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논문 기본 정보

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저자정보
David Tak Wai Lui (The University of Hong Kong) Chi-Ho Lee (The University of Hong Kong) Wing-Sun Chow (The University of Hong Kong) Alan Chun Hong Lee (The University of Hong Kong) Anthony Raymond Tam (The University of Hong Kong) Carol Ho Yi Fong (The University of Hong Kong) Chun Yiu Law (Division of Chemical Pathology Queen Mary Hospital Hongkong) Eunice Ka Hong Leung (The University of Hong Kong) Kelvin Kai Wang To (Department of Microbiology The University of Hong Kong) Kathryn Choon Beng Tan (The University of Hong Kong) Yu-Cho Woo (The University of Hong Kong) Ching Wan Lam (Department of Pathology The University of Hong Kong) Ivan Fan Ngai Hung (The University of Hong Kong) Karen Siu Ling Lam (The University of Hong Kong)
저널정보
대한내분비학회 Endocrinology and Metabolism Endocrinology and Metabolism Vol.36 No.3
발행연도
2021.1
수록면
582 - 589 (8page)

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Background: The occurrence of Graves’ disease and Hashimoto thyroiditis after coronavirus disease 2019 (COVID-19) raised concerns that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may trigger thyroid autoimmunity. We aimed to address the current uncertainties regarding incident thyroid dysfunction and autoimmunity among COVID-19 survivors. Methods: We included consecutive adult COVID-19 patients without known thyroid disorders, who were admitted to Queen Mary Hospital from July 21 to September 21, 2020 and had serum levels of thyroid-stimulating hormone, free thyroxine, free triiodothyronine (fT3), and anti-thyroid antibodies measured both on admission and at 3 months. Results: In total, 122 patients were included. Among 20 patients with abnormal thyroid function tests (TFTs) on admission (mostly low fT3), 15 recovered. Among 102 patients with initial normal TFTs, two had new-onset abnormalities that could represent different phases of thyroiditis. Among 104 patients whose anti-thyroid antibody titers were reassessed, we observed increases in anti-thyroid peroxidase (TPO) (P<0.001) and anti-thyroglobulin (P<0.001), but not anti-thyroid stimulating hormone receptor titers (P=0.486). Of 82 patients with negative anti-TPO findings at baseline, 16 had a significant interval increase in anti-TPO titer by >12 U, and four became anti-TPO-positive. Worse baseline clinical severity (P=0.018), elevated C-reactive protein during hospitalization (P=0.033), and higher baseline anti-TPO titer (P=0.005) were associated with a significant increase in anti-TPO titer. Conclusion: Most patients with thyroid dysfunction on admission recovered during convalescence. Abnormal TFTs suggestive of thyroiditis occurred during convalescence, but infrequently. Importantly, our novel observation of an increase in anti-thyroid antibody titers post-COVID-19 warrants further follow-up for incident thyroid dysfunction among COVID-19 survivors.
#COVID-19 #SARS-CoV-2 #Thyroid function tests #Thyroiditis #Euthyroid sick syndromes #Thyroid gland

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참고문헌 (24)

참고문헌 신청
Wiersinga WJ / 2020 / Pathophysiology, transmission, diagnosis, and treatment of coronavirus disease 2019(COVID-19) : a review / JAMA 324:782~793 google schola Pal R / 2020 / COVID-19 and the endocrine system : exploring the unexplored / J Endocrinol Invest 43:1027~1031 google schola Brancatella A / 2020 / Subacute thyroiditis after SARS-COV-2 infection / J Clin Endocrinol Metab 105:dgaa276 google schola Scappaticcio L / 2020 / Impact of COVID-19 on the thyroid gland : an update / Rev Endocr Metab Disord 25:1~13 google schola Brancatella A / 2020 / Is subacute thyroiditis an underestimated manifestation of SARS-CoV-2 infection? : insights from a case series / J Clin Endocrinol Metab 105:dgaa537 google schola

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