Potential relationships between COVID-19 and the thyroid gland: an update

In this review, I aim to provide a complete overview of recent advances in knowledge regarding severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2)-induced thyroid dysfunction. I discuss the findings regarding the role of SARS-CoV-2 in the development of thyroid dysfunction, including subacute thyroiditis, Graves’ disease, non-thyroidal illness, thyrotoxicosis and Hashimoto’s thyroiditis during and subsequent to coronavirus disease 2019 (COVID-19). The thyroid gland and the entire hypothalamic–pituitary–thyroid (HPT) axis may represent key targets of SARS-CoV-2. Thyroid dysfunction during and subsequent to COVID-19 has been documented in clinical studies and is usually reversible. Most of the thyroid disorders, including Graves’ disease, euthyroid sick syndrome, Hashimoto’s thyroiditis and subacute thyroiditis, have been documented as sequelae to COVID-19, and the SARS-CoV-2 virus has been implicated in the aetiology of each. COVID-19 has been suggested to trigger the activation of pre-existing thyroid disease or autoimmunity. Furthermore, patients with uncontrolled thyrotoxicosis are at risk of SARS-CoV-2 infection-related consequences. Because of the neutropenia caused by antithyroid medications, which may obscure the signs of COVID-19, this group of patients should receive special attention. It is suggested that thyroid dysfunction during COVID-19 is caused by direct infection of the thyroid or “cytokine storm”-mediated autoimmune effects on the thyroid.