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Review
. 2020 Nov-Dec;14(6):2211-2217.
doi: 10.1016/j.dsx.2020.11.012. Epub 2020 Nov 17.

New onset diabetes, type 1 diabetes and COVID-19

Sirisha Kusuma Boddu  1 , Geeta Aurangabadkar  2 , Mohammad Shafi Kuchay  3
Affiliations
Review

New onset diabetes, type 1 diabetes and COVID-19

Sirisha Kusuma Boddu et al. Diabetes Metab Syndr. 2020 Nov-Dec.

Abstract

Background and aims: New data has emerged regarding higher risk of coronavirus disease 2019 (COVID-19), and its severity and complications in patients with type 2 diabetes mellitus (T2DM). However, there is a dearth of evidence regarding type 1 diabetes mellitus (T1DM). This article explores the possibility of COVID 19 induced diabetes and highlights a potential bidirectional link between COVID 19 and T1DM.

Methods: A literature search was performed with Medline (PubMed), Scopus, and Google Scholar electronic databases till October 2020, using relevant keywords (COVID-19 induced diabetes; COVID-19 and type 1 diabetes; COVID-19 induced DKA; new-onset diabetes after SARS-CoV-2 infection) to extract relevant studies describing relationship between COVID-19 and T1DM.

Results: Past lessons and new data teach us that severe acute respiratory syndrome coronaviruses (SARS-CoV and SARS-CoV-2) can enter islet cells via angiotensin converting enzyme-2 (ACE-2) receptors and cause reversible β-cell damage and transient hyperglycemia. There have been postulations regarding the potential new-onset T1DM triggered by COVID-19. This article reviews the available evidence regarding the impact and interlink between COVID-19 and Τ1DM. We also explore the mechanisms behind the viral etiology of Τ1DM.

Conclusions: SARS-CoV-2 can trigger severe diabetic ketoacidosis at presentation in individuals with new-onset diabetes. However, at present, there is no hard evidence that SARS-CoV-2 induces T1DM on it's own accord. Long term follow-up of children and adults presenting with new-onset diabetes during this pandemic is required to fully understand the type of diabetes induced by COVID-19.

Keywords: ACE2 receptors; Hyperglycemia; New-onset diabetes; SARS-CoV-2; Type 1 diabetes; β-cell damage.

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Conflict of interest statement

Declaration of competing interest The authors declare that there are no conflicting interests relevant to this article.

Figures

Fig. 1
Fig. 1
Immuno-pathogenesis of beta cell destruction and type 1 diabetes.
Fig. 2
Fig. 2
The bidirectional dynamic of SARS CoV2 and diabetes.
See this image and copyright information in PMC

References

    1. DIAMOND Project Group Incidence and trends of childhood type 1 diabetes worldwide 1990–1999. Diabet Med. 2006;23:857–866. doi: 10.1111/j.1464-5491.2006.01925.x. - DOI - PubMed
    1. Docherty A.B., Harrison E.M., Green C.A. medRxiv; 2020. Features of 16,749 hospitalised UK patients with COVID-19 using the ISARIC WHO clinical characterisation protocol. - DOI - PMC - PubMed
    1. Chee Y.J., Ng S.J.H., Yeoh E. Diabetic ketoacidosis precipitated by Covid-19 in a patient with newly diagnosed diabetes mellitus. Diabetes Res Clin Pract. 2020;164:108166. doi: 10.1016/j.diabres.2020.108166. - DOI - PMC - PubMed
    1. Sardu C., D’Onofrio N., Balestrieri M.L. Outcomes in patients with hyperglycemia affected by COVID-19: can we do more on glycemic control? Diabetes Care. 2020;43(7):1408–1415. doi: 10.2337/dc20-0723. - DOI - PMC - PubMed
    1. Li J., Wang X., Chen J., Zuo X., Zhang H., Deng A. COVID-19 infection may cause ketosis and ketoacidosis. Diabetes Obes Metabol. 2020 doi: 10.1111/dom.14057. 10.1111/dom.14057. - DOI - PMC - PubMed

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