Endocrine Abstracts

Introduction

Coronavirus disease (COVID-19) caused by SARS-CoV-2 infection, resulted in serious respiratory and other systemic complications, has spread worldwide since December 2019. In patients with the infection, many organ systems can be involved with potentially fatal results due to robust and disorganized systematic immune activation.

The state of the art

Since the outbreak of the SARS-CoV-2 pandemic, many reports of autoimmune diseases related to COVID-19, have been revealed. Regarding thyroid disease, the occurrence of Graves’ disease, Hashimoto’s and postpartum thyroiditis after the viral infection, has been reported. SARS-CoV-2 could act as a trigger of latent or new-onset autoimmunity. Moreover, the molecular mimicry of the viral and thyroid epitope relating to the presentation on HLA molecule, might be a possible mechanism for post-COVID-19 subacute thyroiditis. It has been indicated that antibodies against SARS-CoV-2 spike protein strongly react with thyroid peroxidase and may play also a role in initiating the autoimmune responses. Induction of inappropriate apoptotic reactions seems to be other common features of the virus-induced disease processes. What is more, it has been proven that thyroid gland shows higher expression of the angiotensin-converting enzyme 2 (ACE 2) cell receptors (the main receptors for SARS-CoV-2 acting) compared with the lungs. Thus, the direct cell damage in the thyroid gland may occur and the possibility of thyroiditis may arise. However, during the SARS-CoV 2002 outbreak, the absence of SARS-CoV per se in the damaged thyrocytes in autopsy patients’ material, was strongly indicative of exaggerated innate and adaptive immune responses to COVID-19 (cytokine storm), as a main mechanism leading to damage of tissues and destructive thyroiditis. On the other hand, thyroid hormone abnormalities seem to be associated with an enhanced risk of severe SARS-CoV-2 infection. Thyroid hormones are important in the regulation of innate immune response so their excess or deficiency may lead to its dysregulation. What is more, increased levels of proinflammatory cytokines such as TNF-a and IL-6, were observed in patients with thyroid diseases as well as in ones with severe COVID-19. Moreover, some patients with subacute thyroiditis use corticosteroids – the drugs which have been proven to be associated with higher mortality in COVID-19 patients.

Conclusions

SARS-CoV-2 infection may be associated with the development of thyroid diseases. The several mechanisms have been proposed of thyroid organ damage from the immune overreaction to direct cellular destruction with apoptosis. The presence of thyroid dysfunction may lead to deterioration of the course of COVID-19.