"My symptoms have worsened since I had COVID", "I developed Hashimotos after getting the vaccine", "My well-managed thyroid is now out of control since I had the virus" - this is what I have been hearing in clinic on a weekly basis.
There is now a lot of scientific data to back up the strong impact that COVID has on the thyroid gland, and the data is of major concern.
We need healthy thyroid function to have strong immune system in the first place. We also know that heightened immune system occurs due to and has a direct impact on a cascade of inflammatory cytokines that up or down-regulate hormones, including the hormones of the thyroid gland. Furthermore, we know see how various viruses "mimic" the communication of the human body cells, "tricking" the body into acting the way that is beneficial to the virus.
Here are some of the pathways that have been established on how SARS-CoV-2, the virus responsible for COVID-19, triggers an autoimmune thyroiditis:
1.Molecular Mimicry - is a major mechanism for triggering autoimmune responses, where foreign substances such as viruses resemble self-peptides, activating autoimmune cells inside the human body. Your immune system works to attack and destroy pathogens. Virus creates specific proteins that mimic your own cells, which makes the immune system "confused" and triggers it to attack its own organs and tissues.
2. Thyroid has receptors for COVID - once inside the host the SARS-CoV-2 virus expresses angiotensin-converting enzyme 2 (ACE2), a protein that allows the virus to stick to host cells. Turns out that the thyroid gland is particularly rich in ACE2 receptors, which "invite" the virus into the tissue in great quantities. This leads to a significant number of viral markers in the thyroid gland that the immune system will attempt to destroy, destroying the thyroid tissue in the process.
3. Inflammatory Cytokines - Upon viral infection, the body's immune cells release cytokines as part of the innate immune defense mechanism. This release is triggered by the recognition of viral components by pattern recognition receptors (PRRs) on immune cells, activating signaling pathways that lead to cytokine production. Scientific evidence suggests that excessive cytokine production, known as a "cytokine storm," can contribute to thyroid dysfunction by preventing the thyroid from producing adequate number of hormones, or in rare cases, overproduce these hormones. This hypo and hyper thyroid.
Based on these findings we now understand that COVID infection can either directly communicate with the immune system, attach to thyroid cells in great quantities or cause an inflammatory storm, leading to the exacerbation of pre-existing thyroid disease, or be a trigger of a completely new condition to the individual.
In most scientific analysis we see that the production of T3 (the active thyroid hormone) has been greatly reduced, and an increase in anti-TPG, anti-TG and TRABS - thyroid related autoimmune markers. This dysregulation may result in conditions such as subacute thyroiditis, Graves' disease, and Hashimoto's thyroiditis.
References:
Tutal, E., Ozaras, R., & Leblebicioglu, H. (2022, March 18). Systematic review of COVID-19 and autoimmune thyroiditis.
Rotondi, M., Coperchini, F., Ricci, G., Denegri, M., Croce, L., Ngnitejeu, S. T., Villani, L., Magri, F., Latrofa, F., & Chiovato, L. (2020, October 6). Detection of SARS-COV-2 receptor ACE-2 mRNA in thyroid cells: a clue for COVID-19-related subacute thyroiditis.
Knack, R. S., Hanada, T., Knack, R. S., & Mayr, K. (2021, August 9). Hashimoto's thyroiditis following SARS-CoV-2 infection. Journal of Autoimmunity, 14(8), e244909.
Naguib, R. (2022, February). Potential relationships between COVID-19 and the thyroid gland: an update.
[Journal of Translational Autoimmunity]. (2023, December). SARS-CoV-2 and thyroid diseases. Journal of Translational Autoimmunity, 7, 100214. doi: 10.1016/j.jtauto.2023.100214
[Journal of Clinical and Translational Endocrinology: Case Reports]. (2021, December). Manifestations of thyroid disease post COVID-19 illness: Report of Hashimoto thyroiditis, Graves’ disease, and subacute thyroiditis.
Rojas, M., Restrepo-Jiménez, P., Monsalve, D. M., Pacheco, Y., Acosta-Ampudia, Y., RamÃrez-Santana, C., Leung, P. S. C., Ansari, A. A., Gershwin, M. E., & Anaya, J. M. (2018, December). Molecular mimicry and autoimmunity. Journal of Autoimmunity, 95, 100-123. doi: 10.1016/j.jaut.2018.10.012
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