Effects of Guselkumab on Structural Damage Progression in Patients with Active Psoriatic Arthritis.
Publication Title
Advances in therapy
Document Type
Article
Publication Date
7-1-2026
Keywords
Humans; Arthritis, Psoriatic; Antibodies, Monoclonal, Humanized; Disease Progression; Antibodies, Monoclonal; Interleukin-17; Randomized Controlled Trials as Topic; Antirheumatic Agents; Guselkumab; Interleukin-23; Psoriatic arthritis; Structural damage progression.; washington; swedish
Abstract
Psoriatic arthritis (PsA) is a chronic inflammatory disease with a heterogeneous presentation including peripheral joint arthritis, axial inflammation, enthesitis, dactylitis, and psoriatic skin and nail changes. A substantial proportion of patients develop structural joint damage that can be monitored using standard radiographs. In patients with PsA, structural damage progression has been associated with significant impairment of physical function, health-related quality of life, and work productivity. Tumor necrosis factor inhibitors were the first biologic therapies approved for patients with PsA and have demonstrated efficacy in reducing the rate of structural damage progression in these patients. More recently, biologics targeting the interleukin (IL)-23p19 subunit (guselkumab and risankizumab) and IL-17 (secukinumab, ixekizumab, and bimekizumab) have been approved to treat patients with active PsA and are the subject of this review, with a focus on guselkumab. In separate phase 3, randomized, controlled studies, participants with active PsA treated with guselkumab, secukinumab, ixekizumab, and bimekizumab exhibited less structural damage progression in comparison with placebo. Both guselkumab and risankizumab inhibit the IL-23p19 subunit; however, to date, only guselkumab has demonstrated statistically significant efficacy in inhibiting structural damage progression in this patient population.
Area of Special Interest
Orthopedics & Sports Medicine
Specialty/Research Institute
Rheumatology
Specialty/Research Institute
Orthopedics
DOI
10.1007/s12325-026-03563-x
