Impact of Biologic Therapies on the Risk of Progression from Psoriasis to Psoriatic Arthritis

BACKGROUNDPsoriasis progresses to psoriatic arthritis in up to 30% of patients, causing irreversible joint damage and substantial healthcare burden. Whether biologic therapy reduces psoriatic arthritis risk remains unclear.

OBJECTIVEThe aim of this paper was to evaluate the association between biologic therapy and psoriatic arthritis risk in psoriasis patients.

METHODSWe conducted a systematic review and meta-analysis of cohort studies (PROSPERO: CRD420251240466), searching PubMed, EMBASE, and Cochrane Library from inception to December 2025. We included cohort studies of adults with psoriasis without prior psoriatic arthritis that reported adjusted risk estimates for incident psoriatic arthritis and used an 'on-drug' analytical framework to account for changes in treatment status over time. Pooled hazard ratio (HRs) with 95% confidence interval (CI) were calculated using fixed- or random-effects models.

RESULTSIn total, 15 cohort studies including 124,138 psoriasis patients with over 778,690 person-years of follow-up were included. Biologic use was associated with a 46% lower psoriatic arthritis risk versus non-biologic therapy (pooled HR 0.54, 95% CI 0.43-0.68), consistent versus non-systemic therapies (HR 0.57, 95% CI 0.33-0.97) and methotrexate (HR 0.48, 95% CI 0.45-0.51). Interleukin (IL)-17 inhibitors (HR 0.65, 95% CI 0.49-0.87; 3 studies) and IL-12/23 or IL-23 inhibitors (HR 0.46, 95% CI 0.36-0.60; 4 studies) were associated with lower psoriatic arthritis risk than tumor necrosis factor inhibitors. IL-23 inhibitors showed greater protection than IL-17 inhibitors (HR 0.67, 95% CI 0.58-0.77), while IL-23 inhibitors and IL-12/23 inhibitors did not differ (HR 0.88, 95% CI 0.69-1.13).

CONCLUSIONSBiologic therapy for psoriasis, particularly IL-23/IL-17-targeted agents, is associated with reduced incident psoriatic arthritis risk. These findings suggest early pathway suppression may delay clinical psoriatic arthritis diagnosis, though causal inference is limited by the observational data.

Abstract from PubMed