In dogs, the differentiation between haemolytic and cholestatic
hepatobiliary diseases cannot be achieved by measuring of the unconjugated:conjugated
bilirubin ratio, which is in contrast with generally held clinical concepts. The overlap of the
bilirubin ratios between the two groups of
icterus-generating diseases might in part be explained by deconjugation of conjugated
bilirubin. Enzymatic cleavage by hepatic
beta-glucuronidase might result in higher unconjugated
bilirubin (UCB) fractions in cholestatic disease. The influence of deconjugation of bilirubins by
beta-glucuronidase was investigated in 25 healthy dogs and 35 dogs with spontaneous
hyperbilirubinemia due to either hepatobiliary or haemolytic disease. UCB and its mono- and diconjugates were measured by alkaline methanolysis and HPLC in plasma and liver tissue. The activity of
beta-glucuronidase was also measured in both liver and plasma. In addition, semiquantitative histochemical quantitation of bilirubins in liver tissue was performed. The concentration and the fraction of UCB in plasma of dogs with
hepatobiliary disease were not significantly different from those of dogs with
autoimmune haemolytic anaemia. There was a correlation between the fraction of UCB in liver and plasma of jaundiced dogs (r = 0.42, P less than 0.01) and between the histochemically estimated and the biochemically measured total
bilirubin concentration in liver tissue. There was no correlation between the
beta-glucuronidase activity and either unconjugated or monoconjugated
bilirubin in plasma or liver of diseased animals. The fraction and the concentration of UCB in the liver of dogs with hepatic and with haemolytic disease were identical. It is concluded that
beta-glucuronidase activity is not the significant factor in explaining the similar levels and fractions of UCB in dogs with
hyperbilirubinemia due to either hepatobiliary or haemolytic disease.