COVID-19 Impact: Thyroid Complications and Risks Revealed

The impact of the coronavirus disease 2019 (COVID-19) pandemic has been profound, affecting individuals in various ways. Among the evolving consequences of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are endocrine complications, including thyroid disorders. The entry of SARS-CoV-2 into cells primarily occurs through the angiotensin-converting enzyme 2 (ACE2) receptor, which is also present in the thyroid gland, making it susceptible to viral invasion and potential damage.

Reports have emerged linking COVID-19 to thyroid dysfunction, such as subacute thyroiditis (SAT) and autoimmune thyroid diseases. The expression of ACE2 and other host proteases in thyroid follicular cells enables SARS-CoV-2 invasion, increasing the vulnerability of the thyroid to viral-related injuries. The development of autoimmunity following COVID-19 may lead to thyroiditis, hypothyroidism, or hyperthyroidism. Various studies have highlighted the incidence of thyroid dysfunction post-COVID-19, with differences observed among countries, potentially influenced by population characteristics, infection severity, and treatment interventions.

Thyroiditis, including SAT, painless thyroiditis, and autoimmune thyroiditis, has been reported following acute SARS-CoV-2 infection. While some studies suggest an increased incidence of SAT during the pandemic, others have found no significant rise. Autoimmune thyroid diseases, such as Graves’ disease and Hashimoto’s thyroiditis, have also been linked to COVID-19, with reports of orbitopathy, thyrotoxic periodic paralysis, and thyroid storm post-infection.

Pre-existing thyroid conditions, particularly hypothyroidism, have been associated with worse COVID-19 outcomes in some studies. However, conflicting data exist regarding the impact of thyroid disorders on the severity and prognosis of COVID-19. Thyroid function testing has shown promise in predicting illness severity and mortality risk in hospitalized COVID-19 patients.

The pathophysiological mechanisms underlying thyroid dysfunction post-CO