Can we prevent psoriatic arthritis? Save

Psoriatic arthritis (PsA) can affect up to 30% of patients with psoriasis (PsO). Understanding the factors that predispose patients with PsO who progress to PsA is the first step in understanding how early interventions in PsO may augment the progression to PsA. The majority of patients with PsA present with preceding PsO. 

At #EULAR2024, there are a few presentations on this topic that will help us understand this progression from PsO to PsA better.

C-reactive protein (CRP) is a marker of inflammation that is used routinely inpatient care to monitor disease activity. In Abstract 0402, using high sensitivity (hs) CRP, Eder L et al show that higher levels of hs-CRP are associated with risk of future development of PsA among patients with PsO. This was a prospective cohort of n=589 patients with PsO without PsA at enrolment. Mean duration of follow up was 7.5 years. 57 patients developed PsA during the follow up period (incidence of 1.2 events per year). The mean hs- CRP levels were higher for those who progressed to PsA (5.4±13.1 mg/L) compared to those who did not ( 3.1±5.5 mg/L). There were also higher levels of hs-CRP at baseline in patients with arthralgia, obesity and in females. The association of higher hs-CRP and development of PsA was significant in both uni and multivariate regression analyses.

Can biologics prevent the progression from PsO to PsA?

In OP0010, Joban-Ibanez L et al from the global TRINETX study show that IL12-23 and IL-23 inhibitors reduce the incidence of PsA compared to TNF and IL 17 inhibitors, both in naïve and bio-experienced patients. Using a global network of almost 200 million medical records, the study looked at patients with PsO  without PsA who had started first-line biological treatment with TNF inhibitor (iTNF), iIL12-23, iIL17 and iIL23. After adjusting for different risk factors for PsA, the study showed that first line use of IL 12-23 and IL-23 inhibitors lowered the risk of PsA by 37% and 39% respectively compared to TNFi. In second line treatment, IL12-23i and IL-23i lowered the risk of PsA by 32% and 31% respectively compared to TNFi. IL-23i, both in 1st = and 2nd line present a 47% lower probability of developing PsA than IL-17i at 5 and 3 years.

What is the acceptability of patients participating in clinical trials to prevent the progression of PsO to PsA?

In AB 1643-PARE by Groothuizen S et al, they investigated the minimally accepted level of risk reduction for PsA development and the maximal acceptable risk of side effects for a hypothetical preventive intervention. Patients were asked about a hypothetical baseline risk of developing PsA of 50%, 70% or 90%. Patients chose between preferences for interventions to prevent PsA, in which they chose between no treatment (no benefit and no risks) or a preventive intervention (pharmacological treatment or lifestyle intervention). The study showed 92% would consider a preventive pharmacological intervention. They were willing on average to accept a risk of 45% of developing PsA after starting treatment. Lifestyle interventions were preferred with a risk of developing PsA ≥30% was accepted by 89% of participants. In terms of side effects, the maximum accepted risk of mild side effects was on average 30% and the maximum accepted risk of moderate side effects was on average 25%. The patient perspective is very important and this study showed that the willingness of PsO patients to start therapy to prevent PsA in our study is higher than previous results found for healthy people at risk of developing rheumatoid arthritis and axial spondyloarthritis.