Prolonged cholestasis triggered by hepatitis A virus infection and variants of the hepatocanalicular phospholipid and bile salt transporters.

摘要: Hepatitis A virus (HAV) infection resolves in most patients uneventfully within weeks from the onset of disease. In rare cases, however, it may relapse or cause prolonged cholestasis. Here we present a case 36-year-old female patient who developed severe pruritus and jaundice three after initially uncomplicated hepatitis A. was excluded. Since therapy with colestyramin, antihistaminics, naloxon ursodeoxycholic acid (UDCA) did not improve symptoms, decided to perform plasma absorption start rifampicin therapy. Under these measures, jaundice, as well serum bilirubin levels improved gradually four plasmapheresis sessions were able discharge patient. Genetic testing showed presence two procholestatic polymorphisms, c.3084 [GG] variant gene encoding hepatocanalicular bile salt transporter ABCB11 c.711 [AT] phosphatidylcholine floppase ABCB4. We speculate that this compound ABCB4-ABCB11 genotype led intrahepatic cholestasis setting HAV infection. conclusion, our suggests polymorphisms transporters contribute more pronounced course Although dedicated studies large cohorts are needed confirm observation, carrying hepatobiliary variants benefit vaccination against