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array:24 [ "pii" => "S0025775309012640" "issn" => "00257753" "doi" => "10.1016/j.medcli.2009.07.042" "estado" => "S300" "fechaPublicacion" => "2010-04-03" "aid" => "660" "copyright" => "Elsevier España, S.L. Todos los derechos reservados" "copyrightAnyo" => "2009" "documento" => "simple-article" "crossmark" => 0 "subdocumento" => "cor" "cita" => "Med Clin. 2010;134:423" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 1712 "formatos" => array:3 [ "EPUB" => 6 "HTML" => 1473 "PDF" => 233 ] ] "itemSiguiente" => array:18 [ "pii" => "S0025775309012652" "issn" => "00257753" "doi" => "10.1016/j.medcli.2009.07.043" "estado" => "S300" "fechaPublicacion" => "2010-04-03" "aid" => "661" "copyright" => "Elsevier España, S.L" "documento" => "simple-article" "crossmark" => 0 "subdocumento" => "cor" "cita" => "Med Clin. 2010;134:424" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 7197 "formatos" => array:3 [ "EPUB" => 7 "HTML" => 6312 "PDF" => 878 ] ] "es" => array:10 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Carta al 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=> array:2 [ "nombre" => "Franchek" "apellidos" => "Drobnic" ] ] ] ] ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0025775309012299?idApp=UINPBA00004N" "url" => "/00257753/0000013400000009/v1_201304301843/S0025775309012299/v1_201304301843/es/main.assets" ] "asociados" => array:1 [ 0 => array:18 [ "pii" => "S0025775309012652" "issn" => "00257753" "doi" => "10.1016/j.medcli.2009.07.043" "estado" => "S300" "fechaPublicacion" => "2010-04-03" "aid" => "661" "copyright" => "Elsevier España, S.L" "documento" => "simple-article" "crossmark" => 0 "subdocumento" => "cor" "cita" => "Med Clin. 2010;134:424" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 7197 "formatos" => array:3 [ "EPUB" => 7 "HTML" => 6312 "PDF" => 878 ] ] "es" => array:10 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Carta al Editor</span>" "titulo" => "Respuesta" "tienePdf" => "es" "tieneTextoCompleto" => "es" "paginas" => array:1 [ 0 => array:1 [ "paginaInicial" => "424" ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "Reply" ] ] "contieneTextoCompleto" => array:1 [ "es" => true ] "contienePdf" => array:1 [ "es" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Manuel Ginarte, Jaime Toribio" "autores" => array:2 [ 0 => array:2 [ "nombre" => "Manuel" "apellidos" => "Ginarte" ] 1 => array:2 [ "nombre" => "Jaime" "apellidos" => "Toribio" ] ] ] ] ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0025775309012652?idApp=UINPBA00004N" "url" => "/00257753/0000013400000009/v1_201304301843/S0025775309012652/v1_201304301843/es/main.assets" ] ] "es" => array:12 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Carta al Editor</span>" "titulo" => "Sobre la patogenia del síndrome de Sweet" "tieneTextoCompleto" => true "saludo" => "Sr. Editor:" "paginas" => array:1 [ 0 => array:1 [ "paginaInicial" => "423" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Francisco José Fernández–Fernández, Juan Antonio Garrido, Pascual Sesma" "autores" => array:3 [ 0 => array:5 [ "Iniciales" => "F.J." "nombre" => "Francisco José" "apellidos" => "Fernández–Fernández" "email" => array:1 [ 0 => "fjf-fernandez@terra.es" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">¿</span>" "identificador" => "cor1" ] ] ] 1 => array:2 [ "nombre" => "Juan Antonio" "apellidos" => "Garrido" ] 2 => array:2 [ "nombre" => "Pascual" "apellidos" => "Sesma" ] ] "afiliaciones" => array:1 [ 0 => array:1 [ "entidad" => "Servicio de Medicina Interna, Hospital Arquitecto Marcide, Ferrol, A Coruña, España" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor1" "etiqueta" => "⁎" "correspondencia" => "Autor para correspondencia." ] ] ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "On the pathogenesis of Sweet's syndrome" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p class="elsevierStylePara elsevierViewall">Hemos leído con interés el artículo de revisión sobre el síndrome de Sweet publicado recientemente en su revista<a class="elsevierStyleCrossRef" href="#bib1"><span class="elsevierStyleSup">1</span></a>. Aunque, como los autores indican, la patogenia es desconocida, diversas observaciones indican un trastorno en la regulación de las citocinas como el mecanismo patogénico principal de este síndrome. Entre las citocinas principalmente implicadas se encuentran la interleucina (IL) 1, la IL-6, la IL-8, el factor estimulador de colonias de granulocitos (G-CSF) y el factor estimulador de colonias de granulocitomacrófago (GM-CSF). Los glucocorticoides, tratamiento de primera elección de este síndrome, inhiben la síntesis de casi todas las citocinas conocidas<a class="elsevierStyleCrossRef" href="#bib2"><span class="elsevierStyleSup">2</span></a>. Llevan a cabo esta inhibición fundamentalmente mediante su acción sobre los factores de transcripción inflamatorios factor nuclear kappa B (NF-κB) y proteína activadora-1 (AP-1)<a class="elsevierStyleCrossRefs" href="#bib2"><span class="elsevierStyleSup">2–5</span></a>. Como los Dres. Ginarte y Toribio señalan, la leucemia mieloide aguda es la neoplasia que con más frecuencia se asocia al síndrome de Sweet paraneoplásico, y el G-CSF es el fármaco más comúnmente implicado en la variante farmacológica. Pues bien, las células de la leucemia mieloide aguda<a class="elsevierStyleCrossRef" href="#bib6"><span class="elsevierStyleSup">6</span></a> producen la IL-1 y esta citocina induce la síntesis de los GM-CSF y G-CSF<a class="elsevierStyleCrossRef" href="#bib7"><span class="elsevierStyleSup">7</span></a>. Asimismo, el GM-CSF estimula la producción de IL-8 por los neutrófilos, y esta IL-8 es un potente factor quimiotáctico para los neutrófilos<a class="elsevierStyleCrossRef" href="#bib8"><span class="elsevierStyleSup">8</span></a>. En concordancia con esta base patogénica, recientemente se describió un paciente con un síndrome de Sweet refractario a corticoides, a colchicina, a diversos inmunosupresores y a adalimumab, que se trató con éxito con anakinra<a class="elsevierStyleCrossRef" href="#bib9"><span class="elsevierStyleSup">9</span></a>, un antagonista del receptor de la IL-1.</p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "bibliografia" => array:2 [ "titulo" => "Bibliografía" "seccion" => array:1 [ 0 => array:1 [ "bibliografiaReferencia" => array:9 [ 0 => array:3 [ "identificador" => "bib1" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Síndrome de Sweet" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "M. Ginarte" 1 => "J. 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