An unexpectedly prolonged severe hyperbilirubinemia in a patient with pre-existing hepatitis A: a role of genetic predisposition?

Abstract

Acute hepatitis A virus (AHAV) infection is a self-limited condition that usually spontaneously recovers in 2-8 weeks. While in children under 6 years of age AHAV is often asymptomatic, >70% of adults manifest symptoms together with typical laboratory findings [1]. AHAV is serologically diagnosed by the detection of anti-HAV IgM, which persists 2-6 months after infection. Laboratory results during AHAV show a marked increase (usually 10 to 40 times the upper reference limit [URL]) in serum alanine aminotransferase (ALT) activity, together with high total bilirubin (TB) (average peak of 171.0 μmol/L, mainly consisting of the conjugated form) and moderately (<3 URL) increased alkaline phosphatase (ALP) and γ-glutamyltransferase (GGT) [2]. With resolution of AHAV, conjugated bilirubin (CB) is rapidly cleared and its serum concentrations return to normal quickly. However, 10%-20% of patients develop prolonged cholestasis lasting for >6 months [1].Bilirubin, which is a major end-product of heme breakdown, is physiologically glucuronidated in the liver and then excreted into the bile. The mechanisms of bilirubin excretion, and of hyperbilirubinemia causes, are