Abstract

Graves’ orbitopathy (GO) is an extrathyroid complication of thyroid dysfunction characterized by chronic autoimmune inflammation of soft retrobulbar tissues. The data on the role of oxidative and hypoxic stress in GO are heterogeneous, which necessitates further research.The aim of the study. To evaluate the indicators of oxidative stress and tissue hypoxia at various phases of Graves’ orbitopathy activity.Material and methods. Examination of patients with GO (n = 32), with autoimmune thyroid pathology (n = 18) and healthy individuals (n = 15) was performed. The study included ophthalmological examination and blood sampling to determine the concentration of antibodies to the thyroid-stimulating hormone receptor, interleukin 17A (IL-17A), hypoxia inducible factor 1a (HIF-1a), TBK-active products and calculation of total antioxidant activity.Results. An increase in the concentration of TBK-active products in the clinical group was revealed compared with the control (p < 0.001). The total antioxidant activity was reduced at all phases of GO activity than in the control (p < 0.001). The level of HIF-1α did not differ in the study groups (H = 3.29; p = 0.51). Direct moderate correlations were found between the concentration of IL-17A and the level of TBA-active substances (p = 0.001), as well as inverse moderate correlations with the value of total antioxidant activity (p = 0.007). The activity of GO had weak correlations with total antioxidant activity (p < 0.001). Significant correlations between indicators of oxidative stress and tissue hypoxia were not found.Conclusion. In GO, regardless of the activity phase, there is an imbalance between the parameters of the “lipid peroxidation – antioxidant protection” system, which is manifested by an increase in TBA-active substances while reducing the total antioxidant activity. The indicators of tissue hypoxia did not differ in the study groups. The revealed correlations between the autoimmune inflammation activity in the orbit and oxidative stress emphasize the pathogenetic conditionality of the antioxidant drugs appointment in the therapy of GO.

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