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rRisk of incident thyroid dysfunction in the post-acute phase of COVID-19: a population-based cohort study in Hong Kong.
Endocrine Practice 2024 March 28
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. COVID-19 patients were 1:1 matched to controls based on various variables. The primary outcome was a composite of thyroid dysfunction (hyperthyroidism, hypothyroidism, initiation of anti-thyroid drug [ATD] or levothyroxine [LT4], and thyroiditis). Cox regression was employed to evaluate the risk of incident thyroid dysfunction beyond 30 days after the first positive test.
RESULTS: 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 [CI] 0.979-1.144, p=0.154). Regarding the secondary outcomes, COVID-19 patients did not have increased risk of hyperthyroidism (HR 1.061, p=0.345), hypothyroidism (HR 1.062, p=0.255), initiation of ATD (HR 1.302, p=0.070), initiation of LT4 (HR 1.086, p=0.426), or thyroiditis (p=0.252). 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.
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. COVID-19 patients were 1:1 matched to controls based on various variables. The primary outcome was a composite of thyroid dysfunction (hyperthyroidism, hypothyroidism, initiation of anti-thyroid drug [ATD] or levothyroxine [LT4], and thyroiditis). Cox regression was employed to evaluate the risk of incident thyroid dysfunction beyond 30 days after the first positive test.
RESULTS: 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 [CI] 0.979-1.144, p=0.154). Regarding the secondary outcomes, COVID-19 patients did not have increased risk of hyperthyroidism (HR 1.061, p=0.345), hypothyroidism (HR 1.062, p=0.255), initiation of ATD (HR 1.302, p=0.070), initiation of LT4 (HR 1.086, p=0.426), or thyroiditis (p=0.252). 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.
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