The Link Between COVID & Autoimmune Thyroid Disease
As more data emerges relating to the ongoing health effects of COVID-19, of relevance is the link between the virus and the onset of autoimmune thyroid disease, including Hashimoto’s and Graves.
This two-way interplay between the endocrine and immune systems cannot be denied, particularly as thyroid status could have a direct effect on the course and severity of illness in individuals contracting the virus. Viral infections are known to interact with the thyroid gland through immunomodulatory signalling molecules and of course thyroid hormones. As we know in autoimmunity, the heightened immune response and inflammatory cascade triggered from a variety of factors, including viruses, will initially impact the hypothalamic-pituitary-thyroid (HPT) axis and consequently thyroid function overtime.
So, why might the thyroid gland be more vulnerable to this particular virus?
To break it down a little further, there are some brief technical parts to cover.
COVID-19 is caused by severe acute coronavirus 2 (SARS-CoV-2)
It has been established that angiotensin-converting enzyme-2 (ACE2) is the host receptor in the body for SARS-CoV-2
ACE2 is found in various cells in different organs, including the thyroid gland
With this understanding, thyroid health and function can be affected by COVID-19 either indirectly through any abnormal immune regulation, or directly through the viral infection targeting cells within the endocrine system.
Coinciding with this is the number of pathologies that have emerged and been associated after individual contact with the virus, with many being autoimmune in nature. One study evaluating the thyroid status in 287 patients in non-intensive care unit, showed that COVID-19 cases presented with overt (10.8%) and subclinical (14.6%) thyrotoxicosis (excess circulating thyroid hormones). Without additional data, it can be considered that thyrotoxicosis in these patients may be an initial trigger to the development of an autoimmune thyroid condition.
Additional studies have shown that concentrations of the thyroid hormones TSH and T3 were considerably lower in patients with COVID-19, and that SARS-Cov-2 has a notable effect on TSH-secreting cells and may disrupt numerous pituitary-endocrine feedback loops, not only the HPT-axis.
Whether autoimmune thyroid disease precedes or is consequently triggered by SARS-CoV-2 infection is the question surrounding a lot of the current data. On an individual case basis however, this is something that is certainly being explored and investigated clinically between practitioners and their patients. It is clearly acknowledged that thyroid function can be impacted during the acute phase of infection, yet it is during convalescence that the underlying impacts of COVID-19 on thyroid function and autoimmune disease states need to be explored in greater depth particularly in those that may have a new onset of symptoms, or may have an exacerbation or worsening of their Graves and Hashimoto’s related symptoms.
References:
Naguib R. Potential relationships between COVID-19 and the thyroid gland: an update. Journal of International Medical Research. 2022;50(2). doi:10.1177/03000605221082898
Knack RS, Hanada T, Knack RS, et alHashimoto’s thyroiditis following SARS-CoV-2 infectionBMJ Case Reports CP 2021;14:e244909.
Rotondi M, Coperchini F, Ricci G, et al. Detection of SARS-COV-2 receptor ACE-2 mRNA in thyroid cells: a clue for COVID-19-related subacute thyroiditis. J Endocrinol Invest. 2021;44(5):1085-1090. doi:10.1007/s40618-020-01436-w
Tutal E, Ozaras R, Leblebicioglu H. Systematic review of COVID-19 and autoimmune thyroiditis. Travel Med Infect Dis. 2022;47:102314. doi:10.1016/j.tmaid.2022.102314