Abstract

Tumor necrosis factor alpha targeted therapies have expanded the therapeutic options for patients with inflammatory bowel disease, rheumatoid arthritis, psoriasis and psoriatic arthritis and have significantly improved patients’ quality of life. Paradoxically, anti-TNF-alpha agents may induce psoriatic eruptions or worsen preexisting psoriatic skin disease. The incidence of TNF-induced psoriasis in inflammatory bowel disease is estimated at 1.6% to 2.7%. The mechanism underlying this side effect have yet to be elucidated, however there is mounting evidence of a key innate immune pathway involving plasmacytoid dendritic cell precursors and type 1 interferon production in the pathogenesis of TNF induced psoriasis. The role of interleukin-23/T-helper axis has also been implicated in the pathogenesis of TNF-induced psoriasis. Interestingly, patients with Crohn disease with TNF-alpha induced psoriasis are more likely to be homozygous for polymorphism in the IL-23 receptor gene. Herein we describe a 51- year-old female with history of Crohn’s disease, recently treated with infliximab presented with a generalized erythroderma with an erythematous scaly rash on the hands, arms, abdomen and back studded by pinpoint pustules. No previous history of psoriasis or recent infection identified. The skin biopsy showed an intraepidermal pustular dermatitis with no significant eosinophils and subcorneal pustules, consistent with pustular psoriasis. Based on the clinical and pathologic findings, a diagnosis of paradoxical TNF-alpha induced pustular psoriasis was made. The patient condition improved after infliximab was discontinued and ustekinumab (an IL12/23 inhibitor) in addition to corticosteroid and topical salicylic acid was started. Management of TNF inhibitor psoriasis is challenging, however there is emerging evidence that targeting the IL-23/TH-17 axis is a new potential target for treatment of TNF-induced psoriasis.

Financial Disclosure:
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