Published in:
01-09-2018 | Original Article
Stricturing and Fistulizing Crohn’s Disease Is Associated with Anti-tumor Necrosis Factor-Induced Psoriasis in Patients with Inflammatory Bowel Disease
Authors:
Adam V. Weizman, Robyn Sharma, N. M. Afzal, Wei Xu, Scott Walsh, Joanne M. Stempak, Geoffrey C. Nguyen, Ken Croitoru, A. Hillary Steinhart, Mark S. Silverberg
Published in:
Digestive Diseases and Sciences
|
Issue 9/2018
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Abstract
Background
Paradoxical development of psoriasis in patients on anti-TNF agents has been increasingly reported.
Aim
The aim was to characterize the prevalence and clinical characteristics of anti-TNF-associated psoriasis in a large cohort of inflammatory bowel disease patients.
Methods
Medical records of patients with Crohn’s disease or ulcerative colitis treated with anti-TNF therapy at a single, tertiary IBD center were identified between 2004 and 2016. Patients identified as having developed psoriasis while on anti-TNF underwent detailed retrospective review of dermatologic features and changes in IBD treatment prompted by the development of psoriasis.
Results
Among 676 patients treated with anti-TNF (infliximab or adalimumab), the incidence of psoriasis was 10.7% (N = 72). Female gender (OR 1.88 [95% CI 1.12–3.17], p = 0.017), stricturing or fistulizing Crohn’s disease (OR 1.83 [95% CI 1.04–3.21], p = 0.036) and upper GI Crohn’s disease (OR 3.03 [95% CI 1.06–8.33], p = 0.039) were associated with psoriasis development. The median time to psoriasis onset was 569 days from initiation of anti-TNF, with onset occurring earlier in patients who developed psoriasis on adalimumab versus infliximab (457 vs. 790.5 days, p = 0.008). Overall, in 15/72 (20.8%), cases, cessation of the anti-TNF was required as a result of psoriasis. Plaque psoriasis was the most common type of psoriatic lesion (75%). Topical corticosteroids were the most common treatment for psoriasis.
Conclusion
We report a high incidence of anti-TNF-associated psoriasis that was associated with female gender, foregut disease location, and fistulizing and stricturing disease behavior. More prospective studies and genetic analyses evaluating possible pathophysiologic underpinnings of this problem are needed.