Eczematous drug eruption in patients with psoriasis under anti‐interleukin‐17A: does interleukin‐22 play a key role?

Autor: Cataldo Patruno, Gianmarco Capasso, G. Caiazzo, Maddalena Napolitano, Massimo Mascolo, Daniela Russo, Gabriella Fabbrocini, M Parisi, Matteo Megna, Angelo Ruggiero, Lucia Gallo
Rok vydání: 2022
Předmět:
Zdroj: Clinical and Experimental Dermatology. 47:918-925
ISSN: 1365-2230
0307-6938
Popis: Eczematous drug eruption (EDE) is a spongiotic skin reaction in response to systemic medications. To date, EDE has been described in patients treated with anti-interleukin (IL)-17A monoclonal antibodies with a prevalence of 2.2%-12.1%.To describe the clinical and histological features and the skin cytokine milieu in patients with EDE induced by anti-IL-17A biologics.This was a prospective study, enrolling patients with psoriasis who developed EDE during treatment with two anti-IL-17 biologics, ixekizumab and secukinumab, from June 2019 to April 2021. Skin biopsies were taken from all patients: a 5-mm lesional biopsy (LB) and a 3-mm nonlesional biopsy (NLB). The LB sample was split into two parts, one for histological examination and the other for cytokine profile evaluation.During the study period, treatment with an anti-IL-17A drug was given to 289 patients of whom 8 (2.8%) developed EDE during the treatment. Histopathological evaluation suggested a diagnosis of spongiotic dermatitis in all eight patients. Cytokine gene expression showed a predominance of T helper (Th)2/Th22 cytokines in EDE lesions with a large increase in IL-4, IL-22 and S100A7 levels in both LB and NLB samples compared with healthy skin. IL-4, IL-22 and S100A7 were significantly higher in LB compared with NLB samples. IL-26 levels were also significantly increased in both LB and NLB compared with healthy skin, whereas low levels of IL-23A were found in both LB and NLB.Eczematous drug eruption skin lesions have mainly Th2/Th22 features, with IL-22 playing a major role in their pathogenesis. EDE seems to be the result of an imbalance towards a Th2/Th22 response, secondary to the blockade of IL-17A activity.
Databáze: OpenAIRE
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