Transient pancreatic enlargement with peripancreatic inflammatory changes two days before clinical presentation and diagnosis of atezolizumab-related fulminant type 1 diabetes mellitus followed by pancreatic atrophy: a case report with review of literature.

Immune checkpoint inhibitor (ICI)-related type 1 diabetes is a rare but potentially life-threatening immune-related adverse event, and imaging findings immediately before clinical presentation and diagnosis have rarely been documented. We report a 71-year-old woman with large cell neuroendocrine carcinoma who developed fulminant type 1 diabetes mellitus during carboplatin, nab-paclitaxel, and atezolizumab therapy. The day of clinical presentation and diagnosis was defined as Day 0. On Day -1, she developed nausea and appetite loss without abdominal pain. On Day 0, she presented with impaired consciousness and fever; laboratory evaluation showed plasma glucose 1,435 mg/dL, glycated hemoglobin (HbA1c) 6.9%, marked ketonemia, severe hyperosmolality, negative anti-glutamic acid decarboxylase (GAD) antibody, and near-complete insulin deficiency. The metabolic presentation was interpreted as diabetic ketoacidosis/hyperosmolar hyperglycemic state (DKA/HHS) overlap. Computed tomography (CT) performed on Day -2 showed radiologic enlargement of the pancreatic tail with increased peripancreatic fat attenuation, both of which had resolved on Day 0. Pancreatic volume increased from 46.0 mL at baseline to 82.5 mL on Day -2, decreased to 47.9 mL on Day 0, and further declined to 39.0 mL at 6-month follow-up. This hypothesis-generating case documents incidental transient pancreatic enlargement with peripancreatic inflammatory changes shortly before diagnosis, followed by pancreatic atrophy. This case suggests that incidental pancreatic enlargement during ICI therapy may serve as an early radiologic clue to immune-related diabetes, supporting prompt metabolic evaluation even in the absence of abdominal pain or pancreatic enzyme elevation.