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. 2024 Dec;56(12):2060-2068.
doi: 10.1016/j.dld.2024.05.021. Epub 2024 Jun 13.

Psoriasis induced by antiTNF therapy in inflammatory bowel disease: Therapeutic management and evolution of both diseases in a nationwide cohort study

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Psoriasis induced by antiTNF therapy in inflammatory bowel disease: Therapeutic management and evolution of both diseases in a nationwide cohort study

Patricia Sanz Segura et al. Dig Liver Dis. 2024 Dec.

Abstract

Background: some patients with inflammatory bowel disease (IBD) treated with antiTNF develop drug-induced psoriasis (antiTNF-IP). Several therapeutic strategies are possible.

Aims: to assess the management of antiTNF-IP in IBD, and its impact in both diseases.

Methods: patients with antiTNF-IP from ENEIDA registry were included. Therapeutic strategy was classified as continuing the same antiTNF, stopping antiTNF, switch to another antiTNF or swap to a non-antiTNF biologic. IP severity and IBD activity were assessed at baseline and 16, 32 and 54 weeks.

Results: 234 patients were included. At baseline, antiTNF-IP was moderate-severe in 60 % of them, and IBD was in remission in 80 %. Therapeutic strategy was associated to antiTNF-IP severity (p < 0.001). AntiTNF-IP improved at week 54 with all strategies, but continuing with the same antiTNF showed the worst results (p = 0.042). Among patients with IBD in remission, relapse was higher in those who stopped antiTNF (p = 0.025). In multivariate analysis, stopping antiTNF, trunk and palms and soles location were associated with antiTNF-IP remission; female sex and previous surgery in Crohn´s disease with IBD relapse.

Conclusion: skin lesions severity and IBD activity seem to determine antiTNF-IP management. Continuing antiTNF in mild antiTNF-IP, and swap to ustekinumab or switch to another antiTNF in moderate-severe cases, are suitable strategies.

Keywords: Anti-tumour necrosis factor α; Inflammatory bowel disease; Psoriasis induced by antiTNF.

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Conflict of interest statement

Conflict of interest DCD is partially supported by a Rio-Hortega fellowship from Instituto de Salud Carlos III. IM reports grants and personal fees from MSD, Janssen, Takeda, Kern and Chiesi, during the conduct of the study. AFC has served as a speaker, or has received education funding from Dr. Falk, Janssen, Takeda, Chiesi and Pfizer. MJG has received financial support for travelling and educational activities from Janssen, Pfizer, AbbVie, Takeda, Kern Pharma, Faes Farma and Ferring. IG has served as speaker or has received education funding from Takeda and Tillots. JPG has served as speaker, consultant, and advisory member for or has received research funding from MSD, Abbvie, Pfizer, Kern Pharma, Biogen, Mylan, Takeda, Janssen, Roche, Sandoz, Celgene/Bristol Myers, Gilead/Galapagos, Lilly, Ferring, Faes Farma, Shire Pharmaceuticals, Dr. Falk Pharma, Tillotts Pharma, Chiesi, Casen Fleet, Gebro Pharma, Otsuka Pharmaceutical, Norgine and Vifor Pharma. XC reports grants or contracts from Abbvie, Janssen, Kern, Takeda, Galapagos, Lilly, Sandoz; consulting fees from Janssen; payment or honoraria for lectures, presentations, speakers bureaus, manuscript writing or educational events: AbbVie, Janssen, Takeda, Galapagos, Kern; participation on a Data Safety Monitoring Board or Advisory Board: X Jansen, Galapagos; leadership or fiduciary role in other board, society, committee or advocacy group, paid or unpaid: Past-president, Societat Catalana de Digestologia. BG has served as advisor to Galapagos and Abbvie and as speaker for Abbvie, Jansen, Takeda, Pfizer and Galapagos. REM reports grants and personal fees from Janssen, Pfizer and Ferring. NP has served as speaker, consultant and advisory board of has received research funding from MSD, Abbvie, Janssen, Takeda, Roche, Sandoz, Ferring, Adacyte, Faes Farma, Kern Pharma, Pfizer, Shire Pharmaceuticals, Vifor Pharma, Chiesi and Tillots. SGL has served as a speaker, advisory member for or has received research funding from AbbVie, MSD, Takeda, Janssen and Pfizer.

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