Endocrine Abstracts

Introduction: Research into autoimmune disorders associated with COVID-19 in the middle of an ongoing COVID-19 pandemic is an important and urgent challenge. We focus on the potential relationship between coronavirus infection and other autoimmune diseases, and the positive therapeutic effect of the treatment of severe forms of COVID-19 with drugs traditionally used in the treatment of rheumatological diseases. The results of this study are a starting point for understanding the mechanisms of related to potential breakdown of immunological tolerance and the development of thyroid autoimmune diseases during COVID-19.

Materials and Methods: This prospective single-center, case-control study included 41 patients hospitalized at the National Endocrinology Research Centre with a clinical and laboratory analysis diagnosis of COVID-19 and bilateral polysegmental viral pneumonia, as well as 78 healthy individuals who have never had a coronavirus infection. Both groups were comparable in terms of gender and age. To assess the functional status of the thyroid gland all patients underwent observation of the thyroid-stimulating hormone (TSH), T3free, T4free, antibodies to thyroid peroxidase, antibodies to the TSH receptor. Their thyroid profile was assessed in both the acute period of the disease as well as 6 months after recovery. The markers of the inflammatory process were assessed: 27 signal molecules of cytokines and chemokines. In patients from the first group, the study of the following cytokine levels was carried out in both the acute period of the disease as well as 6 months after recovery: IL-1b, IL-1ra, IL-2, IL-4-10, IL-12, IL-13, IL-15, IL-17, Eotaxin, FGF, GM-CSF, G-CSF, IFN-g, IP-10, MCP- 1, MIP-1a and -1b, PDGF-bb, RANTES, TNF-a, VEGF.

Results: Manifest hypothyroidism was detected in 2.4% of patients, and at subclinical levels in 7.3% of patients 6 months after the onset of coronavirus infection, in addition to an increase in antibodies to thyroid peroxidase 6 months after recovery from coronavirus infection was detected (P= 0.023). In the group of patients with increased antibodies to thyroid peroxidase after undergoing COVID-19, statistically significantly high levels of IL-4 (P= 0.033), IFN-g (P= 0.007), and Eotaxin (P= 0.008) were obtained. An increase in antibodies to the TSH receptor was revealed in the group of patients with severe COVID-19 who did not receive pathogenetic therapy with tocilizumab in the acute period of the disease (P= 0.046).

Conclusion: Our research shows that the COVID-19 may be a trigger of autoimmune thyropathy disorders.