L Croce1,2,3, D Gangemi4, G Ancona4, F Liboà4, G Bendotti4, L Minelli4, L Chiovato5,6. 1. Unit of Internal Medicine and Endocrinology, Laboratory for Endocrine Disruptors, Istituti Clinici Scientifici Maugeri IRCCS, 27100, Pavia, Italy. 2. PHD Course in Experimental Medicine, University of Pavia, 27100, Pavia, Italy. 3. Department of Internal Medicine and Therapeutics, University of Pavia, Via S. Maugeri 4, 27100, Pavia, Italy. 4. Postgraduate School in Endocrinology and Metabolism, University of Pavia, 27100, Pavia, Italy. 5. Unit of Internal Medicine and Endocrinology, Laboratory for Endocrine Disruptors, Istituti Clinici Scientifici Maugeri IRCCS, 27100, Pavia, Italy. luca.chiovato@icsmaugeri.it. 6. Department of Internal Medicine and Therapeutics, University of Pavia, Via S. Maugeri 4, 27100, Pavia, Italy. luca.chiovato@icsmaugeri.it.
Abstract
BACKGROUND: COVID-19 is now a worldwide pandemic. Among the many extra-pulmonary manifestations of COVID-19, recent evidence suggested a possible occurrence of thyroid dysfunction. PURPOSE: The Aim of the present review is to summarize available studies regarding thyroid function alterations in patients with COVID-19 and to overview the possible physio-pathological explanations. CONCLUSIONS: The repercussions of the thyroid of COVID-19 seem to be related, in part, with the occurrence of a "cytokine storm" that would, in turn, induce a "non-thyroidal illness". Some specific cytokines and chemokines appear to have a direct role on the hypothalamus-pituitary-thyroid axis. On the other hand, some authors have observed an increased incidence of a destructive thyroiditis, either subacute or painless, in patients with COVID-19. The hypothesis of a direct infection of the thyroid by SARS-Cov-2 stems from the observation that its receptor, ACE2, is strongly expressed in thyroid tissue. Lastly, it is highly probable that some pharmaceutical agents largely used for the treatment of COVID-19 can act as confounding factors in the laboratory evaluation of thyroid function parameters.
BACKGROUND:COVID-19 is now a worldwide pandemic. Among the many extra-pulmonary manifestations of COVID-19, recent evidence suggested a possible occurrence of thyroid dysfunction. PURPOSE: The Aim of the present review is to summarize available studies regarding thyroid function alterations in patients with COVID-19 and to overview the possible physio-pathological explanations. CONCLUSIONS: The repercussions of the thyroid of COVID-19 seem to be related, in part, with the occurrence of a "cytokine storm" that would, in turn, induce a "non-thyroidal illness". Some specific cytokines and chemokines appear to have a direct role on the hypothalamus-pituitary-thyroid axis. On the other hand, some authors have observed an increased incidence of a destructive thyroiditis, either subacute or painless, in patients with COVID-19. The hypothesis of a direct infection of the thyroid by SARS-Cov-2 stems from the observation that its receptor, ACE2, is strongly expressed in thyroid tissue. Lastly, it is highly probable that some pharmaceutical agents largely used for the treatment of COVID-19 can act as confounding factors in the laboratory evaluation of thyroid function parameters.
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