Eickstaedt, Joshua B.

ImportanceTumor necrosis factor α (TNF) inhibitor–induced psoriasiform eruption is well recognized in adults, but few reports document this paradoxical effect in children.ObjectiveTo characterize the clinical features and the clinical time course of TNF inhibitor–induced psoriasiform eruptions in children.Design, Setting, and ParticipantsA multicenter retrospective case series of children younger than 18 years seen between January 1, 2000, and December 31, 2016, who developed a new-onset psoriasiform eruption while taking a TNF inhibitor for a nondermatologic disorder. Participating sites were members of the Pediatric Dermatology Research Alliance. Data were entered into a Research Electronic Data Capture database at the Mayo Clinic (ie, the coordinating center).ResultsPsoriasiform eruptions were identified in 103 TNF inhibitor–treated patients (median age, 13.8 years [IQR, 11.7-16.4 years]; 52 female patients [50%]; 57 White patients [55%]), with 67 patients (65%) treated with infliximab, 35 (34%) with adalimumab, and 1 (1%) with certolizumab pegol. Most patients had no personal history (101 [98%]) or family history of psoriasis (60 patients [58%]). Inflammatory bowel disease was the most common indication for treatment with TNF inhibitor (94 patients [91%]). The primary extracutaneous disease was under control in 95 patients (92%) who developed the eruption. Most patients (n = 85 [83%]) developed psoriasiform eruptions at multiple anatomic sites, with scalp involvement being most common (65 patients [63%]). Skin disease developed at a median of 14.5 months (IQR, 9-24 months) after TNF inhibitor initiation. To treat the psoriasiform eruption, topical steroidal and nonsteroidal medication was prescribed for all patients. Systemic therapy was added for 30 patients (29%): methotrexate for 24 patients (23%), oral corticosteroids for 8 patients (8%), and azathioprine for 1 patient (1%). For 26 patients (25%), suboptimal effectiveness with topical medications alone prompted discontinuation of the initial TNF inhibitor and a change to a second-line TNF inhibitor with cutaneous improvement in 23 patients (88%) by a median of 3 months (IQR, 2-4 months). Eight patients (31%) who started a second-line TNF inhibitor developed a subsequent TNF inhibitor–induced psoriasiform eruption at a median of 6 months (IQR, 4-8 months). Persistent skin disease in 18 patients (17%) prompted discontinuation of all TNF inhibitors; 11 patients changed to a non-TNF inhibitor systemic therapy, and 7 discontinued all systemic therapy.Conclusions and RelevanceIn this case series, paradoxical TNF inhibitor–induced psoriasiform eruptions were seen in children treated with TNF inhibitors for any indication, and there appears to be a class effect among the varying TNF inhibitors. The majority of these children were able to continue TNF inhibitor therapy with adequate skin-directed and other adjuvant therapies.

Abstract Background Anti–tumor necrosis factor alpha ( TNF ‐α) agents are used to treat a variety of autoimmune and inflammatory conditions, including psoriasis. Paradoxically, numerous reports have documented new‐onset or exacerbation of psoriasis or psoriasiform skin lesions ( PSO ) in patients treated with these agents for conditions other than PSO—particularly in adults with inflammatory bowel disease ( IBD ). Not much is known regarding similar cases in children. Methods A retrospective chart review was performed on children younger than 19 years of age with IBD seen at the Mayo Clinic between 2003 and 2015 who developed new‐onset or recurrent PSO while undergoing anti‐ TNF ‐α therapy. Results Fourteen children developed PSO while undergoing anti‐ TNF ‐α therapy for IBD . All three anti‐ TNF ‐α agents (infliximab, adalimumab, certolizumab) used to treat IBD in this series led to induction or recurrence of PSO lesions. The median time to development of PSO was 11 months (range 0–48 mos), the median age was 15 years (range 12.5–17.5 yrs), and 57% of patients were male. IBD activity was quiescent in 93% of cases at PSO onset. Seven patients (50%) discontinued their initial anti‐ TNF ‐α therapy because of their skin disease. Ultimately, four patients (29%) had to discontinue all anti‐ TNF ‐α therapy to induce PSO resolution. Conclusion TNF ‐α antagonist–induced PSO in children with IBD is a rarely reported adverse reaction. PSO onset has a variable latency, but usually occurs during IBD remission, with a slight male bias. Nearly half of patients required a change in their initial anti‐ TNF ‐α agent despite conventional skin‐directed therapies, and one‐third of patients discontinued all anti‐ TNF ‐α therapy because of PSO .