Pemphigus is a bullous autoimmune disease that affects the skin and mucous membranes. It is very difficult to establish the etiology and the triggering factors that influence reactivations in pemphigus vulgaris (PV). The case of a 33-year-old male with chronic history of intranasal cocaine consumption is presented in this report. We present the clinical case of the patient, followed for a total of 86 weeks, with ten relapses secondary to probable cocaine use. The patient was admitted to the emergency department after presenting polymorphic dermatosis characterized by blisters, vesicles, and excoriations extending from the oral cavity to the thorax, and to the inguinal and genital regions, affecting approximately 35 % of the body surface area with a score of 56 on the Pemphigus Skin Disorder Index. Skin biopsies were compatible with PV diagnosis. The patient had clinical improvement with a combination of methylprednisolone 500 mg intravenously (IV) and cyclophosphamide 500 mg IV every 15 days, along with prednisone 50 mg orally (PO) q24 h and mycophenolic acid 500 mg PO q6 h. Persistent cocaine use is highly likely to be the factor triggering lesion reactivation and responsible for the torpid evolution. We cannot definitively conclude whether the change from azathioprine to mycophenolic acid after the tenth relapse was the adjuvant medication responsible for the end of the consolidation phase and complete remission on therapy. This case study could potentially serve as a guide for management of patients who continuously persist with cocaine use, leading to a clinical picture refractory to multiple therapeutic schemes.Electronic supplementary materialThe online version of this article (10.1007/s13555-018-0271-0) contains supplementary material, which is available to authorized users.
La necrólisis epidérmica tóxica (NET) fue descrita por Lyell en 1956. Es considerada una reacción cutánea adversa grave que consiste en una necrosis generalizada de queratinocitos en el contexto de una activación inmunitaria inapropiada por ciertos fármacos o sus metabolitos. Actualmente, el síndrome de Stevens-Johnson (SSJ) y la NET son reacciones raras y potencialmente mortales, y se consideran dentro del espectro de una misma enfermedad, siendo la forma más grave de expresión la NET cuando hay desprendimiento cutáneo de más del 30% de la superficie corporal total. En el 80% de los casos de SSJ y NET, los fármacos causantes más frecuentes son antiepilépticos (35%), antibióticos (33%) y antinflamatorios no esteroideos (AINE) (24%). La NET afecta principalmente al tronco, la cara, el cuello y las extremidades, con manchas eritematosas, purpúricas y dolorosas (descritas en diana o tiro al blanco), ampollas flácidas con necrosis de piel, desprendimiento cutáneo y signo de Nikolsky positivo. El desprendimiento trascurre de 1 a 3 semanas, y se reepitaliza y deja manchas tipo hiperpigmentadas. El tratamiento comienza con la identificación y el retiro del agente causal, así como con medi-
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