Although these are expected findings for the various types of hepatobiliary disease, they are not diagnostic for the condition. CBC and urinalysis findings can also be very helpful. However, ancillary tests such as imaging studies and biopsy/histopathology are often required to make a definitive diagnosis.

Hepatic trauma

A single physical insult to the liver, as with a vehicle accident, would result in increased activities of leakage enzymes (ALT, AST, SDH, GLDH – varying with the species as described earlier). Since muscle trauma may also occur under these circumstances, the serum activity of a liver-specific enzyme (e.g. GLDH or SDH), could be measured to differentiate the two. If significant blood loss occurred as well, hypoxia could be responsible for release of these enzymes into the circulation. A similar mechanism occurs with acute anemia from other causes, so that marked elevations in hepatic enzyme activities do not necessarily indicate primary hepatic disease.

Hepatitis

Hepatitis is associated with hepatocellular injury. Therefore, the leakage enzymes would be expected to have increased serum activities. Cholestatic enzymes could also be affected, but generally to a lesser degree.

Cholangiohepatitis

In addition to increased serum activities of enzymes indicating hepatocellular injury, indicators of cholestasis will be present with cholangiohepatitis. These could include (depending on the species): ALP, GGT, bilirubin, bile acids.

Biliary tract obstruction/cholestasis

Depending on the cause of the biliary stasis, serum activities of the leakage enzymes may or may not be concurrently elevated along with the indicators of cholestasis. For example, diseases such as hepatic lipidosis in cats result in significant canalicular cholestasis, but may also be associated with hepatocellular damage and release of the leakage enzymes. Changes in the indicators of cholestasis may be dramatic, in the face of only mild changes in the indicators of hepatocellular damage. In those species where ALP activity is a useful measurement, ALP and GGT activities usually change to a similar degree. Hepatic lipidosis in cats is an exception in that ALP activity is usually more dramatically increased than is GGT activity.

Portosystemic shunt (PSS)

PSSs can be either congenital or acquired. Congenital shunts are typically associated with no to mild increases in the activities of leakage and cholestatic enzymes. Increased ALP activity may occur due to the bone-source ALP in young, growing animals with congenital shunts. Typically, indicators of hepatic function will be abnormal. These may include decreases in serum urea, glucose, cholesterol, and protein (particularly albumin). Although baseline bile acids or ammonia may be within RI, postprandial bile acids or ammonia tolerance test results will be abnormal. Animals with congenital shunts do not generally have edema, ascites, or icterus.

Animals with acquired PSSs have usually had significant chronic hepatobiliary disease which led to development of the shunt. The hepatic disease results in loss of normal architecture due to prior or ongoing necrosis, fibrosis, and nodular regeneration (in total, cirrhosis). In addition to abnormal hepatic function, these animals may have increased activities of leakage and cholestatic enzymes, and hyperbilirubinemia. Albumin synthesis may be sufficiently impaired to result in edema and ascites, or milder hypoalbuminemia coupled with portal and lymphatic hypertension may lead to ascites.

Hepatic failure

Hepatic failure can be the result of chronic hepatobiliary disease leading to cirrhosis, as discussed above. Acute diffuse hepatic necrosis, as with toxic or infectious causes, will cause acute hepatic failure. Enzymes indicating hepatocellular injury and cholestasis would be expected to have increased serum activities in acute hepatic failure. Indicators of hepatic function would also be abnormal, though results could be variable depending on the time of testing relative to the insult. For example, the animal may die from acute liver failure before the cessation of albumin synthesis by the liver is reflected in a decreased serum albumin concentration.

Focal hepatic lesions

Focal hepatic necrosis, abscess, or other localized hepatic lesion produces variable results. Indicators of hepatocellular injury may be elevated, but significant hepatic dysfunction or cholestasis would be unlikely. However, an abscess or other space occupying lesion, if compressing the biliary tract, could result in significant increases in cholestatic enzyme activities.

Glucocorticoid hepatopathy

Many drugs induce ALP in dogs. Glucocorticoids initially induce the hepatic isoform of ALP, followed by the corticosteroid isoform. Increased concentrations of endogenous corticosteroids, from hyperadrenocorticism or stress/illness of sufficient magnitude, will also induce ALP. Although ALP activity increases to the greatest degree under the influence of excess corticosteroid, GGT and ALT activities are also increased. Induction of these enzymes may occur; however, leakage due to vacuolar changes and glycogen accumulation is most likely responsible for ALT release. Similarly, hepatocyte swelling associated with glycogen accumulation could contribute to canalicular cholestasis. Serum bilirubin is not usually increased, and indicators of hepatic function are generally unaffected. In addition to glucocorticoids, other drugs can also cause elevated hepatic enzymes. The most common of these are anticonvulsants. Idiosyncratic reactions to a variety of drugs can occur and hepatocyte damage may result, sometimes leading to hepatic failure. Regular monitoring of hepatic enzyme activities and function tests is recommended in animals receiving drugs with potential hepatic side-effects.