Risk of Incident Thyroid Dysfunction in the Post-Acute Phase of COVID-19: A Population-Based Cohort Study in Hong Kong

David Tak Wai Lui, Xi Xiong, Ching-Lung Cheung, Francisco Tsz Tsun Lai, Xue Li, Eric Yuk Fai Wan, Celine Sze Ling Chui, Esther Wai Yin Chan, Franco Wing Tak Cheng, Lanlan Li, Matthew Shing Hin Chung, Chi Ho Lee, Yu Cho Woo, Kathryn Choon Beng Tan, Carlos King Ho Wong, Ian Chi Kei Wong

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2 Citations (SciVal)

Abstract

OBJECTIVE: The evidence of thyroid dysfunction in the post-acute phase of SARS-CoV-2 infection is limited. This study aimed to evaluate the risk of incident thyroid dysfunction in the post-acute phase of COVID-19.

METHODS: This retrospective, propensity-score matched, population-based study included COVID-19 patients and non-COVID-19 individuals between January 2020 and March 2022, identified from the electronic medical records of the Hong Kong Hospital Authority. The cohort was followed up until the occurrence of outcomes, death, or 31 January 2023, whichever came first. Patients with COVID-19 were 1:1 matched to controls based on various variables. The primary outcome was a composite of thyroid dysfunction (hyperthyroidism, hypothyroidism, initiation of antithyroid drug or levothyroxine, and thyroiditis). Cox regression was employed to evaluate the risk of incident thyroid dysfunction during the post-acute phase.

RESULTS: A total of 84 034 COVID-19 survivors and 84 034 matched controls were identified. Upon a median follow-up of 303 days, there was no significant increase in the risk of diagnosed thyroid dysfunction in the post-acute phase of COVID-19 (hazard ratio [HR] 1.058, 95% confidence interval 0.979-1.144, P = .154). Regarding the secondary outcomes, patients with COVID-19 did not have increased risk of hyperthyroidism (HR 1.061, P = .345), hypothyroidism (HR 1.062, P = .255), initiation of antithyroid drug (HR 1.302, P = .070), initiation of levothyroxine (HR 1.086, P = .426), or thyroiditis (P = .252). Subgroup and sensitivity analyses were largely consistent with the main analyses.

CONCLUSION: Our population-based cohort study provided important reassuring data that COVID-19 was unlikely to be associated with persistent effects on thyroid function.

Original languageEnglish
Pages (from-to)528-536
Number of pages9
JournalEndocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
Volume30
Issue number6
Early online date28 Mar 2024
DOIs
Publication statusPublished - Jun 2024

Funding

We thank the Hospital Authority and the Department of Health for the generous provision of data for this study. This work was supported by Collaborative Research Fund, University Grants Committee, The Hong Kong Special Administrative Region (HKSAR) Government (principal investigator, I.C.K.W.; reference no. C7154-20GF); the Health Bureau, HMRF Research on COVID-19, the HKSAR Government (principal investigator [work package 2], E.W.Y.C.; reference no. COVID1903011). I.C.K.W. C.K.H.W. and F.T.T.L. are partially supported by the Laboratory of Data Discovery for Health (D24H) funded by the AIR@InnoHK administered by the Innovation and Technology Commission. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

FundersFunder number
Department of Health and Social Care
Hospital Authority
Innovation and Technology Commission
Laboratory of Data Discovery for Health
University Grants Committee, The Hong Kong Special Administrative RegionCOVID1903011

    Keywords

    • thyroid dysfunction
    • Graves’ disease
    • thyroiditis
    • hyperthyroidism
    • SARS-CoV-2 infection
    • Long COVID
    • hypothyroidism
    • SARS-CoV-2
    • Graves disease

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