ABSTRACT
The liver is capable of transporting IgA from the plasma to bile in several experimental animals. After bile duct ligation, SIgA and free secretory component accumulate in the serum of these animals. In the present study, SIgA was found in the serum of all infants with extrahepatic biliary obstruction, and in 75% of those with intrahepatic cholestasis, but in only one of seven age-matched infants without hepatobiliary disease. Infants with EHBO had significantly higher serum levels of secretory IgA and total IgA than in normal infants or patients with IHC. This result suggests that the human liver is involved in SIgA metabolism and that the elevated serum IgA levels in infants with liver disease are caused by bile duct obstruction or proliferation. Quantitation of SIgA in serum may help to differentiate major categories of obstructive jaundice in infancy. The concentration of SIgA in serum was indicative of the site of obstruction in 12 of 19 infants with hepatobiliary disease.