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机构地区:[1]Department of Medicine,University of Connecticut Health Center,Farmington,CT,USA [2]Department of Medicine,Division of Gastroenterology-Hepatology,University of Connecticut Health Center,Farmington,CT,USA
出 处:《Journal of Clinical and Translational Hepatology》2024年第12期985-987,F0003,共4页临床与转化肝病杂志(英文版)
摘 要:Introduction Serum direct bilirubin levels,consisting mostly of conjugated bilirubin,are often elevated in acute hepatitis due to cholestasis.This usually results in jaundice,which resolves as the hepatitis improves.However,serum direct bilirubin elevations can sometimes persist beyond 4 weeks.1,2 Because bilirubin excretion is an important hepatic function,prolonged direct hyperbilirubinemia may raise concerns about the development of liver failure.2 The incidence of acute liver failure has been reported to be approximately 3,000 cases per year in the U.S.,with about 80%of these cases attributed to acute hepatitis.3 Nevertheless,prolonged direct hyperbilirubinemia is not synonymous with cholestasis,nor is it necessarily a marker of liver failure.For instance,Dubin-Johnson syndrome4 and Rotor syndrome are rare genetic causes of prolonged direct hyperbilirubinemia without cholestasis or liver disease.1 A much more common condition leading to prolonged direct hyperbilirubinemia without cholestasis or liver failure is delta hyperbilirubinemia.Because delta hyperbilirubinemia is relatively common yet often underappreciated,the aim of this article is to update the pathogenesis,clinical significance,and management of delta hyperbilirubinemia.
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