COVID-19 pathophysiology and diabetes mellitus
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Keywords

diabetes
Pathophysiology
Covid-19
SARSCoV-2

How to Cite

Luján, D., Guatibonza-García, V., Pérez-Londoño, A., & Mendivil, C. O. (2020). COVID-19 pathophysiology and diabetes mellitus. Revista Endocrino, 7(2S), 67–71. https://doi.org/10.53853/encr.7.2S.586

Abstract

COVID-19, a disease caused by the coronavirus agent SARSCoV-2, is the current pandemic about which we know very little from the biologic and pathologic perspective, and whose prognosis is darkened by the coexistence of diabetes mellitus (DM). With this motivation, we undertook a bibliographic search about the characteristics of COVID-19 pathophysiology in patients with DM. The evidence revealed that persons with DM have alterations in neutrophil chemotaxis, production of proinflammatory cytokines, phagocytosis and activation of T lymphocytes, which jointly compromise the ability to respond against any pathogen, SARS-CoV-2 included. In addition, advanced glycation end products alter the affinity and opsonizing ability of antibodies. Concerning viruses with respiratory tropism, hyperglycemia favors their proliferation at the affected tissue. SARS-CoV-2 enters cells using its S (Spike) protein, which binds angiotensin-converting enzyme type 2 (ACE2) in the host cell membrane. ACE2 is a transmembrane glycoprotein expressed not only in respiratory epithelium but also in myocardium and pancreatic islets. Hyperglycemia increases the expression of ACE2 in the cell membrane, raising the risk of infection in case the cell enters in contact with the virus. Moreover, epithelial cells from individuals with DM express higher levels of furin, a protease that cleaves the S protein and accelerates viral fusion and entry, favoring the spread of infection and the more severe clinical picture that is observed in practice. There is also evidence that persons with DM who also take ACE inhibitors or angiotensin receptor blockers express more ACE2 in their epithelium. Thus, patients with DM face a harmful combination of increased contagion risk and deregulated humoral and cellular immunity, which leads to a more severe and lethal form of COVID-19.

https://doi.org/10.53853/encr.7.2S.586
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