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Published on: November 5, 2021
The Influence of SARS-CoV-2 Infection on the Thyroid Gland
Aleksandra Piekarska1, Marta Góral1, Marta Kozula1
1Department of Endocrinology, Diabetes and Isotope Therapy, Students Research Association, Wroclaw Medical University, Pasteura Bank 4, 50-367 Wroclaw, Poland.
Abstract:
It is important to acknowledge the impact that COVID-19 has on the thyroid gland and how the thyroid gland status before and during infection affects SARS-CoV-2 severity. To this day those dependencies are not fully understood. It is known that the virus uses angiotensin-converting enzyme-2 as the receptor for cellular entry and it can lead to multiple organ failures due to a cytokine storm. Levels of proinflammatory molecules (such as cytokines and chemokines) which are commonly elevated during infection were significantly higher in observed SARS-CoV-2-positive patients. In terms of hypothyroidism, hyperthyroidism, and autoimmune thyroid diseases, there is no proof that those dysfunctions have a direct impact on the more severe courses of COVID-19. Regarding hyper- and hypothyroidism there was no consequential dependency between the frequency of SARS-CoV-2 infection morbidity and more severe post-infectious complications. When it comes to autoimmune thyroid diseases, more evaluation has to be performed due to the unclear relation with the level of antibodies commonly checked in those illnesses and its binding with the mentioned before virus. Nonetheless, based on analyzed works we found that COVID-19 can trigger the immune system and cause its hyperactivity, sometimes leading to the new onset of autoimmune disorders. We also noticed more acute SARS-CoV-2 courses in patients with mainly reduced free triiodothyronine serum levels, which in the future, might be used as a mortality indicating factor regarding SARS-CoV-2-positive patients. Considering subacute thyroiditis (SAT), no statistically important data proving its direct correlation with COVID-19 infection has been found. Nevertheless, taking into account the fact that SAT is triggered by respiratory tract viral infections, it might be that SARS-CoV-2 can cause it too. There are many heterogenous figures in the symptoms, annual morbidity distribution, and frequency of new cases, so this topic requires further evaluation.
Insights
COVID-19
Area of Science:
- Endocrinology
- Infectious Diseases
- Immunology
Background:
- The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) utilizes angiotensin-converting enzyme-2 (ACE2) for cellular entry, potentially causing multi-organ failure via cytokine storms.
- Proinflammatory molecules like cytokines and chemokines are elevated in SARS-CoV-2 patients, indicating a significant inflammatory response.
Purpose of the Study:
- To investigate the impact of COVID-19 on thyroid gland function and assess how pre-existing thyroid conditions influence SARS-CoV-2 severity.
- To explore the relationship between thyroid status and COVID-19 outcomes, including mortality and autoimmune responses.
Main Methods:
- Review and analysis of existing literature on COVID-19 and its effects on the thyroid gland.
- Examination of data concerning hypothyroidism, hyperthyroidism, autoimmune thyroid diseases, and subacute thyroiditis in relation to SARS-CoV-2 infection.
Main Results:
- No definitive proof links hypothyroidism, hyperthyroidism, or autoimmune thyroid diseases to more severe COVID-19 courses.
- Reduced free triiodothyronine serum levels in SARS-CoV-2 patients may indicate higher mortality risk.
- COVID-19 can potentially trigger immune hyperactivity, leading to new-onset autoimmune disorders and possibly subacute thyroiditis.
Conclusions:
- While established thyroid dysfunctions do not appear to directly worsen COVID-19 severity, SARS-CoV-2 infection can impact thyroid health and immune responses.
- Further research is needed to fully understand the complex interplay between SARS-CoV-2, thyroid disorders, and autoimmune conditions.
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