File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Thyroid Dysfunction in Relation to Immune Profile, Disease Status, and Outcome in 191 Patients with COVID-19

TitleThyroid Dysfunction in Relation to Immune Profile, Disease Status, and Outcome in 191 Patients with COVID-19
Authors
KeywordsCOVID-19
SARS-CoV-2
Thyroid function tests
Thyroiditis
Euthyroid sick syndromes
Thyroid gland
Issue Date2021
PublisherOxford University Press. The Journal's web site is located at https://academic.oup.com/jcem
Citation
The Journal of Clinical Endocrinology & Metabolism, 2021, v. 106 n. 2, p. e926-e935 How to Cite?
AbstractObjective: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)–related thyroiditis is increasingly recognized. The role of thyroid autoimmunity and SARS-CoV-2 viral load in SARS-CoV-2–related thyroid dysfunction is unclear. We evaluated the thyroid function of a cohort of coronavirus disease 2019 (COVID-19) patients, in relation to their clinical features, and biochemical, immunological, and inflammatory markers. Methods: Consecutive adult patients, without known thyroid disorders, admitted to Queen Mary Hospital for COVID-19 from July 21 to August 21, 2020, were included. Serum levels of thyroid-stimulating hormone (TSH), free thyroxine, free triiodothyronine (fT3), and antithyroid antibodies were measured on admission. Results: Among 191 patients with COVID-19 (mean age 53.5 ± 17.2 years; 51.8% male), 84.3% were mild, 12.6% were moderate, and 3.1% were severe. Abnormal thyroid function was seen in 13.1%. Ten patients had isolated low TSH, suggestive of subclinical thyrotoxicosis due to thyroiditis, although the contribution of autoimmunity was likely in 2 of them. Autoimmune thyroiditis probably also contributed to subclinical hypothyroidism in another patient. Ten patients had isolated low fT3, likely representing nonthyroidal illness syndrome. Lower SARS-Cov-2 polymerase chain reaction cycle threshold values and elevated C-reactive protein were independently associated with occurrence of low TSH (P = .030) and low fT3 (P = .007), respectively. A decreasing trend of fT3 with increasing COVID-19 severity (P = .032) was found. Patients with low fT3 had more adverse COVID-19-related outcomes. Conclusion: Around 15% of patients with mild to moderate COVID-19 had thyroid dysfunction. There may be a direct effect of SARS-CoV-2 on thyroid function, potentially leading to exacerbation of pre-existing autoimmune thyroid disease. Low fT3, associated with systemic inflammation, may have a prognostic significance.
Persistent Identifierhttp://hdl.handle.net/10722/294097
ISSN
2019 Impact Factor: 5.399
2015 SCImago Journal Rankings: 2.940
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorLui, DTW-
dc.contributor.authorLee, CH-
dc.contributor.authorChow, WS-
dc.contributor.authorLee, ACH-
dc.contributor.authorTam, AR-
dc.contributor.authorFong, CHY-
dc.contributor.authorLaw, CY-
dc.contributor.authorLeung, EKH-
dc.contributor.authorTo, KKW-
dc.contributor.authorTan, KCB-
dc.contributor.authorWoo, YC-
dc.contributor.authorLam, CW-
dc.contributor.authorHung, IFN-
dc.contributor.authorLam, KSL-
dc.date.accessioned2020-11-23T08:26:17Z-
dc.date.available2020-11-23T08:26:17Z-
dc.date.issued2021-
dc.identifier.citationThe Journal of Clinical Endocrinology & Metabolism, 2021, v. 106 n. 2, p. e926-e935-
dc.identifier.issn0021-972X-
dc.identifier.urihttp://hdl.handle.net/10722/294097-
