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Fulminant type 1 diabetes: recent research progress and future prospects.
Akihisa Imagawa1, Megumi Tachibana1
1Department of Internal Medicine (I), Osaka Medical College, 2-7 Daigaku-cho, Takatsuki, 569-8686 Japan.
Diabetology International
|October 22, 2020
Summary
Anti-PD-1/PD-L1 therapy can cause type 1 diabetes, including fulminant type 1 diabetes. This form shows beta-cell fragility, not regeneration failure, and has genetic links.
Area of Science:
- Immunology
- Endocrinology
- Genetics
Background:
- Anti-programmed cell death 1/programmed cell death ligand 1 (anti-PD-1/PD-L1) therapies can trigger type 1 diabetes.
- Fulminant type 1 diabetes (FT1D) is a severe form requiring urgent characterization.
Purpose of the Study:
- To elucidate the clinical and etiological features of FT1D.
- To differentiate FT1D from other types of type 1 diabetes.
- To investigate the underlying mechanisms of FT1D.
Main Methods:
- Review of patient data with type 1 diabetes post-anti-PD-1/PD-L1 therapy.
- Analysis of induced pluripotent stem (iPS) cell-derived pancreatic beta cells from FT1D patients.
- Examination of clinical, genetic, and cellular characteristics.
Main Results:
- Anti-PD-1/PD-L1 therapy-related type 1 diabetes encompasses both FT1D and acute-onset type 1 diabetes.
- FT1D exhibits beta-cell fragility to inflammatory cytokines, not impaired regeneration, in iPS cell models.
- Severe hyperglycemia is a risk factor for adverse events; diffusion-weighted MRI may aid diagnosis.
- The CSAD/lnc-ITGB7-1 locus is genetically associated with FT1D.
Conclusions:
- FT1D induced by anti-PD-1/PD-L1 therapy presents unique characteristics.
- Beta-cell fragility is a key feature of FT1D, distinct from regeneration failure.
- Multifaceted research, including genetic and cellular analyses, is crucial for understanding FT1D etiology and pathophysiology.
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