COVID-19 may trigger Graves’ disease relapse, subacute thyro
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Approximately 15% of patients with mild to moderate COVID-19 have thyroid dysfunction, and SARS-CoV-2 may directly affect thyroid morphology and function, worsening preexisting autoimmune thyroid disease, data from a review show.

COVID-19, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which has become the most lethal and rapidly-moving pandemic since the Spanish influenza of 1918-1920, is associated with thyroid diseases.

References were identified through searches of PubMed and MEDLINE for articles published by use of the MeSH terms “hypothyroidism”, “hyperthyroidism”, “thyroiditis”, “thyroid cancer”, “thyroid disease”, in combination with the terms “coronavirus” and “COVID-19”.

-- Though pre-existing autoimmune thyroid disease appears unlikely to render patients more vulnerable to COVID-19, some reports have documented relapse of Graves’ disease (GD) or newly diagnosed GD about 1 month following SARS-CoV-2 infection.

-- Investigations are ongoing to investigate molecular pathways permitting the virus to trigger GD or cause subacute thyroiditis (SAT). While COVID-19 is associated with non-thyroidal illness, it is not clear whether it also increases the risk of developing autoimmune hypothyroidism.

-- The possibility that thyroid dysfunction may also increase susceptibility for COVID-19 infection deserves further investigation.

-- Recent data illustrate the importance of thyroid hormone in protecting the lungs from injury, including that associated with COVID-19.

Conclusively, the interaction between the thyroid gland and COVID-19 is complex and bidirectional. COVID-19 infection is associated with triggering of GD and SAT, and possibly hypothyroidism. Until more is understood regarding the impact of coronavirus on the thyroid gland, it seems advisable to monitor patients with COVID-19 for new thyroid disease or progression of pre-existing thyroid disease.