![]() The viruses rapidly spread across China and then all over the world, so on March 11 th 2020, World Health Organization (WHO) declared that COVID-19 reached pandemic levels. The genetic material of the virus was rapidly sequenced ( 2), and the transmission could not be prevented. On January, the virus responsible for the pneumonia was identified as a new coronavirus, later named severe acute respiratory syndrome coronavirus 2, SARS-CoV-2, and the disease was named coronavirus disease 2019 (COVID-19) ( 1). In December, 2019, a pneumonia of unknown origin emerged in Wuhan, China. Thus, future studies are needed to better investigate the pathophysiology of thyroid dysfunction induced by COVID-19 at both molecular and clinical levels. Although the cellular and molecular mechanisms are not completely understood, the evidence suggests that the “cytokine storm” is an important mediator in this context. Overall, the data revealed that abnormal thyroid function may occur during and in the convalescence post-COVID condition phase. In addition, thyroid disease has already been reported as a consequence of the administration of vaccines against SARS-CoV-2. Indeed, a variety of thyroid disorders have been documented in COVID-19 patients, including non-thyroidal illness syndrome (NTIS), subacute thyroiditis and thyrotoxicosis. On the other hand, retrospective observational studies, prospective studies, and case reports published in the last two years reported abnormal thyroid function related to acute SARS-CoV-2 infection or even several weeks after its resolution. However, studies show that patients with controlled hypothyroidism and hyperthyroidism do not have a higher prevalence of COVID-19, nor do they have a worse prognosis when infected with the virus. Immune system cells are targets for thyroid hormones and T3 and T4 modulate specific immune responses, including cell-mediated immunity, natural killer cell activity, the antiviral action of interferon (IFN) and proliferation of T- and B-lymphocytes. In addition, thyroid gland is extremely sensitive to changes in body homeostasis and metabolism. Thyroid gland, as well as hypothalamus and pituitary, which regulate the functioning of most endocrine glands, express angiotensin-converting enzyme 2 (ACE2), the main protein that functions as a receptor to which SARS-CoV-2 binds to enter host cells. Despite being considered a respiratory disease, it is known that other organs and systems can be affected in COVID-19, including the thyroid gland. COVID-19 is a respiratory syndrome that can progress to acute respiratory distress syndrome, multiorgan dysfunction, and eventually death. 4Department of Biorregulation, Health Sciences Institute, Universidade Federal da Bahia, Salvador, BrazilĬoronavirus disease 2019 (COVID-19) was characterized as a pandemic in March, 2020 by the World Health Organization.3Campus Duque de Caxias Professor Geraldo Cidade, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.2Postgraduate Program in Nutritional Sciences, Department of Nutrition, Center for Health Sciences, Universidade Federal da Paraíba, João Pessoa, Brazil.1Institute of Biophysics Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.Camila Lüdke Rossetti 1† Juliana Cazarin 1† Fabio Hecht 1† Fabyan Esberard de Lima Beltrão 2 Andrea Cláudia Freitas Ferreira 1,3 Rodrigo Soares Fortunato 1 Helton Estrela Ramos 4* Denise Pires de Carvalho 1
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