Mehta, A.Awuah, W.A.Yarlagadda, R.Kalmanovich, J.Huang, H.Kundu, M.Nansubuga, E.P.Lopes, L.Ghosh, B.Hasan, M.M.2025-04-012025-04-012022Mehta, Aashna; Awuah, Wireko Andrew; Yarlagadda, Rohan; Kalmanovich, Jacob; Huang, Helen; Kundu, Mrinmoy; Nansubuga, Esther Patience; Lopes, Leilani; Ghosh, Bikona; Hasan, Mohammad Mehedi. Investigating thyroid dysfunction in the context of COVID-19 infection. Annals of Medicine & Surgery 84():, December 2022. | DOI: 10.1016/j.amsu.2022.104806.https://essuir.sumdu.edu.ua/handle/123456789/98680COVID-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.enCC BY 4.0Covid-19thyroid dysfunctioninfectionArticle