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Human leucocyte antigen (HLA)-typing was studied in 82 hepatitis B carriers and 15 cases of autoimmune hepatitis (AIH) to elucidate the genetic factors which may associated with the etio-pathogenesis of chronic hepatitis in Japan. There were two types of HLA phenotypes: HLA A2 was associated with the progression of the disease induced by HBV infection, and HLA A26 and DR5 were related to the retardation of the disease. A family study confirmed the strong association of these HLA phenotypes with the disease induced by HBV infection. In the analysis of AIH, HLA DR4 is a risk factor related to susceptibility of Japanese AIH which shows different clinical manifestations compared to HLA-DR3-positive AIH, dominantly observed in Western countries. These results suggest that genetic background as expressed by HLA, is an important factor in restricting the development of type B hepatitis and AIH, and can explain racial differences of disease susceptibility.

The mechanism of biliary lipid secretion is still controversial and there is no definite information regarding how bilirubin inhibits biliary phospholipid and cholesterol secretions without affecting bile salt secretion. In this study, the effects of bilirubin on intrahepatic vesicular transport and biliary lipid secretion were examined using bile-fistula rats. Horseradish peroxidase (HRP) was used as a tracer of intrahepatic vesicular transport. Bilirubin (5 mg/100 g BW) and/or HRP (5 mg/100 gBW) were injected through the mesenteric vein. Bile flow, biliary bile acid, biliary phospholipid and cholesterol outputs were examined in saline, HRP and HRP + bilirubin groups, respectively. Bile flow and biliary bile acid output were not affected by bilirubin administration. Biliary phospholipid and cholesterol as well as biliary HRP outputs were inhibited just after bilirubin administration, 42.8 +/- 6.1 SD% 47.7 +/- 5.1 SD%, and 33.4 +/- 3.8 SD%, respectively. These results suggested the participation of intrahepatic vesicular transport system in the inhibition of biliary lipid secretion by bilirubin and in its secretory mechanism.