Background. Endocrine ophthalmopathy (EOP) is an autoimmune orbit disease characterized by soft retrobulbar tissues damage. The level of antibodies to the thyroid-stimulating hormone receptor (TSHRAbs) is considered as a laboratory marker of EOP activity. Interleukins 17 (IL-17) and 23 (IL-23) play an important role in the pathogenesis of some autoimmune diseases and directly correlate with clinical activity. At present, there is an open question about the role of these cytokines in EOP and their relationship with TSHRAbs.
Aims. To assess pathogenetic role of IL-17, IL-23 and TSHRAbs in patients with EOP.
Materials and methods. The study included 50 people (100 eyes) at the age of 43 [35; 50] years. Three study groups were formed: 32 patients with moderate severity of EOP (clinical group), 18 patients with thyroid pathology without EOP (comparison group) and 15 healthy subjects (control group). All groups were comparable in age and sex. The diagnosis was verified clinically, laboratory and instrumentally. A comprehensive ophthalmologic examination and blood sampling were performed to determine the concentrations of IL-17, IL-23 and TSHRAbs. Statistical processing of the data was carried out in the program “Statistica 10.0”, StatSoft, Inc.
Results. An increase in the level of TSHRAbs was observed in all phases of EOP activity in comparison with both comparison group and control (p < 0.05). But in the active phase TSHRAbs level reached the maximum values in 100% of patients. An increase in the IL-17 concentration in 5,3 times was found in the active EOP in comparison with the control group (p < 0.05). Concentration of TSHRAbs and IL-17 in blood serum directly correlates with EOP activity (p < 0.001). After carrying out pulse therapy with glucocorticosteroids, the consentration of IL-17 decreased almost to zero. There were no significant differences in the level of IL-23 in the groups (p = 0.56).
Conclusions. Determination of TSHRAbs and IL-17 levels in serum can be used as a laboratory diagnostic marker of EOP activity.
A Role of Insulin-Like Growth Factor I for Follicle-Stimulating Hormone Receptor Expression in Rat Granulosa Cells1
