Checkpoint Inhibitor-Associated Diabetes Mellitus Following Rapid Pancreatic Metastasis Resolution: Implications for...

Checkpoint inhibitor-associated autoimmune diabetes mellitus (CIADM) is a rare complication of immunotherapy, often leading to abrupt insulin deficiency and diabetic ketoacidosis. We present a case arising during atezolizumab therapy following rapid pancreatic metastasis resolution, suggesting a link between tumor regression, local immune activation, and beta-cell injury.

A 67-year-old woman was diagnosed with extensive-stage small-cell lung cancer and a pancreatic metastasis. She began treatment, including atezolizumab, a programmed death-ligand 1 inhibitor. Imaging after 7 weeks of treatment showed complete resolution of the pancreatic lesion. At week 35, she presented with polyuria, polydipsia, and vomiting. Labs confirmed diabetic ketoacidosis, with marked hyperglycemia, low C-peptide, and negative diabetes-related autoantibodies. She was diagnosed with CIADM and required prolonged intravenous insulin followed by basal-bolus therapy. Computed tomography imaging 2 months later demonstrated a 52% reduction in pancreatic volume.

This case highlights the fulminant onset of autoimmune diabetes during immunotherapy, with profound insulin deficiency and pancreatic atrophy. Its onset following rapid pancreatic tumor resolution suggests that localized immune activation may have contributed to beta-cell destruction.

CIADM may emerge as an immune-related adverse event in patients with rapid pancreatic tumor response. Early recognition is essential, particularly in those with pronounced tumor regression, to ensure timely diagnosis and management.