Psoriasis has a known association with inflammatory bowel disease, including Crohn disease and ulcerative colitis. Dermatologists should keep the association in mind when treating their patients with psoriasis.
The idea of discussing all of the potential comorbidities with a patient newly diagnosed with psoriasis can be overwhelming. It is both a lot to say at a new visit for the dermatologist and certainly a lot to understand as the patient. With the growing amount of evidence supporting the increased likelihood of developing multiple comorbidities in psoriasis, it is best to find an approach that works for both you and your patients. I had a patient recently tell me that her first appointment was incredibly emotional. She is not the only one, and I partly have myself to blame for discussing too much with her in that first visit. For most newly-diagnosed patients, learning that they have a life-long chronic disease that could affect joints is already difficult to comprehend; it does not make it easier to hear about all of the scary comorbidities that could be in their future. This was a great lesson for me, and I hope to evolve my practice in a way that will allow me to educate my patients without paralyzing them with fear.
The objective of this article is to share recent data available on inflammatory bowel disease (IBD) and psoriasis as well as discuss screening and best treatment practices based on the literature. IBD and its importance in psoriasis really came to light during clinical trials with IL-17 inhibitors. Since then, several studies and articles have been published trying to discern the true risk of IBD in patients with psoriasis and if screening for symptoms should become standard practice.
Literature Review
According to available literature, the risk of IBD is around four times higher in the psoriasis population, and the risk of Crohn disease (CD) appears to be greater than ulcerative colitis.1,2 This is may be explained by some shared genotypic and immunologic commonalities, such as susceptibility genes that have a shared chromosomal locus (eg, HLA-C and SEL1L) as well as the IL23R and IL12B genes, though more research is needed to understand these associations.3 Both diseases are postulated to result from a combination of environmental and immunologic factors that may lead to impaired interaction between the immune system and microbiota.1,3 IBD traditionally presents with any variation of vomiting, diarrhea, bloody stools, recurrent loss of appetite, abdominal pain, and weight loss.3
A retrospective study looked at patients with concurrent psoriasis and IBD to determine characteristics and trends among this population.2 The researchers found that patients with both psoriasis and IBD were more commonly women and that psoriasis was diagnosed at a younger age and was of more mild severity in this group. The frequency of concomitant psoriatic arthritis was also higher, and these patients were more likely to have other autoimmune diseases. The knowledge of these characteristics could potentially be used to help identify patients that may be at a higher risk for concurrent IBD.
At first glance, it may seem appropriate to change our practices and use medications that can treat both psoriasis and IBD. However, a deeper look at the numbers may support the notion that while we should be aware of this association and screen for signs and symptoms of IBD, a change in prescribing practices is likely not warranted. The overall prevalence of IBD is 0.4%, and studies have found that the prevalence of IBD among psoriasis patients ranges from 1% to 2%.2,4 Screening for family history of IBD and including appropriate questions in the review of systems can hopefully help determine risk and aid in treatment decisions.
Several familiar cytokines, such as tumor necrosis factor (TNF), IL-17, and IL-23, are all involved in the pathogenesis of both psoriasis and IBD,5 so it is not surprising that these diseases share many common treatments. However, new onset and flares of IBD occurred in trials of the three different IL-17 inhibitors approved for psoriasis, suggesting that IL-17 may play a protective role in the gut.6-9 This has been further supported by the demonstration of increased colitis severity in mouse models with IL-17 inhibition.10 A systematic review and meta-analysis of studies conducted from 2010 to 2018 of treatment with IL-17 antagonists in patients with psoriasis, psoriatic arthritis, ankylosing spondylitis, and rheumatoid arthritis contradicts these studies; Burisch et al11 found no increase in IBD incidence in more than 19,000 patients treated with IL-17 inhibitors. However, it appears that many of the studies did not specifically look for IBD as an adverse event and many reported “gastrointestinal disorders” or “diarrhea,” thus muddying this contradiction.11 TNF-α inhibitors have been proven to successfully treat both psoriasis and IBD, but interestingly, there are few reports of patients with IBD developing psoriatic lesions while undergoing treatment with TNF inhibitors.12
Clinical Recommendations
Considering what is known regarding these two entities, my advice is to be aware of this association and add a few IBD symptoms into your review of systems. The joint guidelines of care from the American Academy of Dermatology and National Psoriasis Foundation recommend informing patients of this relationship between psoriasis and IBD.13 Implementing the knowledge we just discovered regarding characteristics of patients most likely to carry both diagnoses can assist us in our treatment decisions. For patients with psoriasis who have a strong family history of IBD or are exhibiting symptoms, choosing a biologic that can potentially assist with both conditions might be the best option, and IL-17 antagonists should likely be avoided. As always, it may be beneficial to develop a relationship with a gastroenterologist who can work closely with you in managing these patients as well as guide patients with psoriasis to seek a consultation with a gastroenterologist if there are digestive symptoms present.
Dr Hawley is an associate clinical professor of dermatology at Michigan State University College of Osteopathic Medicine and medical
director of The Derm Institute of West Michigan in Grand Rapids, MI.
Disclosure: The author reports no relevant financial relationships.
References
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3. Fu Y, Lee CH, Chi CC. Association of psoriasis with inflammatory bowel disease: a systematic review and meta-analysis. JAMA Dermatol. 2018;154(12):1417-1423. doi:10.1001/jamadermatol.2018.3631
4. Cohen AD, Dreiher J, Birkenfeld S. Psoriasis associated with ulcerative colitis and Crohn’s disease. J Eur Acad Dermatol Venererol. 2009;23(5):561-565. doi:10.1111/j.1468-3083.2008.03031.x
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8. van de Kerkhof PC, Griffiths CE, Reich K, et al. Secukinumab long-term safety experience: a pooled analysis of 10 phase II and III clinical studies in patients with moderate to severe plaque psoriasis. J Am Acad Dermatol. 2016;75(1):83-98.e4. doi:10.1016/j.jaad.2016.03.024
9. Targan SR, Feagan B, Vermeire S, et al. A randomized, double-blind, placebo-controlled phase 2 study of brodalumab in patients with moderate-to-severe Crohn’s disease. Am J Gastroenterol. 2016;111(11):1599-1607. doi:10.1038/ajg.2016.298
10. Ogawa A, Andoh A, Araki Y, Bamba T, Fujiyama Y. Neutralization of interleukin-17 aggravates dextran sulfate sodium-induced colitis in mice. Clin Immunol. 2004;110(1):55-62. doi:10.1016/j.clim.2003.09.013
11. Burisch J, Eigner W, Schreiber S, et al. Risk for development of inflammatory bowel disease under inhibition of interleukin 17: a systematic review and meta-analysis. PLoS One. 2020;15(5):e0233781. doi:10.1371/journal.pone.0233781
12. Denadai R, Teixeira FV, Steinwurz F, Romiti R, Saad-Hossne R. Induction or exacerbation of psoriatic lesions during anti-TNF-α therapy for inflammatory bowel disease: a systematic literature review based on 222 cases. J Crohns Colitis. 2013;7(7):517-524. doi:10.1016/j.crohns.2012.08.007
13. Elmets CA, Leonardi CL, Davis DMR, et al. Joint AAD-NPF guidelines of care for the management and treatment of psoriasis with awareness and attention to comorbidities. J Am Acad Dermatol. 2019;80(4):1073-1113. doi:10.1016/j.jaad.2018.11.058
