Retrospective analysis shows increased TSH receptor antibodies and thyroid volume in autoimmune thyroiditis, highlighting immune changes post COVID-19.
Background. The study of post-COVID immune changes, including autoimmune thyroid lesions, remains one of the priority areas of modern endocrinology. The purpose of our study was to compare structural, functional and immune indicators in patients with autoimmune thyroiditis (AIT), depending on the history of COVID-19. Materials and methods. A retrospective analysis of the AIT course depending on the history of COVID-19 was conducted with an assessment of thyroid-stimulating hormone (TSH), thyroid hormones, and antithyroid antibodies. The study group included 200 patients with AIT, 193 women (96.5 %) and 7 men (3.5 %) aged 18 to 62 (mean of 33.80 ± 0.60) years. All patients were divided into 3 groups: group 1 — AIT was diagnosed before COVID-19 (73 patients), group 2 — AIT was diagnosed after COVID-19 (111 people) and the control group — AIT without COVID-19 (16 patients). The levels of TSH, free thyroxine, as well as thyroid peroxidase antibodies, thyroglobulin antibodies, TSH receptor antibodies were determined by the chemiluminescent immunoassay method. Statistical data processing was performed using the Microsoft Excel statistical software package and MedCalc Statistical Software v.19.7.2. The Mann-Whitney test was used to compare groups; differences were considered significant at p < 0.05. Results. After COVID-19, patients have a significant (p < 0.05) increase in the level of blood TSH receptor antibodies, which may indicate the activation of autoimmune processes in the thyroid gland even in the absence of obvious thyroid dysfunction. The thyroid volume significantly (p < 0.05) increased after COVID-19, which may be a manifestation of post-inflammatory or reactive changes in the gland parenchyma in response to viral damage. Conclusions. The levels of classical markers of autoimmune thyroiditis (thyroid peroxidase and thyroglobulin antibodies) remained stable and did not differ between groups, indicating a possible different immune target or mechanism of thyroid damage after COVID-19.
No takes yet. Share an insight, caveat, or question.
Buldygina et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: