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Relevance. Until now, disputes among scientists about its etiology, pathogenesis, nomenclature and risk factors for the development of vulvar lichen sclerosis have not subsided, which actualizes the need for scientific research aimed at solving these problems. The aim of the study - to establish statistically significant clinical and anamnestic risk factors for vulvar lichen sclerosis. Materials and Methods. An electronic database was formed with data from 344 patients with lichen sclerosus of the vulva and 60 women without vulvar diseases aged 20-70 years on hereditary, obstetric-­gynecological, somatic and infectious history. Astatistical comparative correlation analysis of the obtained data was carried out using the Spearman correlation coefficient (R0.15), nonparametric Mann - Whitney U test and Student t test (p0.05), Chi-square tests, Phi and Cramer statistics. Results and Discussion. Statistically significant (p0.05) risk factors for the development of vulvar lichen sclerosus (R, in descending order) were established: the presence of fibrocystic mastopathy (-0.29); late menarche (15 years and older) (-0.28); onset of menopause (-0.25); recurrent vulvo-­vaginal infections (-0.18); recurrent bacterial vaginosis (-0.18); autoimmune thyroiditis(-0.16) and stage II obesity (-0.16). Also, the average number of abortions and births (1.23 and 1.49, respectively) in the group of patients with lichen sclerosis of the vulva is statistically significantly greater (p0.05) than the average value (0.27 and 1.13, respectively) in control group. Conclusion. The data obtained on the impact of obesity and autoimmune thyroiditis on the risk of developing vulvar sclerotic lichen are consistent with the results of global studies and confirm the association of the disease with autoimmune and metabolic disorders. Recurrent vulvo-­vaginal infections and dysbiotic processes in the vagina can be both acause and aconsequence of vulvar lichen. The relationship between fibrocystic mastopathy and vulvar lichen sclerosus remains debatable and requires further research. Late menarche, the onset of menopause, alarge number of abortions and childbirth can also be considered triggers for vulvar lichen sclerosus in patients with agenetic predisposition to the disease.

Aim.The objective is to optimize the diagnosis and management of the atrophic variant of the vulvar lichen sclerosus (LS). Materials and methods. We examined 58 female patients from 20 to 70 years old with the atrophic variant of the vulvar LS. The control group included 30 deemed healthy females 2070 years old. The atrophic variant of LS was diagnosed based on symptoms (dryness and discomfort in the vulva, superficial vulvodynia and dyspareunia, mild itching) and signs (marked atrophy of the external genitalia tissue up to aplasia of the labia minora and clitoris, vaginal stenosis, minimal hypopigmentation, absence of sclerosis). In addition, the following cytokines were measured in the peripheral blood of patients: interleukin (IL)-20, 23, 10, tumor necrosis factor-, and interferon-. The measurements were performed before and after immunotherapy with sodium deoxyribonucleate. Results. In all patients, there was a rapid shrinkage of the labia minora and clitoris, thinning and easy traumatization of the dermis and epidermis, contributing to secondary infection and synechiae formation up to complete vaginal occlusion. An increase in IL-23 (19.01 [18.0; 38.5] vs. 16.6 [12.98; 20.71] in the control group), 2.7-fold (p0.03) decrease in tumor necrosis factor-, interferon- and IL-20 are common for the atrophic variant of LS. The immunomodulatory and clinical efficacy of sodium deoxyribonucleate was demonstrated. Severe vulvodynia before treatment was noted in 29 (50%) patients and no patient (0%) after therapy; 44 (75.8%) patients reported complete reversal of superficial vulvodynia after treatment, and there were no patients without vulvodynia before treatment (0%). Mild itching before treatment was noted by 20 (40%) patients and 2 (3.4%) patients after treatment. Considering the cytokine levels, topical glucocorticoids in atrophic LS are inappropriate and can lead to atrophy and immunosuppression aggravation, contributing to the secondary infection. Conclusion. The observed differences in cytokine levels in patients with atrophic vulvar LS confirm the relevance of LS clinical classification by variants, support their use for LS diagnosis and immunotherapy efficacy control, and also suggest a differentiated approach to the treatment of different LS variants considering the effect of the drugs used on cytokine status.