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Conference Paper: Thyroid Dysfunction in Relation to Immune Profile, Viral Load, Disease Status and Outcome in 191 Patients with COVID-19

TitleThyroid Dysfunction in Relation to Immune Profile, Viral Load, Disease Status and Outcome in 191 Patients with COVID-19
Authors
Issue Date2021
PublisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/
Citation
The 26th Medical Research Conference, Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, 16 January 2021. In Hong Kong Medical Journal, 2021, v. 27 n. 1, Suppl. 1, p. 14, abstract no. 14 How to Cite?
AbstractIntroduction: SARS-CoV-2-related thyroiditis is increasingly recognised. 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 COVID-19 patients, in relation to their clinical features, biochemical, immunological and inflammatory markers. Methods: Consecutive adult patients, without known thyroid disorders, admitted to Queen Mary Hospital for COVID-19 from 21 July to 21 August 2020 were included. Serum levels of thyroid-stimulating hormone (TSH), free thyroxine, free triiodothyronine (fT3) and anti-thyroid 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. 13.1% had abnormal thyroid function. Ten patients had isolated low TSH, suggestive of subclinical thyrotoxicosis due to thyroiditis, although the contribution of autoimmunity was likely in two of them. Autoimmune thyroiditis probably also contributed to subclinical hypothyroidism in another patient. Ten patients had isolated low fT3, likely representing non-thyroidal illness syndrome. Lower SARS-Cov-2 PCR cycle threshold values and elevated C-reactive protein were independently associated with occurrence of low TSH (P=0.030) and low fT3 (P=0.007), respectively. A decreasing trend of fT3 with increasing COVID-19 severity (P=0.032) was found. Patients with low fT3 had more adverse COVID-19-related outcomes, including dexamethasone and/or oxygen requirement (P=0.003), prolonged hospital stay (P=0.018), and clinical deterioration (P<0.001). Conclusion: Around 15% of patients with predominantly 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 preexisting autoimmune thyroid disease. Low fT3, associated with systemic inflammation, may have a prognostic significance.
Persistent Identifierhttp://hdl.handle.net/10722/300966
ISSN
2023 Impact Factor: 3.1
2023 SCImago Journal Rankings: 0.261

 

DC FieldValueLanguage
dc.contributor.authorLui, TWD-
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.accessioned2021-07-06T03:12:42Z-
dc.date.available2021-07-06T03:12:42Z-
dc.date.issued2021-
dc.identifier.citationThe 26th Medical Research Conference, Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, 16 January 2021. In Hong Kong Medical Journal, 2021, v. 27 n. 1, Suppl. 1, p. 14, abstract no. 14-
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/300966-
dc.description.abstractIntroduction: SARS-CoV-2-related thyroiditis is increasingly recognised. 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 COVID-19 patients, in relation to their clinical features, biochemical, immunological and inflammatory markers. Methods: Consecutive adult patients, without known thyroid disorders, admitted to Queen Mary Hospital for COVID-19 from 21 July to 21 August 2020 were included. Serum levels of thyroid-stimulating hormone (TSH), free thyroxine, free triiodothyronine (fT3) and anti-thyroid 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. 13.1% had abnormal thyroid function. Ten patients had isolated low TSH, suggestive of subclinical thyrotoxicosis due to thyroiditis, although the contribution of autoimmunity was likely in two of them. Autoimmune thyroiditis probably also contributed to subclinical hypothyroidism in another patient. Ten patients had isolated low fT3, likely representing non-thyroidal illness syndrome. Lower SARS-Cov-2 PCR cycle threshold values and elevated C-reactive protein were independently associated with occurrence of low TSH (P=0.030) and low fT3 (P=0.007), respectively. A decreasing trend of fT3 with increasing COVID-19 severity (P=0.032) was found. Patients with low fT3 had more adverse COVID-19-related outcomes, including dexamethasone and/or oxygen requirement (P=0.003), prolonged hospital stay (P=0.018), and clinical deterioration (P<0.001). Conclusion: Around 15% of patients with predominantly 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 preexisting autoimmune thyroid disease. Low fT3, associated with systemic inflammation, may have a prognostic significance.-
dc.languageeng-
dc.publisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/-
dc.relation.ispartofHong Kong Medical Journal-
dc.relation.ispartof26th Medical Research Conference, 2021-
dc.rightsHong Kong Medical Journal. Copyright © Hong Kong Academy of Medicine Press.-
dc.titleThyroid Dysfunction in Relation to Immune Profile, Viral Load, Disease Status and Outcome in 191 Patients with COVID-19-
dc.typeConference_Paper-
dc.identifier.emailLui, TWD: dtwlui@hku.hk-
dc.identifier.emailLee, ACH: achlee@hku.hk-
dc.identifier.emailTo, KKW: kelvinto@hku.hk-
dc.identifier.emailTan, KCB: kcbtan@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, TWD=rp02803-
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.natureabstract-
dc.identifier.hkuros323147-
dc.identifier.volume27-
dc.identifier.issue1, Suppl. 1-
dc.identifier.spage14, abstract no. 14-
dc.identifier.epage14, abstract no. 14-
dc.publisher.placeHong Kong-

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