Publications

Kanda et al. investigated the efficacy of second-line b/tsDMARDs in RA patients unresponsive to first-line b/tsDMARDs. Using data from the FIRST registry, the study assessed 687 patients with RA treated with TNFis, IL-6 receptor inhibitors, cytotoxic T-lymphocyte-associated protein 4 immunoglobulin, or JAKis. After propensity score-based adjustment, JAKi showed the highest persistence rate, greatest improvement in CDAI, and highest remission rates at 24 weeks. Among JAKi, UPA was most effective in achieving remission, with a safety profile comparable to other b/tsDMARDs.

Eberhard et al. investigated the effectiveness of JAKi versus bDMARDs on pain reduction in RA patients, using Swedish national register data. JAKi treatment resulted in a significantly greater reduction in pain at three months compared with TNFis, with a higher proportion achieving low pain at 12 months, particularly in those previously treated with multiple bDMARDs.

Gladman et al. assessed the impact of bimekizumab over 1 year on patient-reported symptoms, HRQoL, and work productivity in patients with PsA who were bDMARD-naïve or TNF-IR. The study showed that bimekizumab treatment resulted in sustained improvements across multiple domains, including pain, fatigue, physical function, and work impairment.

Edwards et al. reported that in patients with RA who achieved sustained LDA or remission, tapering baricitinib from 4mg to 2mg allowed most to maintain LDA at 96 weeks. Rescue with 4mg restored control for the majority, demonstrating the feasibility of dose reduction with recovery potential for treatment.

Miyazaki et al. investigated the efficacy and safety of switching to bDMARDs versus cycling among JAKis in RA patients with inadequate JAKi response. Cycling to another JAKi proved more effective in improving disease activity at 26 weeks compared to switching to a bDMARD, and both groups had similar safety profiles.

Zavoriti and Miossec explored the impact of tofacitinib on inflammation and coagulation in RA. Tofacitinib reduced synovial and vascular inflammation by inhibiting IFNɣ, IL-17A, and IL-6 production but failed to prevent the prothrombotic effects of inflammatory cytokines on endothelial cells. These findings suggest that while tofacitinib reduces inflammation, it does not mitigate associated thrombotic risk.

Deodhar et al. conducted a pooled analysis of Phase 2 and 3 RCT data to assess the safety of tofacitinib in AS. The results showed that tofacitinib 5 mg BID had a tolerable safety profile over 48 weeks, consistent with its use in other inflammatory conditions such as RA and PsA.