A 22 year old man presents with a resolving episode of mild jaundice after an influenza-like illness. He reports a previous episode after an appendicectomy, which also resolved spontaneously, but he is worried about the implications of this recurrence. Biochemical records from his surgical admission show a slightly raised bilirubin concentration of 48 µmol/l (normal < 22 µmol/l), but alanine aminotransferase, alkaline phosphatase, γ-glutamyl transferase and albumin were all within normal limits. The history and biochemistry in this patient strongly suggest Gilbert’s syndrome, a hereditary (usually autosomal recessive) condition caused by impaired hepatic bilirubin clearance.1 Gilbert’s syndrome is present in 5-10% of Western European populations with 1 in 3 of those affected unaware that they have it.2 3 Diagnosis of the disorder is often made after an incidental finding of isolated hyperbilirubinaemia on routine liver biochemistry testing. Bilirubin is the normal by-product of the breakdown of red blood cells (haemoglobin). Patients with Gilbert’s syndrome have a defect in the gene that encodes for glucuronyltransferase, which results in a 60-70% reduction in the liver’s ability to conjugate bilirubin. This subsequent increase …