COVID and the Development of Autoimmune Thyroid Disease
May 25, 2021
A recent literature review illuminated the association between both relapsing and newly diagnosed thyroid disease, including Grave’s disease, following a COVID-19 infection. Graves’ disease is an autoimmune disease where the immune system attacks the thyroid, causing an overproduction of hormones (hyperthyroidism).
Reports were usually documented one month after a COVID-19 infection. Cases showed that a COVID-19 infection may aggravate autoimmune thyroid disease through the development of a cytokine storm. Read more about cytokine storms, autoimmune disease, and COVID-19 infection in our article that dives into the juxtaposition of both the Sars-CoV-2 virus and autoimmunity.
Data accumulated in the literature review indicates that the thyroid hormone plays a role in protecting the lungs from injury, including injury from COVID-19. Only a small fraction of the literature covers patients developing autoimmune hypothyroidism, and it has yet to be determined if these cases preceded infection or were triggered by it. The literature is also unclear whether COVID-19 definitively increases the risk of developing autoimmune hypothyroidism. That being said, the “known association between COVID-19, the development of cytokine release syndrome, and the triggering of autoimmunity support the hypothesis of COVID-19 triggering autoimmune thyroid disease, including autoimmune hypothyroidism.”
There has been an influx of literature covering patients with Graves’ disease (one type of hyperthyroidism), including how these patients may experience enhanced symptoms of both Graves’ disease and COVID-19. Additionally, around 15% of patients experiencing mild to moderate cases of COVID-19 have experienced thyroid dysfunction.
Researchers from this study are calling out for thyroid function to be routinely assessed when caring for patients with a COVID-19 infection. Further research must be conducted to clarify whether a SARS-CoV-2 infection targeting the thyroid is influenced by patient comorbidities, genetic factors, or disease history.