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


Other cytosolic liver enzymes include aspartate aminotransferase (AST), alkaline phosphatase (ALP), lactate dehydrogenase (LD) and alanine aminotransferase (ALT). These enzymes also are found with high activity in other tissues, or are inducible. Thus, increases in these enzymes are not specific for liver disease in horses. Because some of these enzymes are frequently reported in equine biochemical profiles, they may serve as a crude indicator of liver disease; however, the limitations of their usefulness must be recognized.

Other nonspecific tests

Additional nonspecific tests of liver disease in the horse include quantitation of bilirubin, albumin, globulins, ammonia, BUN, coagulation proteins, glucose and esterified triglycerides.

Serum bilirubin concentration is not a sensitive indicator of liver disease in horses, as hemolysis, anorexia and the administration of certain drugs will increase the unconjugated bilirubin concentration.

An increase in the conjugated bilirubin fraction is more reliably indicative of hepatic disease in horses than is the unconjugated bilirubin concentration. When the conjugated bilirubin concentration is greater than 25 percent of the total bilirubin value, hepatocellular disease should be suspected. If the conjugated bilirubin concentration is greater than 30 percent of the total value, cholestasis should be suspected.

In normal horses, the total bilirubin concentration is in the range of 0.2 to 5.0 mg/dL, with conjugated bilirubin in the range of 0 to 0.4 mg/dL. Conjugated bilirubin is water-soluble and detectable in the urine of horses only if blood concentrations become sufficiently increased to surpass the renal threshold (Photo 3); thus when urine tests positive for the presence of bilirubin, cholestatic disease should be suspected.

The half-life of albumin in horses is relatively long (19-20 days), thus a decrease in the albumin concentration is rarely detectable until greater than 80 percent of the liver mass is lost for more than three weeks.

The globulin fraction often is increased in chronic hepatic disease as a result of decreased Kupffer-cell mass and thus wider dissemination of enteric-derived foreign antigens.

Plasma cells respond to the general increased antigen load, resulting in polyclonal gammopathy.

Because the liver primarily is responsible for removing ammonia from circulation and converting it to urea for renal excretion, increases in the blood ammonia concentration or a decrease in the blood urea nitrogen (BUN) concentration (<9 mg/dL) may be indicative of chronic hepatocellular disease. Normal values for ammonia vary among laboratories, but have been reported in the range of 13 to 108 microgram/dL.

Because the liver also is responsible for the synthesis of coagulation factors, evaluation of hemostatic function may be useful, especially if one is considering a liver biopsy.

The vitamin K–dependent factor with the shortest half-life is factor VII. Thus, abnormalities are frequently first observed in the prothrombin time (PT). However, adequate evaluation of hemostatic function necessitates determination of the activated partial thromboplastin time (APTT), the fibrinogen and fibrin degradation products (FDP) concentrations and a platelet count. Typically, a 50 percent to 70 percent decrease in the blood concentration of the coagulation factors is necessary before a change in these clotting time-based assays is detectable.

Changes in the blood-glucose concentration are rarely seen in horses with liver insufficiency. Hyperglycemia may be seen with stress-associated catecholamine and glucocorticoid release. Hypoglycemia (glucose <60 mg/dL) may occur in acute massive hepatic failure, but is more likely in chronic liver disease as anorexia progresses, glycogen stores are depleted and gluconeogenesis and glycolysis are impaired by increased glucagon concentrations.

The concentration of blood triglycerides may become increased during hepatic insufficiency as a result of increased mobilization from adipose tissue to support energy-requiring processes, coupled with decreased clearance by the liver.

The second article on this topic will address differential diagnosis and treatment of liver disease in horses.

Michelle Henry Barton is the Josiah Meigs Distinguished Teaching Professor at the University of Georgia's College of Veterinary Medicine, where she is a large-animal internist in academic practice. She received her DVM from the University of Illinois in 1985, her PhD in physiology at the University of Georgia in 1990 and became an ACVIM diplomate in 1990.


Source: DVM360 MAGAZINE,
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