# The impact of COVID-19 on thyroid function and psychological state of Graves’ disease: a one-year prospective study

**Authors:** Lujia Xu, Jianbo Zhang, Riping Cong, Yujian Zhang, Xuenan Song, Wei Wang, Yingli Diao, Haijiao Liu, Kuanxiao Tang

PMC · DOI: 10.3389/fendo.2025.1597083 · Frontiers in Endocrinology · 2025-07-17

## TL;DR

This study examines how a one-year follow-up of Graves’ disease patients with COVID-19 coinfection reveals changes in thyroid function and psychological state.

## Contribution

The study identifies specific risk factors and outcomes for Graves’ disease patients with prolonged COVID-19 infection.

## Key findings

- The number of COVID-19 symptoms is an independent risk factor for hyperthyroidism in Graves’ disease patients.
- Prolonged COVID-19 infection is linked to worsened psychological outcomes and altered thyroid hormone levels.
- Tailored antithyroid drug adjustments and psychological interventions improve outcomes in these patients.

## Abstract

Since the comprehensive lifting of coronavirus disease 2019 (COVID-19) pandemic control measures in mainland China in December 2022, the population has experienced widespread infection with COVID-19. COVID-19 affects multiple systems, including the endocrine system, particularly the thyroid. Graves’ disease, a common autoimmune disorder, may be complicated by COVID-19 infection. Therefore, investigating changes in thyroid function and psychological status in patients with Graves’ disease (GDC) and COVID-19 coinfection holds significant clinical importance.

This study enrolled 110 hyperthyroid patients with COVID-19 coinfection, including 90 GDC patients meeting inclusion criteria. They were prospectively followed for one year at three time points: pre-COVID-19, 3 months, and 1 year post-infection. Patients were categorized by COVID-19 duration: G1 (≤5 days), G2 (6–8 days), and G3 (≥9 days). Follow-up included assessments of COVID-19 and GD symptoms, laboratory tests, psychological evaluations, treatment efficacy, COVID-19 management, and antithyroid medication adjustments. Statistical analyses (rank-sum tests, t-tests, multivariate logistic regression) explored COVID-19-GD associations and changes in thyroid function and psychological status in GDC patients.

Multivariate logistic regression analysis, after covariate adjustment, identified the number of COVID-19 symptoms as an independent risk factor for hyperthyroidism in GDC patients, and COVID-19 duration as an independent risk factor for poor psychological status. At 3 months post-infection, the G3 group showed an increased FT3/FT4 ratio and decreased FT4 levels. Significant intergroup differences were observed in FT4 and TSH changes from pre-infection levels, with the G3 group having the highest anxiety and depression scores. Antithyroid medication and psychological interventions were adjusted based on thyroid function and psychological scores. At 1 year post-infection, TSH levels in the G1 and G3 groups increased compared to 3 months, while psychological scores decreased. The G3 group had significantly higher TSH levels than pre-infection, with significant intergroup differences in FT3 and FT4 levels.

Post-COVID-19 infection, GDC patients may experience hyperthyroidism and psychological distress, which improve with tailored ATD adjustments and psychological interventions. The FT3/FT4 ratio guides (antithyroid drugs) ATDs optimization, while psychological intervention effectively mitigates anxiety and depression in GDC patients.

## Linked entities

- **Diseases:** Graves’ disease (MONDO:0005364), coronavirus disease 2019 (MONDO:0100096), hyperthyroidism (MONDO:0004425), anxiety (MONDO:0005618), depression (MONDO:0002050)

## Full-text entities

- **Genes:** SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, LOC102723407 (immunoglobulin heavy variable 4-38-2-like) [NCBI Gene 102723407] {aka IGHV4, IGHV4-30, IGHV4-38-2, IGHV4-39, IGHV4-b, IGVH4-39}, GAD1 (glutamate decarboxylase 1) [NCBI Gene 2571] {aka CPSQ1, DEE89, GAD, GAD-67, SCP}, THNSL1 (threonine synthase like 1) [NCBI Gene 79896] {aka TSH1}
- **Diseases:** HL (MESH:C538324), depression (MESH:D003866), rheumatic immune diseases (MESH:D012216), Mental Disorders (MESH:D001523), anxiety disorders (MESH:D001008), dry cough (MESH:D003371), Hyperthyroidism (MESH:D006980), hypertension (MESH:D006973), GD (MESH:D006111), anxiety (MESH:D001007), tremors (MESH:D014202), weight loss (MESH:D015431), coronary artery disease (MESH:D003324), -COVID-19 infection (MESH:D000086382), thyroid function (MESH:D013966), autoimmune disease (MESH:D001327), infectious disease (MESH:D003141), goiter (MESH:D006042), GD (MESH:D005776), inflammatory (MESH:D007249), Thyrotoxicosis (MESH:C566386), Hashimoto thyroiditis (MESH:D050031), infection (MESH:D007239), ATDs (MESH:D000081015), diabetes (MESH:D003920), thyroid disease (MESH:D013959), exophthalmos (MESH:D005094), palpitations (MESH:D006331), GAD-7 (MESH:C000726808), hypothyroidism (MESH:D007037), tension (MESH:D018781), increased appetite (MESH:D001068), fever (MESH:D005334)
- **Chemicals:** methimazole (MESH:D008713), alcohol (MESH:D000438), Triiodothyronine (MESH:D014284), iodine (MESH:D007455), Antithyroid (-), thyroxine (MESH:D013974)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12310469/full.md

## References

28 references — full list in the complete paper: https://tomesphere.com/paper/PMC12310469/full.md

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Source: https://tomesphere.com/paper/PMC12310469