A Genetic Study of Neonatal Obstructive Jaundice.

Clarification of the problem of jaundice in the neonatal period began with the discovery of foetomaternal rhesus incompatibility as the usual cause of haemolytic disease of the newborn. After this, the group of infants in whom the jaundice is of obstructive type, with pale stools and bile in the urine, received more attention, and it was soon realized that not all such infants suffered from atresia of the main bile-ducts. In 1952 Craig and Landing described the characteristic histological appearance of the liver in cases with patent bileducts, and the disease has become known as 'neonatal giant cell hepatitis'. Since then various authors have accepted the separation of this disease entity on anatomical and histological grounds, while others have felt that the histological features may be mimicked by other diseases affecting the liver in the foetal or newborn period, of varied causes such as rhesus incompatibility, cytomegalic inclusion cell virus, pyaemic infection or pylephlebitis. It is certainly true that giant cell change may be seen in many of these conditions or in biliary atresia, but consideration of other histological features seems to allow the definition of a group of cases apart from these causes. Biliary atresia may affect any level in the biliary tree, and one newly recognized form involving only the small interlobular radicles exhibits a characteristic clinical course and histological pattern-intrahepatic biliary atresia. Craig and Landing, and most workers since them, have assumed that 'neonatal hepatitis' is due to the infection of the foetus in utero by the virus of infectious hepatitis or of serum hepatitis. Over the years the emphasis has been on the latter virus as the more likely causative agent, and a maternal carrier state has been considered a satisfactory explanation of the often observed occurrence of