Background/Purpose: Paradoxical psoriasis is an increasingly recognized adverse effect of biologic therapy in pediatric rheumatology, most often with TNF-α inhibitors (TNF-i) such as adalimumab and infliximab. Although TNF-i are widely used, well tolerated, and effective for disease control, some patients develop new-onset psoriatic lesions after treatment initiation1. This retrospective study aims to identify and describe pediatric cases in Saskatchewan over the past 10 years in which psoriasis occurred secondary to TNF-i therapy, including demographics, underlying diagnoses, clinical presentation, timing of onset, and management. Findings are compared with existing literature to improve understanding and highlight gaps in the pathophysiology and management of TNF-i–induced psoriasis2.

Methods: A retrospective chart review was conducted of pediatric rheumatology patients treated with adalimumab or infliximab who subsequently developed psoriasis. Cases from a 10-year period were identified from clinic records. Data collected included demographics, underlying diagnosis, TNF-i agent, duration of exposure, and latency to psoriasis onset. Lesion morphology, distribution, severity, and relevant laboratory findings were recorded. Management strategies (topical, systemic, and biologic therapy changes) and treatment outcomes were summarized descriptively.

Results: A total of 6 cases of TNF-i–induced psoriasis were identified among 104 pediatric rheumatology patients started on TNF-i over 10 years (4.8%). One patient refused to participate in the study. Indications for treatment were juvenile idiopathic arthritis (JIA) in 4/5 (80%) and chronic non-bacterial osteitis (CNO) in 1/5 (20%). Both adalimumab (4/5, 80%) and infliximab (1/5, 80%) were implicated as biologic agents potentially contributing to the observed manifestations. Latency to onset ranged from 5.5 to 45 months, with a median of 23.5 months. A personal or family history of psoriasis was present in 1/5 (20%). Plaque-type scalp lesions and palmoplantar involvement were most common (4/5, 80%). Dermatology assessed 4/5 (80%); no biopsies were performed. At data collection, psoriasis was in remission in 3/5 (60%). Two patients (2/5, 40%) had partial improvement with topical and/or systemic therapy while continuing treatment with TNF-i. One JIA patient (1/5, 20%) achieved remission after switching to tocilizumab, while another (1/5, 20%) remained active despite a recent switch to tocilizumab. The CNO patient (1/5, 20%) achieved remission after transitioning to golimumab with intralesional corticosteroids and topical therapy.

Conclusion: TNF-i therapy can paradoxically induce psoriasis in pediatric rheumatology patients, with variable timing and clinical presentations. Most patients can be managed with topical and/or systemic therapy while continuing TNF-i; however, some require switching to a non–TNF-i biologic to achieve remission. Early recognition and counselling are essential. Further research is needed to identify risk factors and guide management strategies.

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ACR Meeting Abstracts - https://acrabstracts.org/abstract/recognizing-paradoxical-psoriasis-in-tnf-inhibitor-treated-pediatric-rheumatic-disease-a-saskatchewan-experience/