{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T14:17:08Z","timestamp":1784557028026,"version":"3.55.0"},"reference-count":0,"publisher":"Bioscientifica","issue":"10","license":[{"start":{"date-parts":[[2021,10,1]],"date-time":"2021-10-01T00:00:00Z","timestamp":1633046400000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["ec.bioscientifica.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2021,10,1]]},"abstract":"<jats:p>\n                    The hypothalamic\u2013pituitary\u2013thyroid hormone axis might be affected in COVID-19, but existing studies have shown varying results. It has been hypothesized that hyperinflammation, as reflected by the secretion of cytokines, might induce thyroid dysfunction among patients with COVID-19. We explored thyroid hormone involvement in the acute phase of symptomatic COVID-19 and its possible associations with cytokine levels and mortality risk. This was a single-center study of 116 consecutive patients hospitalized for moderate-to-severe COVID-19 disease. Serum concentrations of thyroid-stimulating hormone (TSH), free thyroxine (T\n                    <jats:sub>4<\/jats:sub>\n                    ), and 45 cytokines\/chemokines were measured in all patients within 3 days of admission. Data were extracted retrospectively through a manual review of health records. At admission, 95 (81.9%) were euthyroid; while 21 (18.1%) had biochemically thyroid dysfunction including subclinical thyrotoxicosis (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u200911), overt thyrotoxicosis (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20092), hypothyroidism (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20091), non-thyroidal illness (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20092), and normal TSH but high free T\n                    <jats:sub>4<\/jats:sub>\n                    (\n                    <jats:italic>n<\/jats:italic>\n                    \u2009=\u20095). TSH levels were inversely correlated with IL-8 (\n                    <jats:italic>r<\/jats:italic>\n                    <jats:sub>s<\/jats:sub>\n                    \u2009=\u2009\u20130.248), IL-10 (\n                    <jats:italic>r<\/jats:italic>\n                    <jats:sub>s<\/jats:sub>\n                    \u2009=\u2009\u20130.253), IL-15 (\n                    <jats:italic>r<\/jats:italic>\n                    <jats:sub>s<\/jats:sub>\n                    \u2009=\u2009\u20130.213), IP-10 (\n                    <jats:italic>r<\/jats:italic>\n                    <jats:sub>s<\/jats:sub>\n                    \u2009=\u2009\u20130.334), and GM-CSF (\n                    <jats:italic>r<\/jats:italic>\n                    <jats:sub>s<\/jats:sub>\n                    \u2009=\u2009\u20130.254). Moreover, IL-8 levels, IP-10, and GM-CSF were significantly higher in patients with serum TSH &lt; 0.4 mIU\/L. Lastly, a two-fold increment of IL-8 and IL-10 was associated with significantly higher odds of having TSH &lt; 0.4 mIU\/L (odds ratio 1.86 (1.11\u20133.10) and 1.78 (1.03\u20133.06)). Serum TSH was not associated with 30- or 90-day mortality. In conclusion, this study suggests that fluctuations of TSH levels in patients with COVID-19 may be influenced by circulating IL-8, IL-10, IL-15, IP-10, and GM-CSF as previously described in autoimmune thyroid diseases.\n                  <\/jats:p>","DOI":"10.1530\/ec-21-0301","type":"journal-article","created":{"date-parts":[[2021,9,1]],"date-time":"2021-09-01T09:10:42Z","timestamp":1630487442000},"page":"1234-1242","update-policy":"https:\/\/doi.org\/10.1530\/crossmarkpolicy-10","source":"Crossref","is-referenced-by-count":22,"title":["Thyroid function in COVID-19 and the association with cytokine levels and mortality"],"prefix":"10.1530","volume":"10","author":[{"given":"Clara Lundetoft","family":"Clausen","sequence":"first","affiliation":[{"name":"1Center of Research & Disruption of Infectious Diseases, Department of Infectious Diseases, Copenhagen University Hospital, Hvidovre, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"\u00c5se Krogh","family":"Rasmussen","sequence":"additional","affiliation":[{"name":"2Department of Medical Endocrinology and Metabolism, Copenhagen University Hospital, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Trine Holm","family":"Johannsen","sequence":"additional","affiliation":[{"name":"3Department of Growth and Reproduction, Copenhagen University Hospital, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linda Maria","family":"Hilsted","sequence":"additional","affiliation":[{"name":"4Department of Clinical Biochemistry, Copenhagen University Hospital, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Niels Erik","family":"Skakkeb\u00e6k","sequence":"additional","affiliation":[{"name":"3Department of Growth and Reproduction, Copenhagen University Hospital, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pal Bela","family":"Szecsi","sequence":"additional","affiliation":[{"name":"5Department of Clinical Biochemistry, Holb\u00e6k Hospital, Holb\u00e6k, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lise","family":"Pedersen","sequence":"additional","affiliation":[{"name":"5Department of Clinical Biochemistry, Holb\u00e6k Hospital, Holb\u00e6k, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Benfield","sequence":"additional","affiliation":[{"name":"1Center of Research & Disruption of Infectious Diseases, Department of Infectious Diseases, Copenhagen University Hospital, Hvidovre, Denmark"},{"name":"6Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anders","family":"Juul","sequence":"additional","affiliation":[{"name":"3Department of Growth and Reproduction, Copenhagen University Hospital, Copenhagen, Denmark"},{"name":"6Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"416","container-title":["Endocrine Connections"],"original-title":[],"link":[{"URL":"https:\/\/ec.bioscientifica.com\/view\/journals\/ec\/10\/10\/EC-21-0301.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/ec.bioscientifica.com\/downloadpdf\/journals\/ec\/10\/10\/EC-21-0301.xml","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,7,20]],"date-time":"2026-07-20T13:44:44Z","timestamp":1784555084000},"score":1,"resource":{"primary":{"URL":"http:\/\/journals.bioscientifica.com\/ec\/article\/10\/10\/1234-1242\/164"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2021,10,1]]},"references-count":0,"journal-issue":{"issue":"10"},"URL":"https:\/\/doi.org\/10.1530\/ec-21-0301","relation":{},"ISSN":["2049-3614"],"issn-type":[{"value":"2049-3614","type":"electronic"}],"subject":[],"published":{"date-parts":[[2021,10,1]]}}}