Publications

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.

Baraliakos et al. evaluated the long-term safety and efficacy of bimekizumab in axSpA through a 2-year analysis of the BE MOBILE 1 and BE MOBILE 2 studies. Bimekizumab was well tolerated, with a consistent safety profile and no new safety signals. Clinical improvements, including ASAS40 response and MRI remission, were sustained through Wk104.

Gossec et al. demonstrated that tofacitinib significantly reduced fatigue in patients with ankylosing spondylitis, with median times to clinically meaningful improvements of 8 and 12 weeks for initial and stable improvement events, respectively. These changes were observed as early as two weeks and were more pronounced compared to placebo.

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.

Haraoui et al. conducted a subgroup analysis of the CANTORAL study, showing that tofacitinib effectiveness was similar in patients with or without CV risk enrichment. However, AEs, particularly in older patients (≥65 years), were more frequent in the CV+ cohort. These findings highlight the need for tailored CV risk management when treating RA with tofacitinib.

Delcourt et al. conducted a systematic review and meta-analysis revealing that both pharmacological (DMARDs) and non-pharmacological interventions reduce fatigue in axSpA patients over short and medium terms, with greater efficacy seen when combined.

Tanaka et al. observed that in Japanese patients with rheumatoid arthritis treated with tofacitinib, those with absolute lymphocyte counts (ALCs) <0.5x10³ cells/mm³ had a higher risk of serious infections and herpes zoster events compared to patients with higher ALC levels. This threshold may help identify increased infection risk in this population

Goldman, et al. conducted a pharmacovigilance study to evaluate the cardiovascular safety of JAK inhibitors in RA patients. The study demonstrated an increase in the reporting of VTE, stroke, and ischemic heart disease in patients treated with JAK inhibitor compared to bDMARDs, especially within the first year of treatment. This suggests a class effect of JAK inhibitors on cardiovascular risk, emphasising the need for ongoing surveillance and proactive cardiovascular risk management.

Crude gastrointestinal perforation (GIP) incidence rate was higher for the JAKi group compared with those receiving adalimumab, however rates of GIP did not differ between JAKi and adalimumab groups in the weighted and adjusted model. Hoisnard et al compared the risk of GIP in patients initiating treatment with JAKis or adalimumab among real-world patients with rheumatic disease.