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Published on: July 26, 2019
Fulminant type 1 diabetes developed after influenza split vaccination
Toshitaka Sawamura1,2,3, Shigehiro Karashima3, Ai Ohmori1,2
1Department of Internal Medicine, Asanogawa General Hospital, Kosakamachinaka, Kanazawa, Ishikawa, Japan.
Fulminant type 1 diabetes (FT1D) can be triggered by influenza split vaccination. This may occur through the activation of memory CD8-positive T cells into cytotoxic T cells, leading to rapid beta-cell destruction.
Area of Science:
- Immunology
- Endocrinology
- Virology
Background:
- Fulminant type 1 diabetes (FT1D) is a severe form of diabetes with rapid beta-cell destruction and hyperglycemia.
- The exact pathogenesis of FT1D is not fully understood, but viral infections and genetic factors are implicated.
- Immune checkpoint inhibitor use has also been linked to FT1D development.
Purpose of the Study:
- To investigate a potential link between influenza vaccination and the onset of fulminant type 1 diabetes.
- To explore the immunological mechanisms by which influenza vaccination might induce FT1D.
Main Methods:
- Case report of a 51-year-old Japanese man diagnosed with DKA and FT1D.
- Analysis of patient's medical history, including prior influenza infections and recent influenza vaccination.
- Review of immunological mechanisms potentially involved in FT1D pathogenesis.
Main Results:
- The patient developed DKA associated with FT1D 12 days after receiving an inactive split influenza vaccine.
- The patient had a history of influenza infections and non-susceptible HLA class II genotypes.
- The study proposes that inactive split influenza vaccines might induce FT1D by promoting the redifferentiation of memory CD8-positive T cells into cytotoxic T cells.
Conclusions:
- Inactive split influenza vaccines may trigger fulminant type 1 diabetes in susceptible individuals.
- The mechanism may involve the activation and redifferentiation of memory CD8-positive T cells into cytotoxic T cells.
- This case highlights a potential adverse effect of influenza vaccination on glucose metabolism in specific contexts.
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