Indirect hyperbilirubinemia in HBV carriers.
Indirect hyperbilirubinemia without any other abnormalities of liver function tests was seen in 14.3% in HBV carriers and 1.2% in controls in the previous study. In order to clarify the mechanism of hyperbilirubinemia in HBV carriers, 33 HBV carriers with normal liver functions regardless of hyperbilirubinemia and with no past history of acute hepatitis were investigated clinically. Most of HBV carriers with indirect hyperbilirubinemia revealed any other abnormalities of liver functions during the over 2 years observation. Histological examinations of 4 HBV carriers with hyperbilirubinemia presented no evidence of obvious hepatitis. There was no significant correlation between bilirubin, ICG and/or BSP clearance in HBV carriers with hyperbilirubinemia. The above mentioned facts suggest that indirect hyperbilirubinemia in HBV carriers was not caused by organic changes of hepatocytes but might be the results of, at least in part, its functional disturbances. Family studies of HBV carriers with hyperbilirubinemia suggested that some but not all the HBV carriers with indirect hyperbilirubinemia might not have a genetic background in common with patients with Gilbert's syndrome. The persistent infection of HBV in hepatocytes might play an important role of metabolic derangement of bilirubin and make a constitutional defect of bilirubin metabolism manifest.
D001663:Bilirubin / Q000097:blood; D002353:Carrier State / Q000097:blood; D006509:Hepatitis B / Q000097:blood / Q000150:complications* / Q000235:genetics; D006514:Hepatitis B Surface Antigens / Q000032:analysis; D006801:Humans; D006932:Hyperbilirubinemia / Q000150:complications*; D007208:Indocyanine Green; D009539:Nicotinic Acids; D013448:Sulfobromophthalein
D006514:Hepatitis B Surface Antigens; D009539:Nicotinic Acids; D013448:Sulfobromophthalein; D007208:Indocyanine Green; D001663:Bilirubin