Abstract

Changes in serum enzyme activity are routinely used in domestic animal medicine for diagnosis management and prognosis of liver disease.^7,8,9 The liver is the largest gland in the body and performs a multiplicity of functions essential for life.^3,5,10 Hepatocellular damage leads to elevated enzyme release into the circulation. Hepatocellular damage can range from total irreversible cell necrosis to mild reversible alterations.^1,6 Liver disease is usually associated with nonspecific clinical signs,^7,8 which make specific diagnostic tests even more important. Utility of serum enzyme activity for diagnosis of tissue damage is influenced by organ specificity, cellular location, rate of removal from the plasma and the type, severity and duration of the injury or stimulus,^2,7 and may be species specific.⁷

In most terrestrial mammals sorbitol dehydrogenase (SDH) is located primarily in the liver, and serum levels are elevated following acute hepatic insult. The hepatic activity of SDH in most marine mammals is unknown, but elevation may be diagnostically valuable.⁴ Fauquier et al. reported that serum SDH is expected to be the most specific and sensitive indicator of hepatocellular damage in California sea lions (Zalophus californianus), northern elephant seals (Mirounga angustirostris) and harbor seals (Phoca vitulina).⁷

The purpose of this study was to compare SDH to other parameters as possible predictors of hepatocellular damage in California sea lions (n=114), northern elephant seals (n=51) and harbor seals (n=82). The parameters evaluated were SDH, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALK), gamma-glutamyltransferase (GGT), total bilirubin, albumin and globulin. Data were compiled from retrospective analyses of clinical records from stranded animals admitted to The Marine Mammal Center (TMMC) in Sausalito, California. Serum chemistry analyses had been performed at TMMC using an automated chemistry analyzer (Alfa Wasserman). Histopathology was performed by several pathologists, but scoring of liver damage was determined by one veterinarian (FG). The degree of hepatocellular damage was categorized as none, mild, or severe based on the histopathology report. Logistic regressions were performed, and R. Akaike's information criterion (AIC) was used for model selection.

In harbor seals, none of the blood parameters were associated with degree of liver damage. SDH, however, was significantly different in cases with severe versus mild liver damage. In elephant seals, GGT was associated with hepatocellular damage. In California sea lions, the combination of GGT, AST, and albumin was associated with hepatocellular damage, while GGT alone was predictive of severe versus mild liver damage. In sea lions, SDH was not associated with liver damage.

Harbor seals and elephant seals, but not California sea lions, had a significant correlation amongst SDH, ALT and AST. Thus, diagnosis of liver disease in these three pinniped species is dependent on use of a panel of liver enzymes.

Acknowledgements

Thanks to staff and volunteers of The Marine Mammal Center for care for the seals and sea lions. Special thanks to the Vet Science department for the opportunity to do this research, for their support and the knowledge they shared.

References

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