Abstract
Abstract Background Anti-tumor necrosis factor (TNF)-α therapy is frequently used to treat inflammatory bowel disease (IBD). Paradoxical psoriasis (PP) is a known adverse effect of this drug class resulting in disfiguring skin lesions that may impact quality of life and lead to treatment cessation. To date, there are no tools to identify individuals who are susceptible to developing PP. Variations in the IL-23 receptor (IL23R) gene have been linked to psoriasis onset and may be implicated in PP. The aims of this study are 1. to study the incidence and outcomes of PP in anti-TNFα treated IBD patients at an academic centre in London, Ontario, Canada and 2. to examine risk factors associated with PP including the IL23R variant (IL23R1142G>A). Methods We performed a retrospective study of adult IBD patients treated with anti-TNFα therapies at London Health Sciences Centre between 2012 and 2024. Patient charts were reviewed for clinical variables and disease outcomes from the time of anti-TNFα exposure until treatment discontinuation or last follow-up. Patients’ serum was retrospectively genotyped for the IL23R1142G>A variant. Results We identified 496 IBD patients with 570 unique anti-TNFα exposures between 2012 and 2024. 26 patients developed 29 cases of PP while the remaining 473 patients did not develop PP after exposure to 542 anti-TNFα therapies, corresponding to a PP incidence rate of 5.1% in the study population. There was an increased proportion of patients with PP who had a positive family and personal history of psoriasis, though the latter was not significant (Table 1). The IL23R variant was more common in patients who developed PP compared to those who did not (46.2% vs. 5.1%, OR 16.04, 95% CI 6.69-38.41, Figure 1). The average time to develop PP was 9.5 months, with 55% of patients on high-dose anti-TNFα maintenance regimens. Majority of patients had moderate-to-severe disease (72.4%) based on body surface area (BSA) involvement and required treatment cessation (69.0%). All participants had complete resolution of PP following discontinuation of anti-TNFα therapy. Conclusion We identified an increased frequency of the IL23R1142G>A variant in patients who developed PP following anti-TNFα exposure compared to those who did not. Personal and family history of psoriasis were also more common in those who developed PP. Future studies should investigate other drug and disease characteristics that may predict those at highest risk for this anti-TNFα drug effect.
Published Version
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