On the other hand, in a study undertaken in China of 50 patients with COVID-19, Chen et al ( 8) observed a generalized reduction in TSH, total thyroxine (T4), and tri-iodothyronine (T3) more consistent with a nonthyroidal illness pattern.Īlthough these studies provide useful information, they do have limitations. Subacute thyroiditis presenting with overt thyrotoxicosis has been reported with COVID-19 ( 5-7). Currently there is contradictory evidence surrounding the effect of COVID-19 on thyroid function. Thus, the hypothalamic-pituitary-thyroid axis may be susceptible to disturbance in patients with COVID-19. Furthermore, SARS-CoV-2 enters cells using the angiotensin-converting enzyme 2 (ACE2) receptor, which is highly expressed in the thyroid gland ( 4). Additionally, coronaviruses have been detected in the pituitary gland post mortem ( 2), and reduced staining for thyrotropin (TSH) has been observed in the anterior pituitary gland of patients infected with SARS-CoV ( 3). In patients infected with SARS-CoV, a related coronavirus to SARS-CoV-2, damage to the follicular and parafollicular cells of the thyroid was demonstrated at post-mortem ( 1). Coronaviruses are known to have direct effects on several endocrine glands, including the thyroid gland. The coronavirus disease 2019 (COVID-19) pandemic continues to affect the global community, and as understanding of its pathophysiology deepens, so too does interest in the endocrine effects of its causative coronavirus, SARS-CoV-2.