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

IV. Laboratory Assessment of Hepatic Function
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TABLE 13-6 Serum y-Glutamyltransferase (GGT) Activity in Animals with Hepatobiliary
Diseases
Species Condition References
Dog Bile duct obstruction; chronic hepatitis Braun et al . (1983)
Lipidosis; necrosis; cirrhosis; neoplasia Hauge and Abdelkader (1984)
Corticoid therapy De Novo and Prasse (1983)
Cat
Bile duct obstruction; cholangiohepatitis;
cirrhosis; lymphosarcoma; necrosis
Center et al . (1986)
Horse Toxic hepatic failure Divers et al . (1983)
Subclinical hepatopathy Yamaoka et al . (1978)
Hyperlipemia Wensing et al . (1973)
Cow Ragwort poisoning; fascioliasis lipidosis Blackshaw (1978)
Fascioliasis metacercariae migrations and
Simesen et al . (1973)
chronicity
Metacercariae migrations Bulgin and Anderson (1984)
Senecio poisoning Johnson and Molyneux (1984)
Sheep
Bile duct obstruction; sporidesmin; toxicity;
Ford and Evans (1985)
fascioliasis
Lupinosis Malherbe et al . (1977)
Cobalt deficiency (white liver disease) Sutherland et al . (1979)
Ketosis Meissonier and Rousseau (1976)
Pig Cysticercus tenuicollis infection Enigk et al . (1976)
Arsanilic acid toxicity Ferslew and Edds (1979)
mobilization ( “ solubilization ” ) of GGT from its membrane
anchor related to elevated levels of bile salts ( Center,
2007 ).
Highest tissue levels of GGT in the dog and cat are
present in the kidney and pancreas with lesser amounts in
the liver, gallbladder, intestines, spleen, heart, lungs, skeletal
muscle, and erythrocytes (Badylak et al., 1982; Braun
et al., 1983 ; Guelfi et al., 1982 ). The activity of GGT in
serum is derived primarily from the liver although, as
stated previously, there is considerable species variation in
GGT activity within this organ. Hepatic localization has
been demonstrated in the canaliculus, in bile ducts, and in
Zone 1 hepatocytes ( Aronsen et al., 1968 ; Braun et al.,
1983 ; Center, 2005) .
The diagnostic value of GGT has been assessed in clinical
patients with and without liver disease ( Center et al.,
1986, 1992 ; Guelfi et al., 1982 ). Experimental studies in
dogs and cats undergoing acute, severe diffuse necrosis
have shown either no change in serum GGT or only mild
increases in activity (1- to 3-fold normal) that resolve over
the ensuing 10 days. In the dog, extrahepatic bile duct
obstruction causes serum GGT activity to increase 1- to
4-fold within 4 days, and 10- to 50-fold within 1 to 2
weeks. Thereafter, values may plateau or continue to
increase as high as 100-fold that of normal ( Guelfi et al.,
1982 ; Kokot et al., 1965 ; Noonan and Meyer, 1979 ). In
the cat with extrahepatic bile duct obstruction, serum GGT
activity may increase up to 2-fold within 3 days, 2- to 6-
fold within 5 days, and 4- to 16-fold that of normal within
2 weeks ( Meyer, 1983 ; Spano et al., 1983 ).
Glucocorticoids and certain other microsomal enzyme
inducers may stimulate production of GGT in the dog
similar to the influence of such drugs or other xenobiotics
on AP. Administration of dexamethasone (3mg/kg SID)
or prednisone (4.4 mg/kg SID IM) increased GGT activity
within 1 week 4- to 7-fold and up to 10-fold within 2 weeks
( Badylak and Van Vleet, 1981, 1982 ; Stein et al., 1989 ). It
is assumed that the increased production of GGT following
glucocorticoid administration originates in the liver. In
comparison to glucocorticoid induction, dogs treated with
the anticonvulsants phenytoin or primidone develop only
modest increases in serum GGT activity up to 2- or 3-fold
that of normal unless they develop serious anticonvulsant
hepatotoxicosis ( Bunch et al., 1985, 1987 ) .
Some cats with advanced necroinflammatory liver disease,
major bile duct obstruction, or intrahepatic cholestasis
develop relatively greater increases in GGT than in AP
activity ( Center et al., 1986 ). In other species, cholestasis is
known to enhance enzyme synthesis as well as membrane
release of GGT. It remains undetermined whether glucocorticoids
or other enzyme inducers increase the expression
of GGT in cats. It is noteworthy that the normal range
for feline serum GGT activity is narrower and lower than
that of the dog, so the interpretation of feline GGT activity