Multiple endocrine disorders in an adolescent with a history of T-cell acute lymphoblastic leukaemia treatment: a case report

Background. Late endocrine disorders are an important issue after treatment for childhood cancer. Objective: to describe multiple endocrine abnormalities in an adolescent previously trea­ted for T-cell acute lymphoblastic leukaemia and to evaluate the limits of causal interpretation when treatment records are incomplete. Materials and methods. The case report was prepared by retrospectively reconstructing the clinical timeline from the available medical summary and discharge records, with consideration of the CARE recommendations. A targeted narrative search of PubMed and authoritative guideline repositories was conducted through 4 September 2026. Additional relevant sources identified during manuscript revision were also considered. The review was not systematic. Results. T-cell acute lymphoblastic leukaemia was diagnosed at 11 years of age. During induction therapy, the medical record documented acute pancreatitis attributed by the treating team to L-asparaginase, hyperglycaemia described as steroid-induced, hepatotoxicity, and infectious complications. Approximately 27 months after treatment began, the patient developed polydipsia and weight loss. Fasting glucose was 9.4 mmol/L, postprandial glucose reached 15 mmol/L, and HbA1c was 11 %; continuous subcutaneous insulin infusion was started. At the same assessment, thyroid-stimulating hormone was 7.2 mIU/L and free thyroxine was 9.3 pmol/L; thyroid autoantibodies were negative, and levothyroxine was prescribed. At 15 years 8 months, testicular volumes were 2 and 3 mL, luteinising hormone was 15.2 mIU/mL, and follicle-stimulating hormone was 48.6 mIU/mL; the hypergonadotropic profile suggested primary testicular dysfunction. The available records did not contain C-peptide or islet autoantibody results, a complete pancreatic assessment, cumulative doses of gonadotoxic chemotherapy, organ-specific radiation doses, or a complete treatment summary. Conclusions. Diabetes requiring insulin, thyroid dysfunction, and a hypergonadotropic profile supporting primary testicular dysfunction were documented. The available data are insufficient to attribute all abnormalities to a single treatment-related mechanism.