ReviewFrontiers in endocrinology2025
Immune checkpoint inhibitor-associated diabetes mellitus: mechanisms, clinical manifestations, and management strategies.
Review in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The Rise of Oncoendocrinology: How Modern Cancer Therapies Are Reshaping Endocrine Practice.Medical sciences (Basel, Switzerland) · 2026Review
- Severe renal and pancreatic toxicities associated with ipilimumab and nivolumab combination therapy in non-small cell lung cancer: a pharmacovigilance analysis of the FDA adverse event reporting system.Frontiers in immunology · 2026Article
- Case Report: Diabetic ketoacidosis following EGFR-TKIs therapy via aggravated insulin resistance.Frontiers in oncology · 2026Article
- Pembrolizumab-induced type-1 diabetes mellitus: clinical characteristics, therapeutic strategies, and prognosis from a retrospective analysis of 43 published cases.Frontiers in endocrinology · 2026Article
- Tislelizumab-induced hyperosmolar diabetic ketoacidosis complicated with rhabdomyolysis in hepatocellular carcinoma patients: case report.Frontiers in oncology · 2026Article
- Case Report: a three-stage treatment strategy combining immunotherapy with chemoradiotherapy for locally advanced esophageal squamous cell carcinoma.Frontiers in immunology · 2026Article
Corrections and comments
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Authors and funding
3 authors.
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Abstract
Immune checkpoint inhibitor-associated diabetes mellitus (ICI-DM) is a rare but life-threatening endocrine immune-related adverse event characterized by abrupt insulin deficiency and a high incidence of diabetic ketoacidosis (DKA). Unlike classical type 1 diabetes, ICI-DM often develops after only a few treatment cycles, shows a fulminant phenotype with disproportionally modest HbA1c elevation, and is typically irreversible and glucocorticoid-refractory, necessitating permanent insulin therapy. Mechanistically, PD-1/PD-L1 blockade disrupts pancreatic immune tolerance and permits autoreactive CD8
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