sharon sanders
Editor-in-Chief & President
- Letter
- Published: 02 September 2020
- Tim Hollstein,
- Dominik M. Schulte,
- Juliane Schulz,
- Andreas Gl?ck,
- Anette G. Ziegler,
- Ezio Bonifacio,
- Mareike Wendorff,
- Andre Franke,
- Stefan Schreiber,
- Stefan R. Bornstein &
- Matthias Laudes
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Here we report a case where the manifestations of insulin-dependent diabetes occurred following SARS-CoV-2 infection in a young individual in the absence of autoantibodies typical for type 1 diabetes mellitus. Specifically, a 19-year-old white male presented at our emergency department with diabetic ketoacidosis, C-peptide level of 0.62 ?g l[SUP]–1[/SUP], blood glucose concentration of 30.6 mmol l[SUP]–1[/SUP] (552 mg dl[SUP]–1[/SUP]) and haemoglobin A1c of 16.8%. The patient?s case history revealed probable COVID-19 infection 5–7 weeks before admission, based on a positive test for antibodies against SARS-CoV-2 proteins as determined by enzyme-linked immunosorbent assay. Interestingly, the patient carried a human leukocyte antigen genotype (HLA DR1-DR3-DQ2) considered to provide only a slightly elevated risk of developing autoimmune type 1 diabetes mellitus. However, as noted, no serum autoantibodies were observed against islet cells, glutamic acid decarboxylase, tyrosine phosphatase, insulin and zinc-transporter 8.
Although our report cannot fully establish causality between COVID-19 and the development of diabetes in this patient, considering that SARS-CoV-2 entry receptors, including angiotensin-converting enzyme 2, are expressed on pancreatic β-cells and, given the circumstances of this case, we suggest that SARS-CoV-2 infection, or COVID-19, might negatively affect pancreatic function, perhaps through direct cytolytic effects of the virus on β-cells.
https://www.nature.com/articles/s42255-020-00281-8