Thyroid Dysfunction Associated with SARS-CoV-2 Infection
Summary
Emerging evidence over the course of the COVID-19 pandemic has revealed a complex interplay between SARS-CoV-2 infection and thyroid function. A spectrum of thyroid disorders has been observed in patients with COVID-19, ranging from transient thyrotoxicosis and subacute inflammatory thyroiditis to hypothyroidism and nonthyroidal illness syndrome. Clinical presentations may include anterior neck pain, fever, palpitations and fatigue, but many cases run a painless course, especially in hospitalised individuals. Pathophysiologically, direct viral invasion is facilitated by high expression of angiotensin-converting enzyme 2 and TMPRSS2 in thyroid follicular cells, while systemic immune activation and a pronounced cytokine response further perturb the hypothalamic–pituitary–thyroid axis. Autoimmune phenomena such as Graves’ disease and Hashimoto’s thyroiditis have also been reported after SARS-CoV-2 infection, suggesting a potential breaking of self-tolerance. Although most thyroid dysfunction is self-limiting, a subset of patients progress to persistent hypothyroidism requiring long-term levothyroxine. Recognition of these patterns has global significance for clinicians, underlining the importance of thyroid-function monitoring in acute and convalescent phases of COVID-19 and guiding appropriate management to mitigate cardiovascular and metabolic complications.
Research from Nature Portfolio
No recent Nature Portfolio content available.
Research from all publishers
A systematic review of subacute thyroiditis following COVID-19 consolidated data from dozens of case reports and series, confirming that symptom onset typically occurs several weeks after the initial infection. In most patients, corticosteroid therapy achieved rapid relief, although about a quarter developed transient hypothyroidism. A comprehensive review of coronavirus-related thyroid injury highlighted the dual role of direct viral entry via ACE2 receptors and the systemic “cytokine storm” in inducing both destructive and nonthyroidal illness syndromes. This work also noted adaptations in thyroid-cancer care towards telemedicine during the pandemic. An observational cohort study comparing hospitalised COVID-19 patients with controls found mild reductions in thyrotropin and free thyroxine consistent with nonthyroidal illness; in survivors, thyroid function generally returned to baseline, supporting a reversible stress-related aetiology.
Thyroid Dysfunction Associated with SARS-CoV-2 Infection publication trend
The graph below shows the total number of articles in thyroid dysfunction associated with sars-cov-2 infection across all publications each year (not limited to Nature Index journals).
Technical terms
Subacute thyroiditis: A self-limiting inflammatory disorder of the thyroid often triggered by viral infection, characterised by transient thyrotoxicosis and neck pain.
Autoimmune thyroid disease: Immune-mediated destruction or stimulation of thyroid tissue, including Hashimoto’s thyroiditis and Graves’ disease.
Nonthyroidal illness syndrome: Biochemical thyroid-function alterations in systemic illness without intrinsic thyroid pathology, typically showing low thyroid-hormone levels.
Cytokine storm: An excessive immune-mediated release of pro-inflammatory cytokines that can disrupt multiple endocrine axes.
ACE2 receptor: A cell-surface enzyme that serves as the entry point for SARS-CoV-2, highly expressed in thyroid follicular cells.
References
- COVID-induced thyroid autoimmunity. Best Practice & Research Clinical Endocrinology & Metabolism (2023).
- Subacute thyroiditis following COVID-19: A systematic review. Frontiers in Endocrinology (2023).
- Impact of COVID-19 on the thyroid gland: an update. Reviews in Endocrine and Metabolic Disorders (2020).
- Detection of SARS-COV-2 receptor ACE-2 mRNA in thyroid cells: a clue for COVID-19-related subacute thyroiditis. Journal of Endocrinological Investigation (2020).
- Thyroid Function Before, During, and After COVID-19. The Journal of Clinical Endocrinology & Metabolism (2020).
- The cytokine storm and thyroid hormone changes in COVID-19. Journal of Endocrinological Investigation (2021).
About these summaries
This Nature Research Intelligence Topic summary is created with the cited references and a large language model. We take care to ground generated text with facts, and have systems in place to gain human feedback on the overall quality of the process in line with our AI principles. We strive to create accurate and useful summaries for people unfamiliar with the research topic and that supports this goal. These pages are a beta release and will be updated as we learn how best to help people gain value from a research topic summary.
Turn complex research questions into confident strategic decisions
When you're under pressure to set direction, justify investment, or understand your competitive position, you need more than raw data — you need trusted insights you can act on.
Benchmark your performance against global peers using robust, methodologically sound analysis.
Combine quantitative metrics with qualitative expert insight to uncover strengths, gaps and emerging opportunities.
Gain tailored, decision-ready recommendations aligned to your strategic priorities.
Talk to us to learn more about our data dashboards and bespoke strategy reports.
Grow research skills, confidence and careers with training built for every stage of the research lifecycle.
Developed with Nature Portfolio journal Editors and internationally renowned experts. Discover three ways to learn:
Self-paced, online courses in convenient bite-sized units, covering key skills across scientific writing, publishing, grant writing, data analysis, and more.
Expert trainer-led workshops with hands-on exercises and real-time feedback across core research skills, delivered via interactive group sessions.
Editor-led workshops combining core principles in writing and publishing, personalised 1:1 feedback from Nature Portfolio Editors and hands-on exercises.
Explore course catalogues and workshop agendas, enquire about the options or request institutional pricing.