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Year : 2015  |  Volume : 3  |  Issue : 1  |  Page : 81-83

Infliximab-induced psoriasis in a patient with crohn's disease

1 Department of Dermatology, College of Medicine, University of Dammam, King Fahd Hospital of the University, Dammam, Saudi Arabia
2 Department of Internal Medicine, College of Medicine, University of Dammam, King Fahd Hospital of the University, Dammam, Saudi Arabia

Date of Web Publication20-Jan-2015

Correspondence Address:
Abdulaziz A Al-Quorain
Department of Internal Medicine, College of Medicine, University of Dammam, King Fahd Hospital of the University, Dammam
Saudi Arabia
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1658-631X.149695

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Infliximab is a well-known treatment for inflammatory bowel diseases (IBDs) and psoriasis. Paradoxically, there have been numerous reports of new-onset psoriasis following tumor necrosis factor-α antagonist therapy in patients with IBD. Here, we report a case with Crohn's disease who developed Infliximab-induced plaque-type psoriasis 4 months after initiation of treatment with Infliximab.

  Abstract in Arabic 

ملخص البحث:
يعتبر الانفليكسماب علاجًا معروفًا لمرض التهاب الأمعاء التقرحية. والصدفية. لكن هناك تقارير أفادت بظهور حالات صدفية في أعقاب المعالجة بهذا الدواء لدى المرضى المصابين بالتهاب الأمعاء التقرحية. يعرض الباحثون حالة صدفية لمصاب بمرض كرونز. ناجمة عن علاج الانفليكسماب بعد أربعة أشهر من بداية العلاج.

Keywords: Biological therapy, Crohn′s disease, Infliximab, psoriasis, tumor necrosis factor-alpha inhibitors

How to cite this article:
Bukhari I, Alzoubi N, Al-Quorain AA. Infliximab-induced psoriasis in a patient with crohn's disease. Saudi J Med Med Sci 2015;3:81-3

How to cite this URL:
Bukhari I, Alzoubi N, Al-Quorain AA. Infliximab-induced psoriasis in a patient with crohn's disease. Saudi J Med Med Sci [serial online] 2015 [cited 2023 Feb 5];3:81-3. Available from: https://www.sjmms.net/text.asp?2015/3/1/81/149695

  Introduction Top

Biologic therapy has a well-known established role in the management of many inflammatory conditions including inflammatory bowel disease (IBD), rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis and psoriasis. [1],[2],[3],[4],[5],[6],[7],[8] Unfortunately, in recent years a paradoxical effect has been reported with anti-tumor necrosis factor-α (TNF-α) therapy in patients with Crohn's disease (CD), which is the development of psoriatic skin lesions. Numerous case reports, case series, and reviews have been published, mainly describing new-onset or worsening of existing psoriasis and psoriasiform exanthemata in adult patients following TNF-α antagonist therapy. [9],[10],[11],[12],[13] However, researchers have recognized an association between IBD and psoriasis, with an increased prevalence of psoriasis in patients with IBD and vice versa. [14],[15],[16] These data suggest that genetic variants common to both conditions may coexist and research for genetic polymorphisms common to these conditions is being carried-out. [17]

  Case report Top

A 19-year-old Arab female who had been diagnosed with CD the year before was given an infusion of Infliximab which was initiated (5 mg/kg body weight) at weeks 0, 2, 6 with maintenance infusions given every 8 weeks. There was a significant improvement of the bowel disease. However, after the 4 th infusion of Infliximab (4 th months), the patient gradually developed erythematous and scaly plaques all over her body, including the upper and lower limbs [Figure 1]. The rash initially improved with topical steroids then reappeared after each infusion of Infliximab. There were no associated symptoms. Both parents had psoriasis. On physical examination, there were erythematous papules and plaques with silvery scales on the trunk, buttocks, arms, legs and scalp. Skin punch biopsy was consistent with early lesions of psoriasis. A diagnosis of plaque-type psoriasis was made and treatment with calcipotriol/betametasone ointment was initiated. The lesions improved after a few weeks but recurred upon every Infliximab infusion, with a total of four infusion cycles. Since the psoriatic lesions improved with topical treatment and the bowel disease was stable, Infliximab infusion was continued regardless of that side effect.
Figure 1: well demarcated erythematous plaques covered with silvery scales.

