Multimorbidity in vitiligo patients-emphasis on autoimmune diseases and involvement of immune response regulatory genes

The pathogenesis of autoimmune diseases (AD) is based on the “recognition of the body’s own structures by immunocompetent cells and subsequent activation, proliferation, and induction of inflammation. Most lymphocytes directed towards their own antigens are removed in the thymus through apoptosis.” Currently, research is being conducted to investigate the genes involved in the development of autoimmune diseases, specifically in the context of vitiligo, such as HLA genes (HLADR3 associated with a common process, HLADR4 with limited), TNFAIP3 genes, and A20 deficiency haplotype (a product of this gene). The importance of immune inflammation, mononuclear infiltration of marginal zones, and the cytotoxic effect of CD8+ on melanocyte changes in CD4, CD8, and their ratios have been identified as early indicators of vitiligo progression. A local deficiency of SOD, glutathione, and scavengers from ROS regulated through Nrf2 and ARES in the skin and blood of vitiligo patients has also been revealed. This study included 287 patients with non-segmental vitiligo (148 men and 139 women) aged 19-68 years who sought treatment at the Republican Specialized Scientific and Practical Medical Center of Dermatovenerology and Cosmetology between 2018 and 2022. The average age was 28.1\(\pm\)1.3 years, and the duration of the disease was 42.6\(\pm\)3.6 months. Of these patients, 114 (40%) had the debut of vitiligo less than a year before treatment. The study found that the average level of TNF-alpha was higher than the reference interval and the data of the control group, supporting the contribution of inflammation and apoptosis to depigmentation in vitiligo. The study also highlighted the levels of TNF-alpha and IL-21 in patients who had an unfavorable allele for the SNPs among the other patients in the main group.