Abstract
Hepatocellular and hepatobiliary damage was assessed in equine acute, subacute and chronic grass sickness cases (AGS, SAGS, CGS). Histopathological analysis showed that even in some early AGS cases enlarged hepatocytes, hepatocyte vacuolation indicative of lipid accumulation (steatosis), intrahepatocyte, canalicular and periportal deposition of pigments, frequent leucocyte infiltration and cholangitis occurred. Analysis of serum indicated significantly increased levels of unconjugated bilirubin in all groups and conjugated bilirubin in AGS and SAGS groups, increased levels of bile acids in some individuals from each group and significantly increased levels of glutamate dehydrogenase (GLDH) in AGS and SAGS cases. Conjugated bilirubin was significantly elevated in urine of AGS and SAGS cases. The evidence suggests that abnormal liver function involving moderate hepatocellular pathology in conjunction with steatosis and cholestasis may contribute to the pathogenesis of GS.
Published Version
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