Introduction

Gilbert’s syndrome (GS) is a benign hereditary disorder of bilirubin conjugation resulting in an isolated, elevated blood level of unconjugated bilirubin.1 GS affects 2%–10% of the Caucasian population in the Western world.2,3 The inheritance pattern for GS is commonly autosomal recessive, but can be dominant as well; however, genetic counselling is not necessary as there is no impact on life expectancy. For the patient, however, the condition may be an initial cause for concern as they commonly present with painless, non-pruritic jaundice or an incidental finding of hyperbilirubinaemia on routine blood testing. Episodes of jaundice may be exacerbated by heavy physical exertion, fasting, sleep deprivation, alcohol, dehydration, surgery and concurrent illness. Patients will have normal liver enzymes, normal liver synthetic function (clotting, albumin) and a negative haemolysis screen. GS is a diagnosis of exclusion. The primary care practitioners’ main aim is to confirm the diagnosis, reassure the patient and clarify any concerns related to the condition. GS does not require secondary care referral and is largely asymptomatic. Observational studies highlight that the antioxidant effect of unconjugated bilirubin may confer a survival benefit to patients,4,5 and indeed, the greatest risk to those with the condition is in pursuit of an alternative diagnosis. Patients should …