What’s New in Psoriatic Arthritis: A Whirlwind Tour Save

At the "What Is New in Psoriatic Arthritis" session at EULAR 2026, Professor Dennis McGonagle (Leeds, UK) took the audience on a whirlwind yet compact tour of the field, touching on three themes: the pathophysiology of PsA, individualization of clinical management, and emerging research and future directions. Each theme came with its own takeaway, and those takeaways are worth knowing from the start: we are entering the single cell and spatial transcriptomics era in PsA biology; clinical advances are real but individualization is not yet operational; and defining biologically refractory disease, with combination therapy to follow, is the next frontier. 

What follows is a high-level summary, with pointers to the session and key abstracts for those who want to go deeper.

Pathophysiology: Start of the Single Cell Era

Professor McGonagle opened with PsA's defining challenge: pathological heterogeneity. Distinguishing inflammatory from non-inflammatory disease drivers in the same patient remains genuinely hard, and the publication of the first single cell atlas of the enthesis marks the beginning of a more precise era for PsA research.

The mechanistic highlights moved fast. Skin to joint trafficking via mitochondrial variants (Raimondo, Nature Immunology 2026) and entheseal fibroblasts with regulatory T-cell properties (Altaie, ARD 2025) point to a more structured entheseal immune biology than previously appreciated. The persistently inflammatory PsA (PIPsA) versus non-inflammatory PsA (NIPsA) framework (Zabotti, Nature Reviews Rheumatology 2025) draws a clinically important distinction between phenotypes that will not respond to targeted therapy in the same way. On JAK inhibitors, Giryes et al. (AR 2025) showed paradoxical entheseal activation via IL-10 antagonism, and cardiovascular and thrombotic risk data continued to accumulate, with signals that carry real weight in clinical conversations.

Clinical Management: Advances Yes, Individualization Maybe Not Yet

EULAR has formally defined difficult to manage PsA (D2M): failure of two or more bDMARDs or tsDMARDs with distinct mechanisms, management perceived as problematic by rheumatologist or patient, and at least one additional criterion such as failure to achieve low disease activity or objective inflammation. The criteria diverge from GRAPPA and Zabotti PIPsA frameworks on imaging requirements for enthesitis and tender joints, with real implications for who gets labeled refractory.

The axial PsA data were among the most clinically interesting parts of the session. The AXIS study found axial prevalence of 37% by local reader versus 23% by central reader, reflecting how contested axial assessment remains. The topographic anatomy of the sacroiliac joint added nuance: upper SIJ bone marrow edema lesions are linked to BMI, psoriasis severity, and HLA-B27 negativity, while lower SIJ lesions track with the HLA-B27-positive axial spondyloarthritis phenotype (Abacar, Joint Bone Spine, 2026).

Two treatment findings stood out. The guselkumab plus golimumab combination (Scher, AR 2025) achieved minimal disease activity in 32% versus 13% with monotherapy, lending real weight to TNF plus IL-23 dual blockade in refractory disease. TNF inhibitor plus methotrexate was not superior to methotrexate plus corticosteroids in early DMARD naive PsA (De Marco, Lancet Rheumatology 2025), worth noting, though steroid use warrants caution given risks of psoriasis flare and metabolic effects. JAK inhibitor major adverse cardiovascular event rates of 8.5% versus 4% for bDMARDs at two to five years (OP0181, EULAR 2026) continue to inform benefit-risk tradeoffs.

Emerging Research: An Oral Pipeline and an Open Prevention Question

The emerging therapy landscape was genuinely exciting. A late breaking head-to-head at EULAR 2026 showed bimekizumab outperforming risankizumab on ACR50 at 49% versus 38% (p=0.0078). The oral targeted pipeline is growing: icotrokinra, an oral IL-23 receptor peptide in phase 3, zasocitinib, a highly selective TYK2 inhibitor in phase 2b, and deucravacitinib, FDA approved for PsA in March 2026. As small molecules, TYK2 inhibitors offer potential for better tissue penetration at difficult to reach sites like the enthesis compared to large biologic proteins, a rationale that makes this class particularly relevant for enthesitis. Presented at EULAR 2026, the TOGETHER-PsA trial (Merola, Arthritis and Rheumatology 2026) tested ixekizumab plus tirzepatide in PsA patients with overweight or obesity, on the premise that obesity is a key driver of disease activity and that targeting it alongside a biologic lead to better outcomes. Adding tirzepatide to ixekizumab achieved greater disease control than the biologic alone.

On prevention, biologic exposure in psoriasis patients tells a nuanced story. Exposure to two or more biologics carried an increased odds of PsA development (Watad, Rheumatology Therapy 2024), while in the second line setting IL-17 inhibitors were independently associated with a significantly lower PsA risk versus TNF inhibitors (Watad, RMD Open 2026). These findings sit alongside several observational studies supporting IL-23 inhibition as a preventive signal, though Professor McGonagle framed the overall prevention question as still open.

Bottom Line

Professor McGonagle closed with the same three themes he opened with, and by that point in the session, each conclusion felt earned. The single cell era is reshaping how we understand entheseal biology. Clinical frameworks are sharper, even if personalized treatment guided by disease biology is still on the horizon. And the move toward defining biologically refractory disease more precisely, with combination therapy to follow, may be where the most important work in PsA gets done over the next few years.