Jenna Yousif BS, Roudha Al-Dehneem MD MSc, Nadine Kaskas MD, Alice B. Gottlieb MD PhD
Department of Dermatology, Icahn School of Medicine at Mount Sinai, New York, NY
Abstract
Psoriasis vulgaris and eczema are characterized by an imbalance in the Th1 and Th2 immune response and distinct cytokine profiles, where Th1 is more prominent in psoriasis and Th2 is more prominent in eczema. A common treatment for psoriasis is anti-IL-17 therapy, in which inhibition of IL-17 cytokines and the Th1/Th17 immune response may cause a paradoxical shift favoring the Th2 immune response and an eczematous phenotype. Our case series presents three patients who developed a cutaneous eczematous eruption 8-12 weeks following treatment of psoriasis with an IL-17 inhibitor (secukinumab, ixekizumab, or brodalumab) suggesting this phenomenon of shifting cytokine levels away from the phenotype of psoriasis toward the opposing disease.
Psoriasis vulgaris is a chronic relapsing inflammatory skin disease characterized by an upregulation of key cytokines involved in immunopathogenesis.1 Notably, interleukin (IL)-17 is one of several pro-inflammatory cytokines found in lesional skin.1 Thus, treatments targeting IL-17 have been developed to attenuate the immune response.1 A specialized group of biologic treatments aimed at inhibiting either IL-17 or the IL-17 receptor have become widely used amongst psoriasis patients with marked improvement.1 Secukinumab, brodalumab, and ixekizumab are IL-17 inhibitors widely used for the treatment of moderate-to-severe psoriasis vulgaris due to their high safety profile and efficacy based on phase III clinical trial data.2,3 Additionally, the most common adverse effects reported with this class of biologic treatment are minimal and include injection site reactions, headache, oral and vulvovaginal candidiasis, and nasopharyngitis.3 Though fairly uncommon in clinical practice, eczema has been a reported reaction following initiation of IL-17 inhibitor treatment in phase III trials.4 Becoming aware of these adverse events may guide how providers treat and manage these patients.
Herein, we describe a series of three patients who developed eczematous cutaneous eruptions after treatment of psoriasis with an IL-17 inhibitor.
CASE 1
A 46-year-old female with a childhood history of atopic dermatitis (AD) presented to the dermatology clinic with erythematous silvery scaly patches on her scalp and face, and joint pain involving multiple joints. She was diagnosed with psoriasis and psoriatic arthritis. She initially started on secukinumab. Following the loading doses, the patient presented with a new pruritic rash. Physical examination revealed erythematous and eczematous patches and plaques on the scalp, face, ears, anterior neck, and bilateral flexural surfaces of the elbows with superficial fissures and associated burning (Figure 1: A and B). A skin biopsy revealed spongiotic dermatitis, subacute type, and non-specific folliculitis consistent with an eczematous reaction. The decision was made to discontinue the secukinumab and begin a short course of low dose prednisone as a bridge to guselkumab due to her consistent psoriatic lesions. Following the failure of improvement with guselkumab, we started the patient on upadacitinib considering her clinical picture of AD and psoriatic arthritis and she noted a marked improvement in both diseases (Figure 1: C and D).
