Type 1 diabetes mellitus in patients with recurrent acute and chronic pancreatitis: A case series

Harmeet K. Kharoud; Tetyana Mettler; Martin L. Freeman; Guru Trikudanathan; Gregory J. Beilman; Srinath Chinnakotla; Elissa Downs; Sarah J. Schwarzenberg; Melena D. Bellin

doi:10.1016/j.pan.2020.12.006

Type 1 diabetes mellitus in patients with recurrent acute and chronic pancreatitis: A case series

Harmeet K. Kharoud, Tetyana Mettler, Martin L. Freeman, Guru Trikudanathan, Gregory J. Beilman, Srinath Chinnakotla, Elissa Downs, Sarah J. Schwarzenberg, Melena D. Bellin

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Abstract

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 language	English (US)
Pages (from-to)	95-97
Number of pages	3
Journal	Pancreatology
Volume	21
Issue number	1
DOIs	https://doi.org/10.1016/j.pan.2020.12.006
State	Published - Jan 2021

Bibliographical note

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

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 .

Keywords

Autoimmunity
Pancreatitis
Pancreatogenic diabetes
Type 1 diabetes

PubMed: MeSH publication types

Journal Article

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title = "Type 1 diabetes mellitus in patients with recurrent acute and chronic pancreatitis: A case series",

abstract = "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.",

keywords = "Autoimmunity, Pancreatitis, Pancreatogenic diabetes, Type 1 diabetes",

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note = "Funding Information: Dr. Bellin is supported by the following grants from the National Institutes of Health relevant to the current work: U01KD127367 , U01DK126300 , R01DK109124 . 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{\textquoteright}s National Center for Advancing Translational Sciences . ",

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AU - Freeman, Martin L.

AU - Trikudanathan, Guru

AU - Beilman, Gregory J.

AU - Chinnakotla, Srinath

AU - Downs, Elissa

AU - Schwarzenberg, Sarah J.

AU - Bellin, Melena D.

N1 - Funding Information: Dr. Bellin is supported by the following grants from the National Institutes of Health relevant to the current work: U01KD127367 , U01DK126300 , R01DK109124 . 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 .

PY - 2021/1

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N2 - 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.

AB - 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.

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Type 1 diabetes mellitus in patients with recurrent acute and chronic pancreatitis: A case series

Abstract

Bibliographical note

Keywords

PubMed: MeSH publication types

UN SDGs

Access

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