Spondyloarthritis & psoriatic arthritis
Modulation of Interleukin‐23 Signaling With Guselkumab in Biologic‐Naive Patients Versus Tumor Necrosis Factor Inhibitor–Inadequate Responders With Active Psoriatic Arthritis
Authors' conclusion
Guselkumab modulates IL-23 signaling and provides consistent pharmacodynamic effects in both biologic-naive and TNFi-IR PsA patients. Significantly elevated baseline IL-22, TNFα, and BD-2 levels and associations between baseline IL-22, IL-17A, and BD-2 levels and skin responses to guselkumab suggest greater dysregulation of IL-23/Th17 signaling in patients with TNFi-IR.
Study context
- Population
- Participants with active psoriatic arthritis (PsA), biologic-naive or TNFi-IR, treated with guselkumab (IL-23p19 inhibitor) in pooled DISCOVER-1/DISCOVER-2/COSMOS
- Participants
- 251 vs 93
- Comparison
- Biologic-naive vs TNFi-IR participants with active PsA treated with guselkumab 100 mg every 8 weeks
- Biologic-naiven = 251
- TNFi-IRn = 93reference
- Outcome
- Serum biomarker levels at baseline and after guselkumab
- Follow-up
- Week 24
Methodological detailspooled DISCOVER-1/DISCOVER-2/COSMOS data set, serum biomarker analysis
- Pooled DISCOVER-1/DISCOVER-2/COSMOS data set
- Serum biomarker analysis
Main finding
As reported in the abstract
Week 24 IL-17A, IL-17F, IL-22, serum amyloid A, CRP, IL-6 and BD-2 significantly reduced from baseline in both biologic-naive and TNFi-IR (≥1.4-fold difference)
nominal P < 0.05
Further findings
Baseline biomarkers by week 24 clinical response (responders vs nonresponders)
- Higher baseline IL-17A, IL-17F, BD-2 in biologic-naive PASI 90 responders
- nominal P < 0.05
- Higher baseline IL-17A, BD-2 in TNFi-IR IGA 0/1 responders
- nominal P < 0.05
- Higher baseline IL-22, BD-2 in TNFi-IR PASI 90 responders
- nominal P < 0.05
- Trended higher in TNFi-IR ACR20 responders
Original publication
Composed by AI from the published abstract and checked against it. How Briefs are made →