Immune Checkpoint Inhibitor-Induced Diabetes Presenting As Diabetic Ketoacidosis: A Case Report

A 51-year-old woman with BRAF V600E-positive metastatic melanoma developed diabetic ketoacidosis (DKA) three weeks after commencing combination immunotherapy with nivolumab and ipilimumab, despite a normal baseline endocrine and metabolic assessment. She presented with vomiting, dizziness, and profound weakness. Blood gas analysis demonstrated severe DKA (pH 7.09, bicarbonate 7.7 mmol/L, glucose 32.5 mmol/L, ketones 5.6 mmol/L), and laboratory evaluation showed markedly reduced C-peptide with positive anti-glutamic acid decarboxylase (anti-GAD) antibodies, consistent with fulminant, insulin-deficient diabetes secondary to immune checkpoint inhibitor (ICI) therapy. She was treated according to standard DKA protocols, transitioned to long-term insulin therapy, and her immunotherapy was de-escalated to single-agent nivolumab because of concern for recurrent endocrine toxicity. This case illustrates the rapid and unpredictable onset of ICI-induced insulin-deficient diabetes, which occurred despite normal baseline investigations in this patient, and highlights the need for vigilant glucose monitoring in patients receiving combination checkpoint inhibitor therapy.