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CASE REPORT article

Front. Endocrinol.

Sec. Clinical Diabetes

Volume 16 - 2025 | doi: 10.3389/fendo.2025.1697724

Immune Checkpoint Inhibitor Induced Diabetes Can Potentially be Effectively Treated with Infliximab: A case report of two patients

Provisionally accepted
  • 1Yale School of Medicine, New Haven, United States
  • 2VA Connecticut Healthcare System West Haven VA Medical Center, West Haven, United States
  • 3Cedars-Sinai, Los Angeles, United States

The final, formatted version of the article will be published soon.

Immune checkpoint inhibitor-induced diabetes is a potentially severe and life-threatening complication of immune checkpoint inhibitor therapy in patients with advanced malignancies. It is typically an irreversible complication due to complete destruction of pancreatic beta cells that requires ongoing insulin treatment and patients often exhibit labile diabetes. Inflammatory cytokines, including TNF-α, are thought to play a role in the development of this form of diabetes as they do in spontaneous autoimmune diabetes. TNF-α has also been implicated in the development of other immune related adverse events caused by immune therapy and infliximab, a TNF-α monoclonal antibody, has shown efficacy in several of these complications. We tested whether infliximab could preserve beta cell function in immune checkpoint inhibitor-induced diabetes. We present two cases in which infliximab treatment appeared to halt beta cell destruction, as evidenced by maintenance of C-peptide levels, as well as improved clinical outcomes in terms of diabetes control.

Keywords: immune checkpoint inhibitors, Diabetes Mellitus, Immune related adverse events, TNF-α, infliximab

Received: 02 Sep 2025; Accepted: 16 Oct 2025.

Copyright: © 2025 Perdigoto, Savion Gaiger, Hurwitz, Hafez, Kluger and Herold. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Ana Luisa Perdigoto, ana.perdigoto@yale.edu

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