Generalized pustular psoriasis, the most severe form of psoriasis, is a rare variant characterized by widespread sterile pustule associated with systemic inflammation. The disease lacks of specific treatment, drugs approved for plaque psoriasis are used in the clinical practice, with variable results. We present the case of a 41-year old woman affected by a severe form of generalized pustular psoriasis, resistant to several therapies included Tumor Necrosis Factor Antagonist; in our patient we decide to use acitretin plus Secukinumab, an IL-17 inhibitor. The association was effective, achieving the complete resolution of pustulation at month-2; the result was maintained for over 14 months of follow up. No adverse events related to therapy were observed. Generalized pustular psoriasis is related to IL-36RN mutations, which lead to upregulation in IL-36 signaling; IL-36 itself could promote IL-17 pathways. Our case demonstrates that targeting IL-17 eventually associated with systemic retinoids could be a valid therapeutic option for these patients.
Secukinumab Associated with Acitretin in Generalized Pustular Psoriasis
Gisondi, P.;Pizzolato, M.;Girolomoni, G.
2018-01-01
Abstract
Generalized pustular psoriasis, the most severe form of psoriasis, is a rare variant characterized by widespread sterile pustule associated with systemic inflammation. The disease lacks of specific treatment, drugs approved for plaque psoriasis are used in the clinical practice, with variable results. We present the case of a 41-year old woman affected by a severe form of generalized pustular psoriasis, resistant to several therapies included Tumor Necrosis Factor Antagonist; in our patient we decide to use acitretin plus Secukinumab, an IL-17 inhibitor. The association was effective, achieving the complete resolution of pustulation at month-2; the result was maintained for over 14 months of follow up. No adverse events related to therapy were observed. Generalized pustular psoriasis is related to IL-36RN mutations, which lead to upregulation in IL-36 signaling; IL-36 itself could promote IL-17 pathways. Our case demonstrates that targeting IL-17 eventually associated with systemic retinoids could be a valid therapeutic option for these patients.File | Dimensione | Formato | |
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