Abstract

Introduction: TNF-α inhibitors are widely used in the management of Crohn's disease (CD) and psoriasis. These agents can paradoxically cause psoriasis. We present a case report of Crohn's disease patient on infliximab therapy who developed psoriasis. Case report: A 45 year old man with a history of Crohn's colitis, well controlled on infliximab, came to clinic for evaluation of pruritic rash for 2-3 weeks that started on his legs initially and spread to involve his arms, chest, and back. He denied systemic symptoms, use of new medications or skin products, sick contact and recent travel. His CD was in remission for more than 1 year, and the last dose of infliximab was given 4 weeks ago. Skin exam revealed well-demarcated, erythematous plaques with overlying adherent scales involving chest, abdomen, back, legs and extensor surfaces of both arms. The patient was referred to dermatology for further evaluation. Punch skin biopsy revealed psoriasis. It was attributed to the use of infliximab. He was treated with topical steroids and UVB phototherapy with minimal improvement. Infliximab was held and planned to switch to other biologic agents for maintenance of CD. Discussion: CD is characterized by transmural inflammation of the gastrointestinal tract due to inflammatory cytokines such as interleukin (IL)-12 and TNF-α, resulting in symptoms of CD. TNF-α inhibitors, e.g., infliximab are effective in inducing and maintaining remission in moderate to severe CD patients. Plaque-type psoriasis, guttate psoriasis, palmoplantar pustulosis, psoriasis of the nail and scalp have been described in the literature with the use of these agents. Estimated prevalence is 0.6% to 5.3%. Previously reported cases have a wide diversity as far as agent types, gender and age of patients, treatment duration, type of eruption, and presence or absence of personal or family history of psoriasis are concerned. Pustular eruption resembling palmoplantar pustulosis is the most characteristic pattern, and it has been reported in about one-third of all reported cases. Pathogenesis of TNF-α inhibitors induced psoriasis involves a disruption in cytokine balance allowing unopposed interferon-α production by dendritic cells. In most cases, topical steroid therapy is enough. UVB phototherapy or discontinuation of TNF-α inhibitor or switching to an alternative anti-TNF agent is required in severe cases.Figure: Rash on back.Figure: Rash on elbow.

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