Immune checkpoint inhibitor-related diabetes mellitus is a rare but clinically important endocrine adverse event that characteristically presents with abrupt-onset diabetic ketoacidosis, disproportionately normal or near-normal glycated haemoglobin, and evidence of autoimmune beta-cell destruction. We report the case of a 58-year-old woman receiving atezolizumab and bevacizumab for hepatocellular carcinoma who developed new-onset polyuria and polydipsia followed by diabetic ketoacidosis within weeks of commencing immunotherapy. Biochemical evaluation confirmed endogenous hyperinsulinaemia-unrelated hyperglycaemia with strongly positive islet autoantibodies, including glutamic acid decarboxylase (158 IU/mL) and zinc transporter 8 (1,467 U/mL), alongside a urinary C-peptide/creatinine ratio of 0.59 nmol/mmol, consistent with early but rapidly evolving beta-cell failure. She was treated with standard diabetic ketoacidosis care, transitioned to a basal-bolus insulin regimen with continuous glucose monitoring, and discharged with coordinated oncology-endocrinology follow-up. Atezolizumab was held during acute decompensation with plans for re-initiation once metabolic stability was achieved. This case adds to the growing literature on programmed death-ligand 1 inhibitor-induced diabetes in the hepatocellular carcinoma population, where such events are incompletely characterised. Clinicians managing patients on atezolizumab-based regimens should maintain a low threshold for glucose monitoring and early ketone testing in the presence of osmotic symptoms.
Hayat et al. (Fri,) studied this question.