Early insulin averts hyperglycemic crisis in slow-onset durvalumab-induced checkpoint inhibitor-associated autoimmune diabetes mellitus
- VernacularTitle:Early insulin averts hyperglycemic crisis in slow-onset durvalumab-induced checkpoint inhibitor-associated autoimmune diabetes mellitus
- Author:
Takaaki MATSUDA
1
;
Yoshinori OSAKI
2
;
Motohiro SEKIYA
2
;
Hitoshi SHIMANO
2
Author Information
- Keywords: immune checkpoint inhibitors; durvalumab; type 1 diabetes; autoimmune diabetes; hyperglycemic crisis
- From:Journal of Rural Medicine 2025;20(2):150-155
- CountryJapan
- Language:en
- Abstract: Objective: Checkpoint inhibitor-associated autoimmune diabetes mellitus (CIADM), a variant of type 1 diabetes, is a rare immune-related adverse events (irAEs) caused by antibody-based immune checkpoint inhibitors. CIADM typically manifests as fulminant or acute-onset type 1 diabetes in the insulin-depleted state. However, we encountered a patient with slow-onset CIADM who initially presented with hyperglycemia without decreased insulin secretion after treatment with durvalumab (an anti-PD-L1 antibody).Patient: A 60-year-old man diagnosed with small-cell lung cancer on durvalumab combined with dexamethasone treatment experienced an increase in glycated hemoglobin (HbA1c) from 6.4% to 7.8% after three cycles.Results: Despite preserved endogenous insulin secretion (C-peptide, 2.47 ng/mL with a casual plasma glucose level of 287 mg/dL), basal insulin therapy was initiated considering CIADM. HbA1c levels remained stable (8.5–9.2%) for 3 months but increased to 13.4% at 18 weeks, indicative of CIADM. Declining endogenous insulin secretion resulted in ketosis; however, hyperglycemic crisis was prevented through basal insulin therapy.Conclusion: We emphasize that CIADM develops gradually and does not always occur in the course of fulminant or acute-onset type 1 diabetes; therefore, early initiation of insulin in the presence of hyperglycemia is crucial to prevent hyperglycemic crises.
