DR [page 90] [Dermatology Reports 2011; 3:e40] Infliximab-induced intertriginous psoriasis in patient with Crohn’s disease Federica Mola, Alberico Motolese Department of Dermatology, Circolo Hospital and Macchi Foundation, Varese, Italy Abstract Tumor necrosis factor-α (TNFα) inhibition is an effective treatment of moderate-to-severe psoriasis and other diseases (rheumatoid arthritis, ankylosing spondylitis, psoriasis or Crohn’s disease). We report a case of a 32- years-old patient affected by Crohn’s disease since the age of 25 who started infliximab infusion after four years of treatment with prednisone and azathioprine per os without improvement. After the fifth infusion of inflix- imab, he developed a form of intertriginous psoriasis which was approached with topical steroid cream. The patient never presented psoriasis in the past. New onset of psoriasis in patients without history for skin diseases (as in our case) is a quite uncommon complication of TNFα inhibitor therapy. The increased pro- duction of IFNα during TNFα inhibitor therapy is a possible pathophysiologic explanation for this paradoxical effect of the anti-TNFα. Introduction Tumor necrosis factor-α (TNFα) is a proin- flammatory cytokine produced by different cell types (activated T lymphocytes, keratinocytes, Langerhans cells, endothelial cells, cardiac myocytes, adipose tissue etc.) and is involved in the pathogenesis of psoriatic skin lesions. TNFα inhibitors have become established agents in the treatment of inflammatory dis- eases and have shown to be of great benefit in many inflammatory diseases (rheumatoid arthritis, ankylosing spondylitis, psoriasis or Crohn’s disease).1 Case Report We report a case of unexpected induction of Psoriasis due to the use of intravenous TNFα inhibitor. A 32-years-old male patient with recalcitrant Crohn’s disease of the ileum and descending colon (treated without improvement with pred- nisone, mesalazine and azathioprine per os) started treatment with infliximab at the dose of 5 mg/Kg at the week 0, 2, 6 and afterwards every 14 weeks. After the fifth infusion he developed erythematous patches with periph- eral scaling in the axillary folds and inguinal areas, suggesting the diagnosis of flexural pso- riasis (Figure 1). The face and the neck also presented a form of sebopsoriasis (Figure 2). The patient never had psoriasis in the past, and he did not have a familiar history of any skin disease. No signs of infection were shown. The skin biopsy showed psoriasiform hyper- plasia, papillary dermal edema with paraker- atosis and intracorneal microabscesses of neu- trophils (Figure 3). The infliximab infusion was continued (seeing the good response of Crohn’s disease) and a clinical skin improvement was achieved after 40 days of topical steroid treatment. An expanding literature of experience with anti TNFα associated psoriasis is providing abundant information about this paradoxical effect. Many cases are described. The first pub- lished report of this association appeared in 2004 and concerned the development of sym- metrical psoriasiform plaques in a patient treated with infliximab for Crohn’s disease.2 Subsequently plaque, guttate, and pustolar psoriasis have all been noted, and palmoplan- tar pustolar disease appears to be more com- mon than idiopathic psoriasis, accounting for up to the 50% of reported cases. Flexural psori- asis and sebopsoriasis are a rare form of pres- entation. In fact, to our knowledge, ther are only two articles describing cases of flexural psoriasis during infliximab treatment for Crohn’s disease.3,4 Dermatology Reports 2011; volume 3:e40 Correspondence: Federica Mola, Department of Dermatology, Circolo Hospital and Macchi Foundation, viale Borri 75, Varese, Italy. Tel. +39.349.2611869. E-mail: federicamola@yahoo.it Key words: tumor necrosis factor−α, psoriasis, crohn’s disease. Received for publication: 6 June 2011. Accepted for publication: 12 September 2011. This work is licensed under a Creative Commons Attribution NonCommercial 3.0 License (CC BY- NC 3.0). ©Copyright F. Mola and A. Motolese, 2011 Licensee PAGEPress, Italy Dermatology Reports 2011; 3:e40 doi:10.4081/dr.2011.e40 Figure 3. Histologic evaluation demon- strates psoriasiform hyperplasia, papillary dermal edema with parakeratosis and intra- corneal microabscesses of neutrophils. Figure 1. Erythematous patches with peri- pheral scaling in the axillary folds, sugges- tive for the diagnosis of flexural psoriasis Figure 2. Typical erithemato-desquamative patches on the face and neck in sebopsori- asis. No n- co mm er cia l u se on ly [Dermatology Reports 2011; 3:e40] [page 91] It is well recognized that blocking TNFα may actually favour specific autoimmune phenome- na and may activate autoreactive T cells. In addition, with particular relevance to the skin, it may upregulate interferon (IFN)-α activity.5 Immunologically this is not unexpected because TNFα is known to negatively regulate the maturation and function of plasmocytoid dendritic cells, which are the major source of IFN-α. Therapeutic inhibition of TNFα signal- ing would increase IFNα activity and could trigger psoriasis in genetically susceptible individuals.5 On the other hand, some cases can be diag- nosed as an adverse drug reaction and may contribute to stop the treatment. In literature two-thirds of patiens who simply continue anti TNFα therapy improve or resolve the skin dis- ease with steroid treatment. The decisions need to be based on individual circumstances as the extent and severity of the disease, the efficacy of the anti TNFα in treating the condi- tion for which it was initiated and the avail- ability of realistic therapeutic alternatives.5 References 1. Wollina U, Hansel G, Koch A, et al. Tumor necrosis factor-alpha inhibitor-induced psoriasis or psoriasiform exanthemata: first 120 cases from the literature includ- ing a series of six new patients.Am J Clin Dermatol 2008;9:1-14. 2. Baeten D, Kruithof E, Van den Bosch F, et al. Systematic safety follow up in a cohort of 107 patients with spondyloarthropathy treated with infliximab: a new perspective on the role of host defence in the patho- genesis of the disease? Ann Rheum Dis 2003; 62:829-34 3. Peramiquel L, Puig L, Dalmau Jricart E, et al. Onset of flexural psoriasis during infliximab treatment for Crohn's disease. Clin Exp Dermatol 2005; 30:713-4. 4. Avila Alvarez A, Garcia-Alonso L, Solar Boga A, Garcia-Silva J. Flexural Psoriasis induced by infliximab and adalimumab in a patient with Crohn's disease. An Pediatr (Barc) 2009; 70:278-81. 5. Shale M, Ghosh S. Learning the lessons of antitumour necrosis factor therapy-associ- ated psoriasis. Can J Gastroenterol 2009; 23:674-6. Case Report No n- co mm er cia l u se on ly