Paradoxical Psoriasis Induced by Anti-TNFα Treatment: Evaluation of Disease-Specific Clinical and Genetic Markers

Int J Mol Sci. 2020 Oct 23;21(21):7873. doi: 10.3390/ijms21217873.

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.

Keywords: genetic polymorphisms; inflammatory bowel disease; paradoxical psoriasis; psoriasis; tumor necrosis factor-alpha inhibitors.

MeSH terms

  • Adalimumab / administration & dosage*
  • Adalimumab / adverse effects
  • Child
  • Female
  • Genetic Markers
  • Genetic Predisposition to Disease
  • HLA-C Antigens
  • Humans
  • Inflammatory Bowel Diseases / drug therapy*
  • Inflammatory Bowel Diseases / genetics
  • Male
  • Polymorphism, Single Nucleotide*
  • Psoriasis / chemically induced
  • Psoriasis / drug therapy*
  • Psoriasis / genetics
  • Sex Characteristics
  • Tumor Necrosis Factor-alpha / genetics*

Substances

  • Genetic Markers
  • HLA-C Antigens
  • TNF protein, human
  • Tumor Necrosis Factor-alpha
  • Adalimumab