Introduction. PPARγ is the most studied PPAR subtype and is expressed predominantly in adipose tissue, heart, colon, kidney, spleen, intestine, skeletal muscle, liver, macrophages, and skin. In the skin, PPARγ controls the genetic regulation of gene network expression involved in cell proliferation, differentiation, and inflammatory responses. PPARγ (Peroxisome proliferator-activated receptor gamma) has only recently come to be considered a key player in the development and pathogenesis of psoriasis and psoriatic inflammatory conditions.Aim of the study. To study PPARγ gene expression in the affected skin of psoriasis patients in comparison with visually unaffected skin. To study changes in PPARγ gene expression level in psoriasis affected skin in comparison with unaffected skin in patients before and after treatment with low-level laser radiation with a wavelength of 1.27 μm.Materials and methods. Twelve patients with psoriasis participated in the study. Biopsies from unaffected skin areas were taken at a distance of about 3 cm from the affected skin. Analysis was performed by real-time PCR.Results and Discussion. We quantitatively measured PPARγ gene expression using RT-PCR in the affected skin of patients with psoriasis in comparison with visually unaffected skin in the same patients before and after treatment with low-level laser radiation with a wavelength of 1.27 μm (the short-wave part of the infrared range). The study experimentally showed a 1.3 ± 0.27-fold decrease in PPARγ gene expression in the affected skin of psoriasis patients on average. Significant increase in over-expression of PPARγ gene up to 2,13 ± 0,47 times was observed after treatment of patients with low-level laser radiation.Conclusions. PPARγ gene expression may be an indicator of the efficacy of psoriasis treatment at the molecular level, as well as become a new therapeutic target.

Psoriasis is a chronic inflammatory skin disease that is currently viewed as a systemic process due to its association with many comorbid conditions. With the appearance of genetically engineered biological drugs (GEBDs), the treatment of psoriasis has undergone significant changes due to their high efficiency and favorable safety profile. It has been clinically proven that the use of this type of therapy has a positive effect, including on comorbid diseases. However, it must be highlighted that some types of drugs can have a negative effect on the course of these conditions. The characteristics of each individual drug, such as the rate of onset of remission, long-term efficacy, safety profile and effect on comorbidities are different. A better understanding of these characteristics leads to the correct personalized choice of therapy, hence to improved survival of drugs, patient satisfaction and minimization of the impact of psoriasis on the quality of life of patients.This article examines the efficacy and safety of biological drugs in patients with psoriasis, discusses their effect on concomitant diseases pathogenetically associated with psoriasis.To date it is known that the signaling pathway IL-23 / IL-17 plays a key role in the pathogenesis of psoriasis. Promising results are shown by the use of a biological drug aimed at inhibiting IL-23, namely the IL-23 blocker guselkumab. In addition to the high level of therapeutic response in psoriasis, other properties oa the drug have been identified - it has also shown efficacy in patients with concomitant Crohn's disease. Studies describe positive responses in the guselkumab treatment of psoriasis with “difficult” localisations, psoriatic arthritis and Hidradenitis Suppurativa, and its use in patients with cardiovascular risks did not lead to any manifestations of negative dynamics. Thus, further study of the effect of the IL-23 blocker on comorbid pathologies in psoriasis is a promising area.

Psoriasis is a chronic immune-mediated disease that is accompanied by a significant number of comorbid pathologies. Damage to the nail plates (psoriatic onychodystrophy) is widespread among patients with psoriasis and is associated with significant functional as well as psychosocial impairments. Despite the fact that nails constitute a small percentage of the surface of the human body, the damage to this particular area can lead to a deterioration in the quality of life and irreversible disability. In addition, studies have shown that nail psoriasis is indicative of a more severe course of the disease and it can also be associated with psoriatic arthritis or it can be a predictor of its development. Current treatment options for psoriasis accompanied by the nail plates damage include many topical and systemic methods, however, patients often report dissatisfaction with the results of treatment due to low efficacy or many side effects. Achieving higher efficiency is possible with the use of biologic therapy. Currently, a wide range of biologics have been developed that modulate key elements in the immunopathogenesis of psoriasis.The pathogenesis of psoriasis is a multifactorial process, however, it is the IL23 / Th17 signaling pathway that is key in this process. Interleukin-17A is the principal effector of this pathway and overexpression of IL-17A leads to epidermal hyperplasia and an excessive inflammatory response seen in psoriasis. Therefore, interleukin-17A is a promising therapeutic target.Considering the critical pathogenetic role as well as the high efficacy and safety of IL-17A inhibitors, the study of their effect on the psoriatic onychodystrophy manifestations is of great clinical importance.Netakimab is the first Russian original IL-17 inhibitor which is a promising modern agent for the treatment of moderate-to-severe plaque psoriasis. The obtained real clinical data indicate the high efficacy and safety of the use of Netakimab in patients with both plaque psoriasis and «severe» psoriasis in difficult to treat localizations, such as damage of the nail plate.

Introduction. Recommendations cover the current state of diagnosis and treatment of mastocytosis.Aim — а consolidation of the Russian experts’ opinion on treatment for adult mastocytosis.Main findings. The recommendations have been developed taking into account foreign literature, national experience and world clinical evidence on therapy for systemic and cutaneous mastocytoses, mast cell leukaemia and other mastocytosis forms. The significance of bone marrow and peripheral blood molecular genetic testing for the presence of KITD816V gene variants is demonstrated. The treatment regimens described are based on midostaurin, imatinib, cladribine, hydroxycarbamide, interferon alfa and haematopoietic stem cell transplantation. Prognosis in different forms of mastocytosis is provided.