition, feline
*Alkaline phosphatase, alanine aminotransferase, bile acids, ammonia.
hepatic AP concentrations are low; there-
fore, the sensitivity of AP in detecting feline liver disease is low. ally have higher GGT concentrations than AP. GGT concen-
The highest concentrations of plasma AP in cats often occurs trations are usually only mildly elevated in feline idiopathic
with hepatic lipidosis. hepatic lipidosis (Center et al, 1986).

Gamma Glutamyl Transferase Alanine Aminotransferase and Aspartate
Hepatic γ-glutamyl transferase (GGT) is associated with hepa- Aminotransferase
tocyte canalicular membranes and bile ducts. Highest concen- Alanine aminotransferase (ALT) and aspartate aminotrans-
trations generally are associated with disease of biliary epithe- ferase (AST) were known in the older nomenclature as GPT
lium such as bile duct obstructions or cholangitis. Cats with and GOT, respectively.They are often collectively referred to as
cholangitis, biliary tract disease or hepatobiliary disease gener- “hepatic leakage” enzymes. ALT is very liver-specific in dogs