Abstract / Summary
Background: Increasing evidence suggests that COVID-19 can induce or exacerbate autoimmune disorders, including immune-mediated thyroid dysfunction. The most common autoimmune thyroid diseases are Graves' disease and Hashimoto's thyroiditis; the mechanisms by which viral infections like SARS-CoV-2 trigger these diseases are not fully understood. Objectives: This study aims to systematically review published clinical evidence on the presentation, laboratory characteristics, and outcomes of autoimmune thyroid diseases after COVID-19 infection. Methods: The review followed the PRISMA 2020 framework. Scopus, Web of Science, and PubMed were searched for English-language studies between January 2020 and December 2025 using the terms COVID-19, SARS-CoV-2, autoimmune thyroiditis, Graves' disease, Hashimoto's thyroiditis, and autoimmune thyroid disease. Results: In total, 46 studies (five cohort studies and 41 case reports/series) involving 3856 patients were analyzed. The findings indicate that a significant increase in TPOAb prevalence occurs post-COVID-19 infection (15.7% vs. 7.7% in controls). New-onset Graves' disease (GD) post-COVID-19 presented with higher fT3/fT4 ratios and more aggressive thyrotoxicosis compared to non-viral cases. Rare but severe manifestations included thyrotoxic periodic paralysis, Hashimoto's encephalopathy, and dilated cardiomyopathy. Conclusions: SARS-CoV-2 may act as a trigger for autoimmune thyroid diseases, particularly in moderate-to-severe infections; however, the strength of this association warrants further investigation with controlled prospective data. Standard therapy remains effective, but thyroid function monitoring is advisable during post-COVID-19 recovery. An interdisciplinary approach is essential for early diagnosis and management of systemic complications.
Primary Source
International journal of environmental research and public health
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