Page 905 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
P. 905

880                                        CHAPTER 5



  VetBooks.ir  relate to the remaining effective functional cellular   concentrations of  liver enzymes  may be associ-
                                                          ated with a poorer prognosis, this association is not
           mass, rather than to those cells that have been dam-
           aged. Thus, serum enzymes generally offer an indi-
                                                          centrations and perhaps, more consistently, with cer-
           cation of ongoing hepatic insult whereas functional   strong. It may only apply to markedly increased con-
           indicators reflect the impact that the hepatic damage   tain enzymes such as GGT and ALP, rather than
           has had.                                       GLDH and AST. There may be additional useful
             The potential restriction or diversity of tissue   differential information in the pattern of enzyme
           sources of serum enzymes clearly impacts greatly   abnormalities, in that GGT and ALP are generally
           on diagnostic usefulness. Enzymes such as aspar-  regarded as reflecting damage primarily to the biliary
           tate aminotransferase (AST) and lactate dehydroge-  epithelium, whereas enzymes such as GLDH, SDH,
           nase (LDH) may come from multiple tissue types,   LDH and AST are generally regarded as reflecting
           although liver and muscle appear to be the main   parenchymal hepatocellular damage.  Liver disease
           origin of increased serum concentrations. Although   in horses will almost invariably be associated with
           glutamate dehydrogenase (GLDH) and sorbitol    insult to both the hepatocellular and biliary popula-
           dehydrogenase (SDH) are widely regarded as liver   tions, but where there are clearly disproportionate
           specific, this assumption lacks an evidence basis in   effects on the two enzyme groups then diagnostic
           horses and other tissues such as the gastrointesti-  inferences can be made.
           nal (GI) tract appear to be the source of increases   A common clinical dilemma facing equine prac-
           in serum concentrations in some cases. The liver is   titioners  is  when  serum  biochemical  indicators of
           also widely regarded as the specific source of high   liver disease are found in apparently healthy horses.
           serum gamma-glutamyltransferase (GGT) concen-  Under  such  circumstances  there  are  two  possible
           trations, although it is also accepted that rare cases   fundamental explanations: firstly, the laboratory
           of pancreatic disease might contribute high serum   results are correct and the horse does indeed have
           GGT levels. Renal tubules are also known to be a   liver disease, but that it is subclinical; and secondly,
           rich source of GGT, alkaline phosphatase (ALP) and   the laboratory results incorrectly imply hepatic
           GLDH, although damage to such cells is assumed   disease and the horse is either healthy or has non-
           to result in enzyme appearance in urine rather than   hepatic  disease. As previously mentioned, subclinical
           serum. There is a widely-recognised association   liver disease is not a surprising or unusual concept,
           between mild to moderately increased liver enzymes   given the large reserve capacity of the liver and this
           and primary GI diseases such as colon impaction,   is certainly a common and plausible explanation for
           colon displacement and gastric ulceration. Clinical   apparently healthy horses to have increased serum
           experiences support these observations, although   concentrations of liver-derived enzymes. On the
           it is unclear whether this might reflect primary GI   other hand, given that reference intervals are gen-
           sources of such enzymes, or whether a primary GI   erally calculated to include approximately 95%
           disease may secondarily cause hepatic insults via   of a normal population, it should be expected that
           physical pressure, or via injurious GI-derived sub-  around 2.5% (1 in 40) of normal horses will show a
           stances carried to the liver via the hepatic portal vein.   value greater than the reference interval when a sin-
             Although there is no disputing the diagnostic   gle analyte is measured, with about 10% of normal
           value of liver-derived enzymes in the evaluation of   horses  demonstrating  at  least  one  increased  value
           suspected hepatic insult, it is important to remem-  out of  a panel of four serum enzymes. However,
           ber that no enzyme is entirely specific for liver dis-  this statistical certainty can only be used to explain
           ease, nor will it be found to be abnormal in every   mild increases above the reference interval, as more
           case of liver disease. Thus, such enzymes are useful   marked increases will be extremely uncommon
           alongside other diagnostic data to raise the suspicion   in entirely normal horses. When higher values of
           of liver disease in an individual horse, or group of   serum enzymes (e.g. greater than 3 or 4 standard
           horses, but clinicians should be constantly aware of   deviations above the mean) are found in horses with
           their diagnostic limitations. Although high serum   no corroborative evidence of hepatic disease found in
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