Publications

Kristensen et al. compared 14 PsA drugs across five treatment classes, evaluating their real-world effectiveness over three months. Ixekizumab showed rapid effectiveness on joint disease activity and skin outcomes, performing better than IL-12/23i and IL-23i, and comparable to TNFi and JAKi. More patients with active psoriasis achieved minimal disease activity with Ixekizumab than other therapies.

Mease et al. assessed the comparative effectiveness of bimekizumab and risankizumab in patients with PsA over 52 weeks using a matching-adjusted indirect comparison (MAIC). The study included patients who were biologic disease-modifying anti-rheumatic drug (bDMARD) naïve or had a prior inadequate response or intolerance to tumour necrosis factor inhibitors (TNFi-IR).

Genetic variants in TNFα, NLRP3, MYD88, and FcRγ genes were associated with a response to TNFi, when assessing several inflammatory diseases together. Al-Sofi et al. conducted a systematic review and meta-analysis on single nucleotide polymorphism (SNP) genetic markers and their response to biologics in psoriasis, PsA, RA, IBD, and across all chronic inflammatory diseases together.

Compared with placebo, bimekizumab-treated patients displayed a rapid clinically meaningful improvement in PsAID-12 scores at Week 4, which continued to Week 16 and was sustained to 1 year. Gossec et al. assessed 1-year bimekizumab efficacy from the patient perspective using the PsAID-12 questionnaire in bDMARD-naïve (BE OPTIMAL) and TNFi-IR (BE COMPLETE) patients with active PsA.

Results of this analysis by Hernández-Cruz, et al. show that infections, herpes zoster and gastrointestinal AEs in patients with RA tended to be more frequent with JAKi treatment versus TNFi. They also found that treatment persistence was similar with JAKi and TNFi in patients with RA and axSpA, and only slightly higher for TNFi in patients with PsA.

Risk of composite CV endpoints combining all ischaemic CV events and heart failure were similar for individual and combined TOF doses versus TNFi. The totality of CV risk (MACE-8 plus VTE) was higher with TOF 10mg twice daily versus TNFi. Buch et al conducted a post-hoc analysis on the ORAL Surveillance trial to assess risk across extended MACE endpoints in RA patients treated with either TOF 5mg, TOF 10mg, or TNFi.

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.

This post hoc analysis of ORAL Surveillance showed that incidence of venous thromboembolism (VTE) events was higher in patients with RA treated with tofacitinib (10>5mg BID) versus TNFi. Across treatments, VTE risk factors (age, BMI, and VTE history) were aligned with previous studies in the general RA population.

The results of the meta-analysis show that TNFi, IL-17i, and JAK inhibitor treatments significantly improved sacroiliac joint SPARCC scores in patients with axSpA or AS at Weeks 12–16. However, there were no significant differences in mean improvement between the treatment groups.

This study by Cho, et al. did not find any significant differences in remission rates in South Korean patients with RA that were treated with tofacitinib versus TNFi in a real-world setting. Remission rates were significantly higher for patients naïve to both JAKi and bDMARDs treated with tofacitinib versus TNFi.