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Immune Checkpoint Inhibitor-Induced (Type 3) Autoimmune Pancreatitis

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Abstract

Purpose of Review

Immune checkpoint inhibitors (ICI) have revolutionized cancer care and work primarily by blocking CTLA-4 (cytotoxic T-lymphocyte-associated protein 4), and/or PD-1 (programmed cell death protein 1), and/or PD-L1 (programmed death-ligand 1), thereby providing highly efficacious anti-tumor activity. However, this unmitigated immune response can also trigger immune related adverse events (irAEs) in multiple organs, with pancreatic irAEs (now referred to as type 3 Autoimmune pancreatitis (AIP) being infrequent.

Recent Findings

Type 3 AIP is a drug-induced, immune mediated progressive inflammatory disease of the pancreas that may have variable clinical presentations viz., an asymptomatic pancreatic enzyme elevation, incidental imaging evidence of pancreatitis, painful pancreatitis, or any combination of these subtypes. Management is largely supportive with intravenous fluid hydration, pain control and holding the inciting medication. Steroids have not been shown to demonstrate a clear benefit in acute management. A rapid development pancreatic atrophy is observed on imaging as early as 1 year post initial injury.

Summary

Type 3 AIP is a chronic inflammatory disease of the pancreas that though predominantly asymptomatic and mild in severity can lead to rapid organ volume loss regardless of type of clinical presentation and despite steroid therapy.

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Data Availability

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Contributions

Anusha Shirwaikar Thomas: review of literature, drafting of the manuscript, critical revision of the manuscript for intellectual content and prepared Fig. 1; Suresh T. Chari: study concept and design; analysis and interpretation of data; critical revision of the manuscript for intellectual content.

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Correspondence to Suresh T. Chari.

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Shirwaikar Thomas, A., Chari, S.T. Immune Checkpoint Inhibitor-Induced (Type 3) Autoimmune Pancreatitis. Curr Gastroenterol Rep 25, 255–259 (2023). https://doi.org/10.1007/s11894-023-00885-6

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