Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

IV. Laboratory Assessment of Hepatic Function
397
FIGURE 13-4 Formation, excretion, and enterohepatic circulation of
bilirubin and other bile pigments associated with overproduction of bilirubin
as a result of hemolysis.
by intestinal bacteria is remarkably reduced, and the test
for urinary urobilinogen is characteristically negative in
complete extrahepatic obstruction ( Fig. 13-6 ). The therapeutic
administration of oral, broad-spectrum antibiotics to
patients may diminish the metabolic activity of intestinal
bacteria and result in a spuriously negative test for urobilinogen
in the urine in the absence of cholestasis.
The biochemical differentiation between unconjugated
and conjugated hyperbilirubinemia using the van den
Bergh reaction can be useful in the assessment of prehepatic
or posthepatic causes of hyperbilirubinemia. In severe
primary hepatitic diseases of varying cause, the excretory
steps of uptake, conjugation, and excretion all may be
deranged and result in elevations of both conjugated and
unconjugated pigment.
Important species characteristics should be considered
when interpreting results of the van den Bergh reaction.
In general, the interpretation in dogs and cats is similar.
Typically, in cholestatic disease, the conjugated fraction
is elevated, representing 50% to 75% of the total serum
bilirubin ( Fig. 13-7 ). The normal horse has a much higher
total serum bilirubin than any of the other domestic species
( Fig. 13-8 ), and values as high as 4.0 mg/dl or higher have
been observed in otherwise healthy individuals. In addition
to hepatic and hemolytic diseases, hyperbilirubinemia
is observed in horses with intestinal obstruction and in a
variety of other serious systemic diseases. Food restriction
alone causes an abrupt increase in the unconjugated serum
bilirubin of the horse ( Gronwall and Mia, 1972 ; Tennant
et al., 1975 ), and decreased bile flow is a probable factor
of the hyperbilirubinemia observed in fasting horses
( Fig. 13-9 ).
In cattle and sheep, hyperbilirubinemia of sufficient
magnitude to produce clinical icterus ( 3 mg/dl) is caused
FIGURE 13-5 Formation, excretion, and enterohepatic circulation of
bilirubin and other bile pigments associated with hepatocellular injury
and intrahepatic cholestasis.
FIGURE 13-6 Formation, excretion, and enterohepatic circulation of
bilirubin and other bile pigments in extrahepatic bile duct obstruction.
most frequently by hemolytic disease. Biochemical hyperbilirubinemia
(1 to 2 mg/dl) without clinical icterus may be
observed in sheep and in cattle with fatty liver associated
with ketosis/acetonemia, and in such cases, the predominant
pigment is unconjugated bilirubin. Greater elevations
in serum bilirubin and clinical icterus in ruminants associated
with fatty liver and ketosis are unusual. Mild to
moderate conjugated hyperbilirubinemia has been observed
in sheep with sclerosing cholangitis caused by Fasciola
hepatica infestation ( Hjerpe et al., 1971 ) and in cattle with
hepatic cirrhosis ( Finn and Tennant, 1974 ).