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  Discussion Top

Psoriasis is a chronic skin disorder affecting almost 2% of the population. Biologic therapy is one of the treatment options for resistant cases of psoriasis. Unfortunately, it can be seen as a paradoxical side effect with biologics. In the literature, there are 209 cases of anti-TNF-α induced or exacerbated psoriasis. [9],[18] IBD accounts for 20% of all the reported cases, a vast majority of which have CD. [9],[19] In a cohort of >700 Infliximab treated patients with CD, a variety of skin eruptions occurred, almost 10% of which were severe enough to warrant dermatology consultation, and for which psoriasiform exanthema was confirmed. [20] It has been suggested that these skin eruptions are different from classic psoriasis when there is no anti-TNF-α exposure, and the preferred term here is "psoriasiform". The onset of psoriasis following TNF-α antagonists does not appear to be drug specific, and there is a risk of recurrence following the use of an alternate anti-TNF-α agent. [21] It may occur at any age (mean: 30.1 years), and in most patients, there is no personal or family history of psoriasis. [9] The development of the psoriatic lesions may occur any time after the introduction of anti-TNF-α. [9] Clinically, palmoplantar pustular psoriasis is the predominant form (52-56%), followed by plaque psoriasis (49-50%), and guttate lesions (12-15%). [9],[22] In IBD patients, the majority of cases described are plaque-type (61%), [9] mainly affecting the palmo-plantar region (82%). [19] The study by Seneschal et al. of skin biopsy specimens from 11 patients who developed psoriasiform lesions following TNF-α antagonist therapy showed the following variable histologic features: Spongiosus, increased type 1 Interferon expression and increased expression of the chemokine receptor (CXCR). [21] Different reports indicate that patients continued Infliximab therapy because their skin eruptions were successfully treated with topical therapy. [12],[18] However, Rahier et al. and Cullen et al., [12],[13] reported that up to 40% of patients with IBD with a new-onset or worsening existing psoriasiform skin lesions discontinued anti-TNF-α therapy. The pathogenesis of this paradoxical process is not yet fully understood, but there is evidence to support the role of increased interferon-alpha expression as a result of TNF-α blockade. It is possible that variants in the IL-23 axis play a role in the development of this paradoxical adverse event. In a study done by Sherlock et al., a significant association was found between polymorphisms in the IL-23R gene and the subsequent development of psoriasis/psoriasiform lesions, indicating that variants in the IL-23 axis play a role in the development of this side-effect. [18] An explanation for the occurrence of psoriasis in IBD patients could simply be the simultaneous concurrence of the two diseases, [23] as the incidence of psoriasis in patients with IBD ranges from 6-11%, compared to 2-3% in the general population. [12] However, the majority of reported cases [9],[10],[11],[12],[19],[22],[23] had no history of psoriasis before the start of biological therapy and upon withdrawal of the drug there was a complete regress of the clinical lesions. [9],[19],[24],[25] This adverse event seems to indicate a true increase in the prevalence in anti-TNF-α treated patients and the Food and Drug Administration now recommends that manufacturers of TNF-α antagonist products record this in the prescribing information of the product.

