A M Casali1, G Carbone, G Cavalli. 1. Institute of Histology and General Embryology, University of Genova, Italy.
Abstract
AIMS: Intrahepatic bile duct volume density has been evaluated in four cases of primary sclerosing cholangitis (PSC) by applying a semiautomatic image analysis system to histological sections of surgical biopsies. Comparison was made between normal livers and cases of primary biliary cirrhosis. METHODS AND RESULTS: A marked decrease in both bile duct volume density in liver (up to 50% of normal value) and bile duct volume density in portal tracts (up to 21% of normal value) was found. The analysis of correlations between the portal tract size and the portal tract volume fraction constituted by bile ducts confirms that the destruction mainly affects small and medium-sized ducts. The ratio of bile duct to arterial component volume fractions in portal tracts turned out to be inverted with respect to that determined in normal liver, showing a decrease of up to 30% of normal value. CONCLUSIONS: The features observed in primary sclerosing cholangitis, as well as the extent of bile duct loss proved to be quite similar to what we had previously described in primary biliary cirrhosis. Thus, regardless of the causes and mechanisms leading to the bile duct loss, the quantification of ductopenia produced results which are alike for the two distinct cholestatic diseases.
AIMS: Intrahepatic bile duct volume density has been evaluated in four cases of primary sclerosing cholangitis (PSC) by applying a semiautomatic image analysis system to histological sections of surgical biopsies. Comparison was made between normal livers and cases of primary biliary cirrhosis. METHODS AND RESULTS: A marked decrease in both bile duct volume density in liver (up to 50% of normal value) and bile duct volume density in portal tracts (up to 21% of normal value) was found. The analysis of correlations between the portal tract size and the portal tract volume fraction constituted by bile ducts confirms that the destruction mainly affects small and medium-sized ducts. The ratio of bile duct to arterial component volume fractions in portal tracts turned out to be inverted with respect to that determined in normal liver, showing a decrease of up to 30% of normal value. CONCLUSIONS: The features observed in primary sclerosing cholangitis, as well as the extent of bile duct loss proved to be quite similar to what we had previously described in primary biliary cirrhosis. Thus, regardless of the causes and mechanisms leading to the bile duct loss, the quantification of ductopenia produced results which are alike for the two distinct cholestatic diseases.