Псориатический артрит: патогенетическое обоснование современных терапевтических подходов

Abstract

Objective of the Review: To analyse and summarise information on the pathogenesis of psoriatic arthritis (PsA); to discuss therapeutic targets, actual and long-term drug therapy strategies for this disease. Key Points. PsA pathogenesis is still a matter of argument; some of its mechanisms are still studied poorly. It is assumed that, in patients with genetic predisposition, the disease is triggered by the environmental factors, dysbiosis, infections, stress, that can cause and maintain aberrant activation of the innate and adaptive immune system. We found out that increased expression of such cytokines as IL-6, TNF-α and IL-17A causes synovitis; activates neoangiogenesis, bone resorption and erosion; leads to destruction and inflammation of cartilage as a result of induction of several molecular paths in synovial fibroblasts and macrophages, endothelial cells, osteoblasts, osteoclasts, cartilage cells, and immune cells. Taking into account available information on pathogenic mechanisms of PsA and psoriasis, we have developed several drugs targeting cells, cytokines or other mediators, playing a central role in the pathogenesis of the disease. Conclusion. Currently, treatment of psoriasis and PsA involves the use of traditional basic synthetic anti-inflammatory medicines, genetically engineered biological agents, and target oral synthetic medications, particularly phosphodeisterase-4 inhibitors and Janus kinase inhibitors, a majority of which can treat the entire range of skin and bone manifestations of the disease. Taking into account the varying PsA phenotype, comorbidities and a wide range of medicinal products that can be used by medical professionals, a majority of authors are of the opinion that it is necessary to improve the algorithms of individual approaches to the management of each patient. Keywords: psoriatic arthritis; immunopathogenesis; genetically engineered biological agents.