Liver disease in the horse: clinical signs and diagnostic aids - DVM
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Liver disease in the horse: clinical signs and diagnostic aids


Diarrhea and hemostasis

Photo 3: Grossly brown-green discolored urine from increased conjugated bilirubin in a horse with obstructive cholelithiasis.
Diarrhea may infrequently accompany chronic hepatic insufficiency in horses. Alterations in the intestinal microflora, portal hypertension and deficiency of bile acids may be involved in the pathogenesis.

Because the liver is responsible for the synthesis of numerous factors involved in coagulation, abnormal hemostasis may be a sequela to hepatic insufficiency. Clinical signs may vary from ecchymotic hemorrhages, to hemorrhage after trauma or venipuncture, to spontaneous hemorrhage (Photo 2).

Especially sensitive to hepatic disease is the synthesis of fibrinogen and the vitamin K-dependent factors (II, VII, IX, X), which have relatively short half-lives.

Although not common, a fever may be present in horses with hepatic abscesses, acute hepatitis, chronic active hepatitis, obstructive cholelithiasis, fatty liver failure or neoplasia.

Intravascular hemolysis is a rarely seen, but grave prognostic indicator of fulminate hepatic failure in horses. The exact cause of hemolysis is not known, but is believed to be the result of increased erythrocyte fragility.

Hypoalbuminemia and water retention can occur with chronic liver failure and may result in dependent edema. Because the half-life of albumin is relatively long in the horse, edema is a rare clinical sign. Dependent abdominal edema may form if there is significant portal hypertension and ascites.

The Kupffer cell plays an important role in removing bacterial endotoxin that is normally absorbed from the lumen of the intestinal tract and carried to the liver via the portal circulation. Failure of Kupffer-cell phagocytosis of endotoxin may result in clinical and laboratory evidence of endotoxemia.

Laboratory findings of hepatic insufficiency

Because massive hepatic disease must be present before alterations are seen with some laboratory tests, and because different liver functions are variably altered by disease, the laboratory diagnosis of hepatic disease can be challenging.

The most useful diagnostic tests for evaluation of hepatic disease in horses are quantitation of sorbitol dehydrogenase (SDH) and gamma-glutamyl transpeptidase or -transferase (GGT) activity and serum bile acids concentration (SBA).

In the face of clinically significant liver disease, at least one of the three former serum tests typically is abnormal. Although increases in SDH, GGT and SBA are highly specific for liver disease, they are not specific for the type of disease.

Sorbitol dehydrogenase (SDH) has been widely used in the evaluation of acute liver disease in horses. The short half-life of this liver cytosolic enzyme makes it ideal for the evaluation of acute ongoing disease, as values usually return to baseline within three to five days after a transient hepatic insult. Its short half-life necessitates analysis within hours of collection.

Although mild variations exist between laboratories, the normal blood activity SDH in horses is usually less than 8 units/L. Gamma-glutamyl transpeptidase or transferase (GGT) is primarily associated with microsomal membranes in the biliary epithelium. Production and release of GGT is induced by cholestasis.

Some clinicians consider GGT the test of highest sensitivity in evaluating horses for liver disease. The half-life of GGT is about three days, and it is stable two days in serum at room temperature.

Mild increases may be seen following acute hepatocellular necrosis and may continue to rise for one to two weeks despite improvement in clinical signs. Increases are more persistent in chronic disease, especially with cholestasis. Normal values for GGT in adult horses typically are less than 30 units/L, but may be two to three times greater in healthy donkeys, burros and asses.

The normal liver removes greater than 90 percent of bile acids from the enterohepatic circulation. Thus, the blood concentration of bile acids may be increased with liver disease and quantitation provides an excellent screen of liver function.

The concentration of total serum bile acids is not affected significantly by fasting or eating, so only a single blood sample is needed. Increased serum bile acid concentrations are highly specific for the presence of liver disease (may increase within 24 to 48 hours after the onset of hepatic disease), but are not specific for the type of liver disease.

A value less than 20 micromolel/L appears to be a good predictor in ruling out significant functional liver disease and should be included in the evaluation of horses suspected to have hepatic disease. Bile acid concentrations are highest in biliary obstructive diseases and portosystemic shunts.


Source: DVM360 MAGAZINE,
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