dc.description.abstractObjective: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)–related thyroiditis is increasingly recognized. The role of thyroid autoimmunity and SARS-CoV-2 viral load in SARS-CoV-2–related thyroid dysfunction is unclear. We evaluated the thyroid function of a cohort of coronavirus disease 2019 (COVID-19) patients, in relation to their clinical features, and biochemical, immunological, and inflammatory markers. Methods: Consecutive adult patients, without known thyroid disorders, admitted to Queen Mary Hospital for COVID-19 from July 21 to August 21, 2020, were included. Serum levels of thyroid-stimulating hormone (TSH), free thyroxine, free triiodothyronine (fT3), and antithyroid antibodies were measured on admission. Results: Among 191 patients with COVID-19 (mean age 53.5 ± 17.2 years; 51.8% male), 84.3% were mild, 12.6% were moderate, and 3.1% were severe. Abnormal thyroid function was seen in 13.1%. Ten patients had isolated low TSH, suggestive of subclinical thyrotoxicosis due to thyroiditis, although the contribution of autoimmunity was likely in 2 of them. Autoimmune thyroiditis probably also contributed to subclinical hypothyroidism in another patient. Ten patients had isolated low fT3, likely representing nonthyroidal illness syndrome. Lower SARS-Cov-2 polymerase chain reaction cycle threshold values and elevated C-reactive protein were independently associated with occurrence of low TSH (P = .030) and low fT3 (P = .007), respectively. A decreasing trend of fT3 with increasing COVID-19 severity (P = .032) was found. Patients with low fT3 had more adverse COVID-19-related outcomes. Conclusion: Around 15% of patients with mild to moderate COVID-19 had thyroid dysfunction. There may be a direct effect of SARS-CoV-2 on thyroid function, potentially leading to exacerbation of pre-existing autoimmune thyroid disease. Low fT3, associated with systemic inflammation, may have a prognostic significance.-
dc.languageeng-
dc.publisherOxford University Press. The Journal's web site is located at https://academic.oup.com/jcem-
dc.relation.ispartofThe Journal of Clinical Endocrinology & Metabolism-
dc.subjectCOVID-19-
dc.subjectSARS-CoV-2-
dc.subjectThyroid function tests-
dc.subjectThyroiditis-
dc.subjectEuthyroid sick syndromes-
dc.subjectThyroid gland-
dc.titleThyroid Dysfunction in Relation to Immune Profile, Disease Status, and Outcome in 191 Patients with COVID-19-
dc.typeArticle-
dc.identifier.emailLui, DTW: dtwlui@hku.hk-
dc.identifier.emailLee, CH: pchlee@hku.hk-
dc.identifier.emailChow, WS: chowws01@hkucc.hku.hk-
dc.identifier.emailLee, ACH: achlee@hku.hk-
dc.identifier.emailFong, CHY: kalofong@hku.hk-
dc.identifier.emailTo, KKW: kelvinto@hku.hk-
dc.identifier.emailTan, KCB: kcbtan@hkucc.hku.hk-
dc.identifier.emailWoo, YC: wooyucho@hku.hk-
dc.identifier.emailLam, CW: ching-wanlam@pathology.hku.hk-
dc.identifier.emailHung, IFN: ivanhung@hkucc.hku.hk-
dc.identifier.emailLam, KSL: ksllam@hku.hk-
dc.identifier.authorityLui, DTW=rp02803-
dc.identifier.authorityLee, CH=rp02043-
dc.identifier.authorityTo, KKW=rp01384-
dc.identifier.authorityTan, KCB=rp00402-
dc.identifier.authorityLam, CW=rp00260-
dc.identifier.authorityHung, IFN=rp00508-
dc.identifier.authorityLam, KSL=rp00343-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1210/clinem/dgaa813-
dc.identifier.pmid33141191-
dc.identifier.pmcidPMC7665541-
dc.identifier.scopuseid_2-s2.0-85100357954-
dc.identifier.hkuros318962-
dc.identifier.volume106-
dc.identifier.issue2-
dc.identifier.spagee926-
dc.identifier.epagee935-
dc.publisher.placeUnited States-
dc.identifier.issnl0021-972X-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats