Publications

Hernández-Hernández et al. showed that in a real-world clinical settings, UPA persistence is lower among RA patients who have received prior IL-6i treatment; and that treatment strategies to avoid UPA in patients with cardiovascular risk (CVR) appear to be primarily driven by pivotal safety studies rather than regulatory guidance.

Schaefer et al. showed that treatment with JAKis (predominantly BARI and TOF) was associated with an increased HR of malignancies compared to treatment with bDMARDs in the overall study cohort, consistent with results from the ORAL surveillance trial. To better understand the complex role of JAKis in cancer development in RA patients, Schaefer et al. estimated the effects of JAKis compared to bDMARDs on the risk of malignancy (excluding NMSC) in patients with RA.

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.

Edwards et al. report on real-world data for baricitinib monotherapy in rheumatoid arthritis, showing significant disease activity reduction across multiple registries and observational studies. These findings reinforce the viability of baricitinib monotherapy in clinical practice for RA patients, complementing existing guidelines.

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.

Unadjusted time to all-cause discontinuation was significantly longer with baricitinib treatment versus TNFi (estimated median prescription survival time of 704 days versus 448 days; log-rank P<0.01). This difference increased when only comparing differences for b/tsDMARD-naïve patients treated with baricitinib versus tofacitinib.

The observed benefit:risk ratio strongly favours JAKi use in the majority of patients, and HCPs should consider and adhere to guidance on high-risk patients where applicable. Szekanecz et al summarised the safety and efficacy of approved JAKis tofacitinib, baricitinib, upadacitinib, and filgotinib to aid in clinical decision making.

This pooled analysis of four Phase 3 RCTs investigated the long-term efficacy baricitinib in patients with active RA who were MTX-IR, csDMARD-IR, or bDMARD-IR. They found that baricitinib demonstrated efficacy up to 6.5 years and was well tolerated.