Comparative study of the efficacy and safety of tofacitinib, baricitinib, upadacitinib, and filgotinib versus methotrexa
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Rheumatologie Originalien Z Rheumatol https://doi.org/10.1007/s00393-020-00889-x Accepted: 30 August 2020 © Springer Medizin Verlag GmbH, ein Teil von Springer Nature 2020 Redaktion U. Müller-Ladner, Bad Nauheim U. Lange, Bad Nauheim
Introduction Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic synovial joint inflammation, leading to disability and reduced quality of life [31]. Methotrexate (MTX), an effective disease-modifying antirheumatic drug (DMARD) [10], is one of the most widely used DMARDs in the treatment of RA [17]. Nevertheless, not all patients are responsive to the drug as 30% of patients discontinue therapy within 1 year of commencement due to, in most cases, the lack of efficacy or undesirable adverse effects [2]. Therefore, an alternative to MTX in RA patients who cannot take or tolerate MTX may be required. Furthermore, although current guidelines recommend MTX as initial DMARD therapy for patients with RA, use of corticosteroids has been recommended to bridge treatment response due to slow onset of MTX [30, 32]. Hence, novel therapies with rapid onset may obviate the need to use corticosteroid as bridge therapy with MTX, thereby eliminating the toxicities that have been identified with corticosteroid treatment.
Y.-K. Sung1 · Y. H. Lee2 1
Department of Rheumatology, Hanyang University Hospital for Rheumatic Diseases, Seoul, Korea (Republic of) 2 Department of Rheumatology, Korea University College of Medicine, Seongbuk-gu, Seoul, Korea (Republic of)
Comparative study of the efficacy and safety of tofacitinib, baricitinib, upadacitinib, and filgotinib versus methotrexate for disease-modifying antirheumatic drug-naïve patients with rheumatoid arthritis The intracellular pathways involving the Janus kinases (JAKs; JAK1, JAK2, JAK3) and tyrosine kinase 2 (Tyk2) are critical to immune cell activation, pro-inflammatory cytokine production, and cytokine signaling [12]. In the past decade, small-molecule JAK inhibitors were clinically developed for the treatment of RA [27]. Among these
is tofacitinib, an orally administered JAK inhibitor [7]. It selectively inhibits JAK-1, JAK-2, and JAK-3, with a functional cellular specificity for JAK-1 and JAK-3 over JAK-2 [8, 24]. Baricitinib, another JAK inhibitor, is a potent, selective JAK1 and JAK2 inhibitor [29]. Baricitinib shows similar inhibitory activities against both JAK1 and JAK2, but Fig. 1 9 Evidence network diagram of the comparators in the network meta-analysis. The width of each edge is proportional to the number of randomized controlled trials comparing each treatment pair. The size of each treatment node is proportional to the number of randomized participants (sample size). A methotrexate, B tofacitinib 5 mg, C baricitinib 4 mg, D upadacitinib 15 mg, and E filgotinib 200 mg Zeitschrift für Rheumatologie
Originalien Table 1 Study
Characteristics of the individual studies included in the network meta-analysis—JAK inhibitors Subjects Total Drugs, mean No. of No. No. No. number dosage patients achieving achieving achieving
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