ReviewBiomedicines2023
The Influence of SARS-CoV-2 Infection on the Thyroid Gland.
Review in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Post-COVID-19 Thyroid Dysfunction and Autoimmune Ultrasound Changes: A 12-Month Prospective Cohort Study.Medicina (Kaunas, Lithuania) · 2026Article
- Appropriately designed studies are required before valproic acid, carbamazepine, and oxcarbazepine can be blamed for thyroid dysfunction.Revista da Associacao Medica Brasileira (1992) · 2025Article
- Case Report: SARS-CoV-2-associated immune dysfunction manifesting as concurrent fulminant type 1 diabetes mellitus and subacute thyroiditis.Frontiers in medicine · 2025Article
- Comparative analysis of clinical profile, laboratory profile and outcome in COVID-19 patients with and without hypothyroidism.Ghana medical journal · 2024Observational
- Thyroid dysfunction in COVID-19.Nature reviews. Endocrinology · 2024Review
- CT semi-quantitative score used as risk factor for hyponatremia in patients with COVID-19: a cross-sectional study.Frontiers in endocrinology · 2024Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
It is important to acknowledge the impact that COVID-19 has on the thyroid gland and how the thyroid gland status before and during infection affects SARS-CoV-2 severity. To this day those dependencies are not fully understood. It is known that the virus uses angiotensin-converting enzyme-2 as the receptor for cellular entry and it can lead to multiple organ failures due to a cytokine storm. Levels of proinflammatory molecules (such as cytokines and chemokines) which are commonly elevated during infection were significantly higher in observed SARS-CoV-2-positive patients. In terms of hypothyroidism, hyperthyroidism, and autoimmune thyroid diseases, there is no proof that those dysfunctions have a direct impact on the more severe courses of COVID-19. Regarding hyper- and hypothyroidism there was no consequential dependency between the frequency of SARS-CoV-2 infection morbidity and more severe post-infectious complications. When it comes to autoimmune thyroid diseases, more evaluation has to be performed due to the unclear relation with the level of antibodies commonly checked in those illnesses and its binding with the mentioned before virus. Nonetheless, based on analyzed works we found that COVID-19 can trigger the immune system and cause its hyperactivity, sometimes leading to the new onset of autoimmune disorders. We also noticed more acute SARS-CoV-2 courses in patients with mainly reduced free triiodothyronine serum levels, which in the future, might be used as a mortality indicating factor regarding SARS-CoV-2-positive patients. Considering subacute thyroiditis (SAT), no statistically important data proving its direct correlation with COVID-19 infection has been found. Nevertheless, taking into account the fact that SAT is triggered by respiratory tract viral infections, it might be that SARS-CoV-2 can cause it too. There are many heterogenous figures in the symptoms, annual morbidity distribution, and frequency of new cases, so this topic requires further evaluation.
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Registered trials
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