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. 2020 Mar 26;139:109699. doi: 10.1016/j.mehy.2020.109699

Hyperglycemia and the novel Covid-19 infection: Possible pathophysiologic mechanisms

Ioannis Ilias 1, Lina Zabuliene 2
PMCID: PMC7203506  PMID: 32240876

Acutely ill patients present often with hyperglycemia (caused among other factors by endogenous stress-induced glucocorticoid hypersecretion) [1]. In preliminary reports, presenting clinical characteristics of patients with the novel Covid-19 infection, hyperglycemia was noted in 51% of cases [2]. Interestingly, transient hyperglycemia was also noted in patients with SARS (Severe Acute Respiratory Syndrome in 2003, caused by another coronavirus, closely related to Covid-19, SARS-CoV) [3]; the virus leads to transient impairment of pancreatic islet cell function [3]. Additionally, the also closely related, Middle Eastern Respiratory Syndrome (MERS in 2013) coronavirus (MERS-CoV) as well as human coronavirus-EMC are anchored to host cells via dipeptidyl peptidase 4 (DPP-4, which physiologically is implicated in the modulation of insulin action and as an enzyme plays a major role in glucose metabolism and is responsible for the degradation of incretins such as glucagon like peptide −1, GLP-1) [4], [5]. Thus, we believe that the hyperglycemia noted in patients with Covid-19 may be caused via such (or analogous) mechanisms; this remains to be assessed by ulterior studies. Nevertheless, the issue of hyperglycemia should not be overlooked, since it may lead to additional immune suppression and further complications [6].

Declaration of Competing Interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

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