Abstract
The SARS-CoV-2 virus is the pathogenic agent of the COVID-19 disease, which pandemic had caused 6.8 million deaths worldwide by February 2023. In the course of the disease, involvement of the thyroid gland is observed. The pathomechanism of damage to the thyroid gland is bidirectional – direct cytotoxicity of the virus and the indirect effect of a cytokine storm. Circulating pro-inflammatory cytokines lead to deiodinase activity dysregulation, resulting in changes in plasma concentrations of TSH, fT3, and fT4. These hormone abnormalities are observed in about 16% of patients during COVID-19 and may also result from the treatment itself – systemic corticosteroids. Dysregulation of the immune system also leads to autoinflammatory thyroid diseases. It seems crucial to monitor thyroid hormones to detect subclinical forms of thyroiditis early. This paper presents the prevalence and potential pathomechanism of thyroid disorders observed during SARS-CoV-2 infection – subacute thyroiditis, low T3 syndrome, Graves-Basedow disease, and Hashimoto’s disease.
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