Abstract

Paradoxical psoriasis (PP) may occur during treatment with anti-tumor necrosis factor-alpha (TNF-α) drugs in various chronic immune-mediated diseases, mainly inflammatory bowel diseases (IBD) and psoriasis. In this study, clinical and genetic characteristics of PP arising in IBD and psoriatic patients were investigated to identify disease-specific markers of the paradoxical effect. A total of 161 IBD and psoriatic patients treated with anti-TNF-α drugs were included in the study. Of these patients, 39 developed PP. All patients were characterized for the main clinical–pathologic characteristics and genotyped for six candidate single nucleotide polymorphisms (SNPs) selected for their possible role in PP susceptibility. In IBD patients, the onset of PP was associated with female sex, presence of comorbidities, and use of adalimumab. IBD patients with PP had a higher frequency of the TNF-α rs1799964 rare allele (p = 0.006) compared with cases without the paradoxical effect, and a lower frequency of the human leucocyte antigen (HLA)-Cw06 rs10484554 rare allele (p = 0.03) compared with psoriatic patients with PP. Overall, these findings point to specific clinical and genetic characteristics of IBD patients with PP and provide data showing that genetic variability may be related to the paradoxical effect of anti-TNF-α drugs with possible implications into clinical practice.

Highlights

  • Paradoxical psoriasis (PP) represents a peculiar type of psoriasis that may occur de novo or as the exacerbation of pre-existent psoriatic lesions during treatment with biological drugs [1]

  • inflammatory bowel diseases (IBD) patients with PP significantly differed from IBD patients without PP in relation to sex (p < 0.001), presence of comorbidities (p = 0.01), and the biological drug used (p < 0.001)

  • The infliximab was the most widely used anti-TNF-α drug, the PP was most frequently observed in patients treated with adalimumab

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Summary

Introduction

Paradoxical psoriasis (PP) represents a peculiar type of psoriasis that may occur de novo or as the exacerbation of pre-existent psoriatic lesions during treatment with biological drugs [1]. The first case of PP induced by anti -TNF-α treatment was described in a patient affected by inflammatory bowel diseases (IBD) more than 15 years ago [5], and later, an increasing number of cases of PP has been reported in the literature, mainly due to the widespread use of anti-TNF-α drugs [6,7,8,9,10,11] For their good safety profile and high sustainability, TNF-α inhibitors have revolutionized the management of numerous chronic immune-mediated inflammatory diseases, including IBD and psoriasis [12,13,14,15]. The most frequently reported clinical presentations of PP are palmoplantar pustular eruption, plaque-type and guttate psoriasis, and nail and scalp involvement have been described [23,24,25,26]

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