6 Scopus citations


Background/objectives: Pancreatogenic diabetes mellitus has been assumed to result from non-immune beta cell destruction when the pancreas is replaced by fibrotic tissue secondary to acute and chronic pancreatitis. We hypothesize that recurrent episodes of pancreatic inflammation may increase the risk for developing β-cell autoimmunity in susceptible individuals. Methods: We describe 11 patients who had both recurrent acute and/or chronic pancreatitis and type 1 diabetes (T1D) requiring insulin therapy. Results: All 11 patients had positive autoantibodies and 8 patients tested had minimal to undetectable (7/8) or moderate (1/8) stimulated C-peptide at 12 months after T1D onset. Three had biopsy confirmation of insulitis. Conclusions: These cases lend support to the theory that pancreatitis may increase risk for T1D. We postulate that the pro-inflammatory conditions of pancreatitis may increase posttranslational protein modifications of β-cell antigens and neoepitope generation, which are potential initiating events for loss of β-cell self-tolerance.

Original languageEnglish (US)
Pages (from-to)95-97
Number of pages3
Issue number1
StatePublished - Jan 1 2021

Bibliographical note

Funding Information:
M. Bellin discloses financial relationships with Dexcom (research support), Viacyte (research support) and Insulet (DSMB membership), and medical advisory roles with ARIEL Precision Medicine and MissionCure. All other authors have no conflicts to disclose. The authors also acknowledge Clinical Translational Science Institutes support from UL1TR002494 from the National Institutes of Health’s National Center for Advancing Translational Sciences .

Funding Information:
Dr. Bellin is supported by the following grants from the National Institutes of Health relevant to the current work: U01KD127367 , U01DK126300 , R01DK109124 .

Publisher Copyright:
© 2020 IAP and EPC


  • Autoimmunity
  • Pancreatitis
  • Pancreatogenic diabetes
  • Type 1 diabetes

PubMed: MeSH publication types

  • Journal Article


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