COVID-19 and thyroid function: What do we know so far?

Abstract

Coronavirus disease 2019 (COVID-19) was characterized as a pandemic in March, 2020 by the World Health Organization. COVID-19 is a respiratory syndrome that can progress to acute respiratory distress syndrome, multiorgan dysfunction, and eventually death. Despite being considered a respiratory disease, it is known that other organs and systems can be affected in COVID-19, including the thyroid gland. Thyroid gland, as well as hypothalamus and pituitary, which regulate the functioning of most endocrine glands, express angiotensin-converting enzyme 2 (ACE2), the main protein that functions as a receptor to which SARS-CoV-2 binds to enter host cells. In addition, thyroid gland is extremely sensitive to changes in body homeostasis and metabolism. Immune system cells are targets for thyroid hormones and T3 and T4 modulate specific immune responses, including cell-mediated immunity, natural killer cell activity, the antiviral action of interferon (IFN) and proliferation of T- and B-lymphocytes. However, studies show that patients with controlled hypothyroidism and hyperthyroidism do not have a higher prevalence of COVID-19, nor do they have a worse prognosis when infected with the virus. On the other hand, retrospective observational studies, prospective studies, and case reports published in the last two years reported abnormal thyroid function related to acute SARS-CoV-2 infection or even several weeks after its resolution. Indeed, a variety of thyroid disorders have been documented in COVID-19 patients, including non-thyroidal illness syndrome (NTIS), subacute thyroiditis and thyrotoxicosis. In addition, thyroid disease has already been reported as a consequence of the administration of vaccines against SARS-CoV-2. Overall, the data revealed that abnormal thyroid function may occur during and in the convalescence post-COVID condition phase. Although the cellular and molecular mechanisms are not completely understood, the evidence suggests that the “cytokine storm” is an important mediator in this context. Thus, future studies are needed to better investigate the pathophysiology of thyroid dysfunction induced by COVID-19 at both molecular and clinical levels.

Post-COVID Syndrome in Adults—An Overview

“…Proposed underlying mechanisms related to the development and manifestation of post-COVID syndrome can include (1) viral persistence upon initial infection of host cells by SARS-CoV-2, (2) cellular damage due persistent hyperinflammation, (3) immunologic aberrations caused by molecular mimicry, epitope spreading, bystander activation, or superantigen, and (4) hemostatic changes, predominantly characterized by coagulation abnormalities [ 23 , 24 , 25 , 26 , 27 , 28 ]. Some of these mechanisms and abnormal or misdirected drivers are displayed in Figure 1 and discussed in more detail below.…”

“…Viral persistence also triggers long-term stimulation of the adaptive immune system, thereby activating autoreactive T lymphocytes through antigen-presenting cells. For example, T cell-mediated abnormalities in post-COVID syndrome can become evident by autoimmune thyroid dysfunction [ 27 ]. Likewise, persistent B cell activation and subsequent production of autoantibodies that are detected in more than 50% of patients with post-COVID condition can induce a variety of autoimmune disorders (e.g., antiphospholipid syndrome, lupus erythematosus, thyroid disease, among others, see Section 5.2.4.1 .)…”

“…Likewise, persistent B cell activation and subsequent production of autoantibodies that are detected in more than 50% of patients with post-COVID condition can induce a variety of autoimmune disorders (e.g., antiphospholipid syndrome, lupus erythematosus, thyroid disease, among others, see Section 5.2.4.1 .) [ 17 , 25 , 26 , 27 , 28 ].…”

SARS-CoV-2 infection and its effects on the endocrine system

“…Future studies will be needed to assess whether this observed increase in the incidence of Graves‘ disease is sustained for a long period of time. Patients with controlled hypothyroidism and hyperthyroidism do not have a higher prevalence of COVID-19, nor do they have a worse prognosis when infected with the virus [92] .…”

“…Furthermore, autoimmune thyroiditis or Graves’ disease has been described [91] . In addition, thyroid disease has been reported as a consequence of the administration of vaccines against SARS-CoV-2 [92] . Future studies will be needed to assess whether this observed increase in the incidence of Graves‘ disease is sustained for a long period of time.…”