Intrahepatic cholestasis is known as uncontrollable and sometimes fatal complication often seen infants receiving TPN from neonatal period. Though many etilogical concepts on this disorder have been proposed, the details of its mechanism remain obscure. Seven infants receiving TPN for 17 days to 2 yrs 4 mos from neonatal period were subjected to the present study and pathophysiological investigation of the cholestasis was carried out by immunoelectron-microscopic localization of IgA, SC (markers derived from biliary epithelia) and C_3, C_4 (markers derived from hepatic cells) in the liver. Consequently, cholestasis containing IgA and SC began from at the level of bile canaliculi, which suggested that initial site of biliary obstruction located at the canals of Hering or their a little distal bile ductules. Then, as hepatic cells and biliary epithelia received more damage, cholestasis developed proximally to the hepatic cells and distally to the interlobular bile ducts. Every cholestasis contained IgA, SC as well as C_3, C_4. Positive staining of C_3, C_4 in the bile suggested that the complements were transferred from hepatic cells into bile canaliculi. In conclusion, the present study using IgA, SC and C_3, C_4 as markers derived from biliary epithelia and hepatic cells respectively, revealed more clearly the mechanism and process of intrahepatic cholestatic disease associated with TPN. Immunological analysis of the results obtained from this study should be achieved in the future.
