Investigating thyroid dysfunction in the context of COVID-19 infection.
Journal
Annals of medicine and surgery (2012)
ISSN: 2049-0801
Titre abrégé: Ann Med Surg (Lond)
Pays: England
ID NLM: 101616869
Informations de publication
Date de publication:
Dec 2022
Dec 2022
Historique:
received:
27
08
2022
accepted:
23
10
2022
pubmed:
8
11
2022
medline:
8
11
2022
entrez:
7
11
2022
Statut:
ppublish
Résumé
COVID-19 is a contagious viral infection caused by severe acute respiratory syndrome coronavirus 2 (Sars-CoV-2). One of the key features of COVID-19 infection is inflammation. There is increasing evidence pointing to an association between cytokine storm and autoimmunity. One autoimmune disease of interest in connection to COVID-19 is hyperthyroidism. COVID-19 has been shown to decrease TSH levels and induce thyrotoxicosis, destructive thyroiditis, and de novo Graves' disease. It has also been suggested that the immune response against SARS-CoV-2 antigens following vaccination can cross-react through a mechanism called molecular mimicry which can elicit autoimmune reactivity, potentially leading to potential thyroid disease post vaccine. However, if the COVID-19 vaccine is linked to reduced COVID-19 related serious disease, it could potentially play a protective role against post COVID-19 hyperthyroidism (de novo disease and exacerbations). Further studies investigating the complex interplay between COVID-19 or COVID-19 vaccine and thyroid dysfunction can help provide substantial evidence and potential therapeutic targets that can alter prognosis and improve COVID-19 related outcomes in individuals with or without preexisting thyroid disease.
Identifiants
pubmed: 36339111
doi: 10.1016/j.amsu.2022.104806
pii: S2049-0801(22)01566-7
pmc: PMC9621589
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
104806Informations de copyright
© 2022 Published by Elsevier Ltd on behalf of IJS Publishing Group Ltd.
Déclaration de conflit d'intérêts
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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