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Hollstein, T.* ; Schulte, D.M.* ; Schulz, J.* ; Glück, A.* ; Ziegler, A.-G. ; Bonifacio, E.* ; Wendorff, M.* ; Franke, A.* ; Schreiber, S.* ; Bornstein, S.R.* ; Laudes, M.*

Autoantibody-negative insulin-dependent diabetes mellitus after SARS-CoV-2 infection: A case report.

Nat. Metab. 2, 1021-1024 (2020)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
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 mu g l(-1), blood glucose concentration of 30.6 mmol l(-1) (552 mg dl(-1)) 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 beta-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 beta-cells.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Glutamic-acid Decarboxylase; Cell; Coronavirus; Hemoglobin; Covid-19; Children; Onset; Risk; Ace2
ISSN (print) / ISBN 2522-5812
e-ISSN 2522-5812
Zeitschrift Nature metabolism
Quellenangaben Band: 2, Heft: 10, Seiten: 1021-1024 Artikelnummer: , Supplement: ,
Verlag Springer
Verlagsort London
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed