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Severe Acute Respiratory Syndrome Coronavirus-2 Infection and New Changes in Thyroid Function Parameters During
Francisca Leitão Henriques1, Catarina Pestana Santos2, Ana Quítalo1
1ULS Almada-Seixal, Endocrinology, Portugal, Almada.
Abstract:
Severe acute respiratory syndrome coronavirus-2 infection is a systemic disease associated with metabolic and hormonal disturbances, including thyroid dysfunction such as primary hypothyroidism, subacute thyroiditis, and non-thyroidal illness syndrome. This study aimed to investigate the association between severe acute respiratory syndrome coronavirus-2 infection and changes in thyroid function during hospitalization and follow-up and evaluate whether these alterations are related to disease severity. We retrospectively analyzed a random cohort of 500 patients admitted to the Medicine Department of a central hospital between March 2020 and 2022. After excluding deaths, prior thyroid disease, and cases without thyroid evaluation, 218 patients were included. Serum thyroid-stimulating hormone, free triiodothyronine and free thyroxine values were measured at admission and after hospitalization. Patients were classified as having thyrotoxicosis, hypothyroidism, isolated hypothyroxinemia, and non-thyroidal illness syndrome. Thyroid dysfunction was defined by compatible biochemical findings with serological and/or imaging evidence of thyroid pathology and/or the need for therapy. COVID-19 cases were grouped by severity. Non-thyroidal illness syndrome was the most frequent abnormality, followed by isolated hypothyroxinemia and primary hypothyroidism. Non-thyroidal illness syndrome was more common in severe cases of COVID-19, although no statistically significant association was found between disease severity and type of thyroid abnormality. Most reassessed patients showed normalization of thyroid function during follow-up. The small sample size may have limited statistical power. Thyroid function alterations are common in severe acute respiratory syndrome coronavirus-2 infection, transient, and more frequent in severe disease. These findings suggest an adaptive response to systemic stress and inflammation. Larger prospective studies are needed to clarify evolution and clinical impact.
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