Early insulin averts hyperglycemic crisis in slow-onset durvalumab-induced checkpoint inhibitor-associated autoimmune diabetes mellitus.

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.