Since Peden and associates reported the development of hepatic cholestasis and cirrhosis in a premature infant receiving total parenteral nutrition (TPN), the liver damage has been reported bv many authors as the major metabolic complication of XPN in newborn infants. We have experienced cholestasis and abnormal hepatic function in 9 of 17 newborn infants receiving TPN over 1 month. In 6 of the 9 patients, the total bilirubin levels and liver function tests returned to normal after discontinuation of TPN. However the remaining 3 patients receiving TPN more than 6 months died from liver failure. The pathophysiology of the liver disease accompanied by TPN remains obscure. In order to study the mechanism of cholestasis during TPN, we performed immunohistochemical studies using IgA and SC as markers in 4 infants receiving long term TPN. Cholestasis containing IgA and SC limited to the bile canaliculi was seen even when the serum bilirubin levels were still in normal range. Localization of IgA and SC in the bile cananiculi suggested that the cholestasis was responsible for biliary ductal obstruction about the Hering canal. Then the cholestasis developed proximally to the hepatic cells and distally to the bile ductules.
