PMID- 37664349 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20230905 IS - 2168-8184 (Print) IS - 2168-8184 (Electronic) IS - 2168-8184 (Linking) VI - 15 IP - 8 DP - 2023 Aug TI - Paradoxical Tumor Necrosis Factor-Alpha (TNF-alpha) Inhibitor-Induced Psoriasis: A Systematic Review of Pathogenesis, Clinical Presentation, and Treatment. PG - e42791 LID - 10.7759/cureus.42791 [doi] LID - e42791 AB - Tumor necrosis factor-alpha (TNF-alpha) inhibitors have been shown to be well tolerated among patients with rheumatoid arthritis, inflammatory bowel disease, and psoriasis. Meanwhile, more recently, clinical practice and research efforts have uncovered increasing cases of psoriatic lesion development tied to initiating treatment with a TNF-alpha inhibitor. The underlying mechanisms associated with this occurrence have yet to be fully elucidated. A review and analysis of cases of paradoxical psoriasis currently published in the literature is warranted. In addition, exploring possible mechanisms of action and potential treatment options associated with favorable outcomes is much needed. A systematic literature review was performed utilizing PubMed and Google Scholar databases (1992-present), in which 106 cases of paradoxical psoriasis were reviewed. The most common morphology developed was plaque psoriasis vulgaris. There was a female predominance (61.3%), and the most common underlying autoimmune disease was rheumatoid arthritis (45.3%). In addition, the most commonly associated drug with the onset of psoriatic lesions was infliximab (62.3%). Furthermore, the findings suggest that the most well-supported mechanism of action involves the uncontrolled release of interferon-alpha (IFN-alpha) from plasmacytoid dendritic cells (pDCs) after TNF-alpha inhibition. While TNF-alpha inhibitors have been shown to have great benefits to patients with rheumatologic diseases, cases of paradoxical psoriasis demonstrate the importance of close monitoring of patients on TNF-alpha inhibitors to allow for early recognition, treatment, and potentially change to a different mechanism of action of the medication used to prevent further progression of the inflammatory lesions. CI - Copyright (c) 2023, Chokshi et al. FAU - Chokshi, Aditi AU - Chokshi A AD - Dermatology, Nova Southeastern University Dr. Kiran C. Patel College of Osteopathic Medicine, Davie, USA. FAU - Demory Beckler, Michelle AU - Demory Beckler M AD - Microbiology and Immunology, Nova Southeastern University Dr. Kiran C. Patel College of Allopathic Medicine, Davie, USA. FAU - Laloo, Anita AU - Laloo A AD - Rheumatology, Nova Southeastern University Dr. Kiran C. Patel College of Osteopathic Medicine, Davie, USA. FAU - Kesselman, Marc M AU - Kesselman MM AD - Rheumatology, Nova Southeastern University Dr. Kiran C. Patel College of Osteopathic Medicine, Davie, USA. LA - eng PT - Journal Article PT - Review DEP - 20230801 PL - United States TA - Cureus JT - Cureus JID - 101596737 PMC - PMC10469896 OTO - NOTNLM OT - paradoxical OT - pathogenesis OT - psoriasis OT - tnf-a inhibitor OT - treatment COIS- The authors have declared that no competing interests exist. EDAT- 2023/09/04 06:42 MHDA- 2023/09/04 06:43 PMCR- 2023/08/01 CRDT- 2023/09/04 05:12 PHST- 2023/07/06 00:00 [received] PHST- 2023/07/31 00:00 [accepted] PHST- 2023/09/04 06:43 [medline] PHST- 2023/09/04 06:42 [pubmed] PHST- 2023/09/04 05:12 [entrez] PHST- 2023/08/01 00:00 [pmc-release] AID - 10.7759/cureus.42791 [doi] PST - epublish SO - Cureus. 2023 Aug 1;15(8):e42791. doi: 10.7759/cureus.42791. eCollection 2023 Aug.