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Results of studying the clinical efficacy and safety of tofacitinib in the treatment of psoriatic arthritis
Author(s) -
Т. В. Коротаева,
Е. Ю. Логинова
Publication year - 2019
Publication title -
sovremennaâ revmatologiâ
Language(s) - English
Resource type - Journals
eISSN - 2310-158X
pISSN - 1996-7012
DOI - 10.14412/1996-7012-2019-2-112-118
Subject(s) - tofacitinib , medicine , psoriatic arthritis , psoriasis , rheumatoid arthritis , disease , quality of life (healthcare) , oncology , intensive care medicine , immunology , nursing
The paper reviews of the data available in the literature on the clinical efficacy and safety of tofacitinib (TOFA) in the treatment of psoriatic arthritis (PsA). It considers the mechanism of action of TOFA, which is mainly in the selective inhibition of signal transmission due to its effect on the activity of JAK3 and/or JAK1, the enzymes that ensure the function of turning on and turning off the signals transmitted by cytokines. TOFA is noted to directly or indirectly act on a wide range of a number of molecules that play an important role in the pathogenesis of PsA. The paper analyzes the current data on the clinical efficacy of TOFA in treating PsA, which have been obtained in the 12-month OPAL Broaden study including patients with PsA and an inadequate response to synthetic disease-modifying anti-rheumatic drugs and in the 6-month OPAL Beyond study enrolling those with PsA and an inadequate response to tumor necrosis factor-α (TNF-α) inhibitors. It is noted that the results of these studies confirmed the efficacy of the drug in treating PsA not only according to the data of objective (medical) monitoring, but also to the subjective characteristics of pain, to the global assessment of disease activity, fatigue, as well as the mental and physical components of the SF-36 quality of life questionnaire. It is concluded that the current findings allow JAK inhibitors to be recommended as a new pathogenetically sound approach to treating PsA and suggest that TOFA has benefits in managing patients unresponsive to therapy with TNF-α inhibitors. 

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