Immune Checkpoint Inhibitor-Associated Diabetes: A Single-Institution Experience

• Published in: Diabetes care Vol. 43; no. 12; pp. 3106 - 3109
• Main Authors: Byun, David J, Braunstein, Rebecca, Flynn, Jessica, Zheng, Junting, Lefkowitz, Robert A, Kanbour, Sarah, Girotra, Monica
• Format: Journal Article
• Language: English
• Published: United States American Diabetes Association 01.12.2020
• Subjects: Apoptosis; Atrophy; Autoantibodies; Carcinoma; Cell death; Diabetes; Diabetes mellitus; Diabetic ketoacidosis; Glucose; Immune checkpoint inhibitors; Immunotherapy; Inhibitors; Ketoacidosis; Novel Communications in Diabetes; Pancreas; PD-1 protein; PD-L1 protein; Proteins; Research design
• ISSN: 0149-5992; 1935-5548
• DOI: 10.2337/dc20-0609

To characterize immune checkpoint inhibitor-associated diabetes mellitus (ICI-DM) in a single-institution case series. Retrospective chart review of 18 patients with new-onset ICI-DM following anti-programmed cell death protein 1 (PD-1)/anti-programmed cell death protein ligand 1 (PD-L1) therapy for advanced carcinomas. Of 18 patients, 9 had diabetic ketoacidosis (median glucose 27.92 mmol/L; median glucose before presentation 6.35 mmol/L). Median C-peptide at ICI-DM diagnosis was low, and it declined during follow-up. Median anti-PD-1/anti-PD-L1 duration before ICI-DM was 3.65 months (range 0.56-12.23 months). Time to ICI-DM onset was a median 1.4 months/3 ICI cycles and 6 months/10 cycles in those patients who were positive and negative for GAD65 autoantibodies, respectively. Time to ICI-DM onset was a median 2.5 months/3 ICI cycles and 4.8 months/8 cycles after anti-PD-L1 or anti-PD-1 therapy, respectively. Significant pancreatic atrophy was seen radiographically. ICI-DM presents abruptly, appears irreversible, is characterized by pancreatic atrophy, and may occur both earlier following PD-L1 blockade compared with PD-1 inhibition and in those who have positive GAD65 autoantibodies.