Chemotherapy-Induced Unconjugated Hyperbilirubinemia Complicated by Other Trigger Factors in a Child with T-Cell Acute Lymphoblastic Leukaemia and UGT1A1 Mutation-Associated Gilbert Syndrome

Gilbert syndrome (GS) is an inherited disorder characterised by unconjugated hyperbilirubinemia due to a deficiency in hepatic UDP-glucuronosyltransferase 1A1 (<i>UGT1A1</i>) enzyme activity, responsible for bilirubin glucuronidation. This results in decreased bilirubin conjugation and excretion, leading to elevated serum unconjugated bilirubin levels. In T-cell acute lymphoblastic leukaemia (T-ALL), treatment typically involves intensive chemotherapy regimens that include agents metabolised by the liver, requiring careful consideration of liver function and bilirubin metabolism in patients with concurrent GS. We present the case of a 15-year-old male who was diagnosed with T-ALL and treated with a chemotherapy regimen following the modified Dutch Child Oncology Group ALL-9 (High Risk) protocol. Concurrently, the patient was observed to have persistent unconjugated hyperbilirubinemia aggravated by infection and fasting despite normal to mildly deranged liver function, which was initially assumed to be attributed by 6-Mercaptopurine (6-MP). Further workup confirmed a diagnosis of GS based on clinical history, laboratory findings, and genetic testing. We recommend performing a genetic analysis of <i>UGT1A1</i> in patients presenting with chemotherapy-induced hyperbilirubinemia with no signs of liver impairment. This aims to prevent unnecessary alterations in chemotherapy regimens that could potentially increase the risk of relapse.