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ABSTRACT
Introduction: During the COVID-19 pandemic thyroid gland alteration/dysfunction has been emerged as a possible endocrine complication. The present review is focused on inflammatory and autoimmune thyroid complications triggered by SARS-CoV-2 infection by searching through databases like MEDLINE and Scopus up to April 2021.
Areas covered: Beside the occurrence of ‘non-thyroidal illness’ in severe clinical conditions, alterations of thyroid function and structure may occur during COVID-19 as a consequence of either direct or indirect effects of SARS-CoV-2 infection on the gland. On the one hand, SARS-CoV-2 uses ACE2 as a receptor to infect the host cells and ACE2 is highly expressed by follicular thyroid cells. On the other hand, COVID-19 is associated with a systemic inflammatory and immune response, involving Th1/Th17/Th2 lymphocytes and proinflammatory cytokines, which resembles the immune activation that occurs in immune-mediated thyroid diseases. COVID-19-related thyroid disorders include destructive thyroiditis and onset or relapse of autoimmune thyroid disorders, leading to a broad spectrum of thyroid dysfunction ranging from thyrotoxicosis to hypothyroidism, that may worsen COVID-19 clinical course and affect prognosis.
Expert opinion: Physicians should be aware of the possible occurrence of thyroid dysfunction during and after SARS-CoV-2 infection. Further longitudinal studies are warranted to evaluate potential long-term sequelae.
Article highlights
SARS-CoV-2 infectious promotes the release of several pro-inflammatory cytokines (IL-1β, IL-6, TNFα, and IFN-γ being the key pathogenic ones), leading to immune response hyperactivity and uncontrolled systemic inflammatory response, the so-called ‘cytokine storm’.
Enhanced Th1/Th17 immune responses and cytokine pathways involved in SARS-CoV2 infectious resemble, at least in part, the immune activation that occurs in immune-mediated thyroid diseases.
Thyroid function test alterations are quite common in the course of COVID-19 as a consequence of either non-thyroidal-illness or thyroidal gland involvement in the context of hypercytokinemia, as a consequence of hyperinflammatory response (subacute thyroiditis) or T-lymphocyte triggered autoimmunity (painless thyroiditis).
Thyroid inflammation/damage may be also the consequence of a direct action of the SARS-CoV-2 virus on thyroid cells through ACE2 receptor.
Excessive cytokine production and immune system dysregulation may favor the development/relapse of autoimmune disorders in genetically susceptible individuals. Future researches would investigate the intriguing connections and mutual relationships between SARS-CoV-2 and thyroid autoimmunity and the potential long-term increase of autoimmune thyroid disease after the COVID-19 outbreak.
Declaration of interest
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewers disclosure
Peer reviewers on this manuscript have no relevant financial relationships or otherwise to disclose.
Author agreement
All authors have seen and approved the final version of the manuscript and warrant that the article is the authors’ original work, has not received prior publication and is not under consideration for publication elsewhere.