Abstract

The paper considers the modern concepts of the etiology and pathogenesis of psoriatic arthritis (PsA). The latter is currently indicated as a T-cell-mediated disease that is based on the activation of cellular immunity, followed by the hyperproduction and imbalance of key pro- and anti-inflammatory cytokines, such as tumor necrosis factor-α (TNF- α), interleukin-1β (IL-1β), IL-6, IL-12/23, and IL-17. The paper presents the basic principles of diagnosis and clinical manifestations of the disease and notes the importance of screening questionnaires, the use of which allows specialists to diagnose PsA early, by actively identifying articular complaints, the characteristic clinical and radiological signs of damage to the joint, spine, and entheses. It is pointed out that the key target of pharmacotherapy for PsA is to achieve remission or minimal activity of the main clinical manifestations of the disease, to slow down or prevent its radiographic progression, to increase the length and quality of life in patients, and to reduce the risk of comorbidities. The authors characterize the major groups of used drugs: nonsteroidal anti-inflammatory drugs, conventional and targeted synthetic disease-modifying antirheumatic drugs, and biological drugs (inhibitors of TNF-α, IL-12/23, and IL-17). The key Treat-to-target principles of patient management are considered; it is noted that strict control over disease activity and treatment results provides suppression of all major clinical manifestations of PsA. The paper also shows the basic principles of the creation and further development of the All-Russian Registry of PsA patients, which makes it possible to optimize management decision-making on the provision of high-tech medical care and drugs for this cohort of patients.

Highlights

  • Рассмотрены современные представления об этиологии и патогенезе псориатического артрита (ПсА)

  • The paper considers the modern concepts of the etiology and pathogenesis of psoriatic arthritis (PsA)

  • The latter is currently indicated as a T-cell-mediated disease that is based on the activation of cellular immunity, followed by the hyperproduction and imbalance of key pro- and anti-inflammatory cytokines, such as tumor necrosis factor-α (TNFα), interleukin-1β (IL-1β), IL-6, IL-12/23, and IL-17

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Summary

Introduction

Рассмотрены современные представления об этиологии и патогенезе псориатического артрита (ПсА). Что в настоящее время ПсА рассматривают как Т-клеточно-опосредованное заболевание, в основе которого лежит активация клеточного иммунитета с последующей гиперпродукцией и дисбалансом ключевых про- и антивоспалительных цитокинов – фактора некроза опухоли α (ФНОα), интерлейкина 1β (ИЛ1β), ИЛ6, ИЛ12/23, ИЛ17.

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