  References Top

Hyams J, Crandall W, Kugathasan S, Griffiths A, Olson A, Johanns J, et al. Induction and maintenance infliximab therapy for the treatment of moderate-to-severe Crohn's disease in children. Gastroenterology 2007;132:863-73.  Back to cited text no. 1
Hanauer SB, Feagan BG, Lichtenstein GR, Mayer LF, Schreiber S, Colombel JF, et al. Maintenance infliximab for Crohn's disease: The ACCENT I randomised trial. Lancet 2002;359:1541-9.  Back to cited text no. 2
Alonso-Ruiz A, Pijoan JI, Ansuategui E, Urkaregi A, Calabozo M, Quintana A. Tumor necrosis factor alpha drugs in rheumatoid arthritis: Systematic review and metaanalysis of efficacy and safety. BMC Musculoskelet Disord 2008;9:52.  Back to cited text no. 3
van der Heijde D, Dijkmans B, Geusens P, Sieper J, DeWoody K, Williamson P, et al. Efficacy and safety of infliximab in patients with ankylosing spondylitis: Results of a randomized, placebo-controlled trial (ASSERT). Arthritis Rheum 2005;52:582-91.  Back to cited text no. 4
Antoni CE, Kavanaugh A, Kirkham B, Tutuncu Z, Burmester GR, Schneider U, et al. Sustained benefits of infliximab therapy for dermatologic and articular manifestations of psoriatic arthritis: Results from the infliximab multinational psoriatic arthritis controlled trial (IMPACT). Arthritis Rheum 2005;52:1227-36.  Back to cited text no. 5
Chaudhari U, Romano P, Mulcahy LD, Dooley LT, Baker DG, Gottlieb AB. Efficacy and safety of infliximab monotherapy for plaque-type psoriasis: A randomised trial. Lancet 2001;357:1842-7.  Back to cited text no. 6
Gottlieb A, Korman NJ, Gordon KB, Feldman SR, Lebwohl M, Koo JY, et al. Guidelines of care for the management of psoriasis and psoriatic arthritis: Section 2. Psoriatic arthritis: Overview and guidelines of care for treatment with an emphasis on the biologics. J Am Acad Dermatol 2008;58:851-64.  Back to cited text no. 7
Reich K, Nestle FO, Papp K, Ortonne JP, Evans R, Guzzo C, et al. Infliximab induction and maintenance therapy for moderate-to-severe psoriasis: A phase III, multicentre, double-blind trial. Lancet 2005;366:1367-74.  Back to cited text no. 8
Collamer AN, Battafarano DF. Psoriatic skin lesions induced by tumor necrosis factor antagonist therapy: Clinical features and possible immunopathogenesis. Semin Arthritis Rheum 2010;40:233-40.  Back to cited text no. 9
Ko JM, Gottlieb AB, Kerbleski JF. Induction and exacerbation of psoriasis with TNF-blockade therapy: A review and analysis of 127 cases. J Dermatolog Treat 2009;20:100-8.  Back to cited text no. 10
Wollina U, Hansel G, Koch A, Schönlebe J, Köstler E, Haroske G. Tumor necrosis factor-alpha inhibitor-induced psoriasis or psoriasiform exanthemata: First 120 cases from the literature including a series of six new patients. Am J Clin Dermatol 2008;9:1-14.  Back to cited text no. 11
Rahier JF, Buche S, Peyrin-Biroulet L, Bouhnik Y, Duclos B, Louis E, et al. Severe skin lesions cause patients with inflammatory bowel disease to discontinue anti-tumor necrosis factor therapy. Clin Gastroenterol Hepatol 2010;8:1048-55.  Back to cited text no. 12
Cullen G, Kroshinsky D, Cheifetz AS, Korzenik JR. Psoriasis associated with anti-tumour necrosis factor therapy in inflammatory bowel disease: A new series and a review of 120 cases from the literature. Aliment Pharmacol Ther 2011;34:1318-27.  Back to cited text no. 13
Yates VM, Watkinson G, Kelman A. Further evidence for an association between psoriasis, Crohn's disease and ulcerative colitis. Br J Dermatol 1982;106:323-30.  Back to cited text no. 14
Lee FI, Bellary SV, Francis C. Increased occurrence of psoriasis in patients with Crohn's disease and their relatives. Am J Gastroenterol 1990;85:962-3.  Back to cited text no. 15
Cohen AD, Dreiher J, Birkenfeld S. Psoriasis associated with ulcerative colitis and Crohn's disease. J Eur Acad Dermatol Venereol 2009;23:561-5.  Back to cited text no. 16
Najarian DJ, Gottlieb AB. Connections between psoriasis and Crohn's disease. J Am Acad Dermatol 2003;48:805-21.  Back to cited text no. 17
Sherlock ME, Walters T, Tabbers MM, Frost K, Zachos M, Muise A, et al. Infliximab-induced psoriasis and psoriasiform skin lesions in pediatric Crohn disease and a potential association with IL-23 receptor polymorphisms. J Pediatr Gastroenterol Nutr 2013;56:512-8.  Back to cited text no. 18
Fiorino G, Allez M, Malesci A, Danese S. Review article: Anti TNF-alpha induced psoriasis in patients with inflammatory bowel disease. Aliment Pharmacol Ther 2009;29:921-7.  Back to cited text no. 19
Fidder H, Schnitzler F, Ferrante M, Noman M, Katsanos K, Segaert S, et al. Long-term safety of infliximab for the treatment of inflammatory bowel disease: A single-centre cohort study. Gut 2009;58:501-8.  Back to cited text no. 20
Seneschal J, Milpied B, Vergier B, Lepreux S, Schaeverbeke T, Taïeb A. Cytokine imbalance with increased production of interferon-alpha in psoriasiform eruptions associated with antitumour necrosis factor-alpha treatments. Br J Dermatol 2009;161:1081-8.  Back to cited text no. 21
Collamer AN, Guerrero KT, Henning JS, Battafarano DF. Psoriatic skin lesions induced by tumor necrosis factor antagonist therapy: A literature review and potential mechanisms of action. Arthritis Rheum 2008;59:996-1001.  Back to cited text no. 22
Costa-Romero M, Coto-Segura P, Suarez-Saavedra S, Ramos-Polo E, Santos-Juanes J. Guttate psoriasis induced by infliximab in a child with Crohn's disease. Inflamm Bowel Dis 2008;14:1462-3.  Back to cited text no. 23
Passarini B, Infusino SD, Barbieri E, Varotti E, Gionchetti P, Rizzello F, et al. Cutaneous manifestations in inflammatory bowel diseases: Eight cases of psoriasis induced by anti-tumor-necrosis-factor antibody therapy. Dermatology 2007;215:295-300.  Back to cited text no. 24
Laga AC, Vleugels RA, Qureshi AA, Velazquez EF. Histopathologic spectrum of psoriasiform skin reactions associated with tumor necrosis factor-a inhibitor therapy. A study of 16 biopsies. Am J Dermatopathol 2010;32:568-73.  Back to cited text no. 25


  [Figure 1]

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