Clinical and Biochemical Recovery From Immune Checkpoint Inhibitor-Induced Diabetes With Seroconversion of GAD Antibodies.

Abstract

Immune checkpoint inhibitors (ICIs) improve outcomes across multiple cancers but may cause immune-related adverse events, including ICI-induced diabetes (ICI-D). ICI-D typically presents abruptly with severe insulin deficiency, and published cases have largely described irreversible loss of endogenous insulin secretion. We report a novel case of clinical and biochemical recovery of ICI-D. Following melanoma treatment with ipilimumab plus nivolumab, then nivolumab monotherapy, the patient developed abrupt-onset symptomatic hyperglycemia with mild ketosis and positive GAD and insulin autoantibodies, consistent with ICI-D. The patient subsequently received infliximab for ICI-related arthritis. Insulin requirements progressively declined, allowing discontinuation of insulin therapy. GAD antibodies normalized within ∼2 months and later became undetectable. Urine C-peptide-to-creatinine ratios increased over time, consistent with endogenous insulin secretion. Recovery from ICI-D may occur. The temporal association suggests infliximab may have contributed, warranting further study as a potential disease-modifying therapy.