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  • Linear immunoglobulin A der...
    Prieto‐Barrios, M.; Velasco‐Tamariz, V.; Tous‐Romero, F.; Burillo‐Martinez, S.; Zarco‐Olivo, C.; Rodriguez‐Peralto, J.L.; Ortiz‐Romero, P.L.

    British journal of dermatology (1951), March 2018, 2018-03-00, 20180301, Letnik: 178, Številka: 3
    Journal Article

    Summary A 65‐year‐old pluripathological woman attended our hospital with a cutaneous eruption of sudden appearance after vancomycin treatment. She presented targetoid lesions affecting approximately 25–30% of her body surface, large erosions with mucosal lesions and positive Nikolsky sign. Under the initial clinical suspicion of toxic epidermal necrolysis (TEN), and considering the recent literature of successful use of etanercept in these cases, she was treated with a single dose of this antitumour necrosis factor (anti‐TNF) agent. Subsequently, the exanthema progression stopped and resolution of the lesions happened in a few days. Later on, histopathology revealed a subepidermal blister with dense neutrophilic infiltrate and linear deposits of immunoglobulin A (IgA) on the dermoepidermal junction, allowing us to establish the diagnosis of drug‐induced linear IgA dermatosis mimicking TEN. Linear IgA dermatosis can have severe clinical manifestations, even mimicking TEN, and can have high mortality, especially in drug‐induced cases. We have not found any other report of linear IgA dermatosis treated with etanercept in the English literature. Anti‐TNF medications could represent useful therapeutic alternatives in this dermatosis. What's already known about this topic? Linear IgA dermatosis is an autoimmune bullous dermatosis that can have multiple clinical presentations including a severe one that mimics toxic epidermal necrolysis. Drug‐induced cases are frequently more serious. Apart from drug suspension no medication has been proven to modify its natural course. What does this study add? We could not find any previous report of linear IgA dermatosis treated with etanercept. We report a more rapid than expected improvement of this disease, which we believe was due to this therapy. This could point to a more important role of tumour necrosis factor (TNF)‐α in this dermatosis. Anti‐TNF agents could represent alternative therapies.