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Review
. 2023 Jul;37(4):101759.
doi: 10.1016/j.beem.2023.101759. Epub 2023 Mar 3.

COVID-19 vaccination and thyroiditis

Süleyman Nahit Şendur  1 , Seda Hanife Oğuz  1 , Uğur Ünlütürk  2
Affiliations
Review

COVID-19 vaccination and thyroiditis

Süleyman Nahit Şendur et al. Best Pract Res Clin Endocrinol Metab. 2023 Jul.

Abstract

At the end of 2019, the world began to fight the coronavirus disease 2019 (COVID-19) pandemic caused by the severe acute respiratory syndrome coronavirus-2. Many vaccines have quickly been developed to control the epidemic, and with the widespread use of vaccines globally, several vaccine-related adverse events have been reported. This review mainly focused on COVID-19 vaccination-associated thyroiditis and summarized the current evidence regarding vaccine-induced subacute thyroiditis, silent thyroiditis, Graves' disease, and Graves' orbitopathy. The main clinical characteristics of each specific disease were outlined, and possible pathophysiological mechanisms were discussed. Finally, areas lacking evidence were specified, and a research agenda was proposed.

Keywords: COVID-19; Graves’ disease; Hashimoto thyroiditis; SARS-CoV-2; painless thyroiditis; subacute thyroiditis; thyroiditis; vaccination; vaccine.

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Conflict of interest statement

Conflict of interest The authors declare no conflict of interest.

Figures

Fig. 1
Fig. 1
Approach to patients with SARS-CoV-2 vaccine-induced SAT.
Fig. 2
Fig. 2
Approach to patients with SARS-CoV-2 vaccine-induced Graves’ disease and Graves’ orbitopathy.
Fig. 3
Fig. 3
Vaccines against SARS-CoV-2 consist of an inactivated whole-virion or encode for the synthesis of viral S protein to induce an immune response. The S protein of SARS-CoV-2 and certain human proteins share a considerable number of peptides, including thyroid peroxidase. As a result of this molecular mimicry, pathogen-specific antibody responses may interact with thyroidal structures following vaccination. Vaccine adjuvants are used to strengthen the immune response and cause higher antibody titers. However, they may trigger autoimmunity in susceptible individuals. Whether adjuvants increase the risk of developing molecular mimicry-related autoimmunity in susceptible subjects by increasing autoantibody production is unclear. Genetic predisposition (e.g., carrying HLA-B*35, HLA-C*04, and maybe HLA-A*11 alleles) appears to be the key in the pathogenesis of SARS-CoV-2 vaccine-induced SAT, since only a small percentage of individuals develop autoimmune disorders after receiving a SARS-CoV-2 vaccine. HLA: human leukocyte antigen, TPO: thyroid peroxidase.
See this image and copyright information in PMC

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