STING-associated vasculopathy with onset in infancy (SAVI) presenting with skin lesions

STING-associated vasculopathy with onset in infancy (SAVI) is caused by pathogenic gain-of-function variants in the gene TMEM173 (also named stimulator of interferon genes, STING1). This report details the case of an 11-year-old girl with SAVI who presented with skin-limited symptoms and discusses t...

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Detalles Bibliográficos
Autores: Latour-Alvarez, I, Murcia-Clemente, L, Vazquez-Pigueras, I, Garramone-Ramírez, JE, Clemente, D, Sanz, V, Torrelo, A
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2024
País:España
Institución:Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana (FISABIO)
Repositorio:r-FISABIO. Repositorio Institucional de Producción Científica
OAI Identifier:oai:fisabio.fundanetsuite.com:p17045
Acceso en línea:https://fisabio.portalinvestigacion.com/publicaciones/17045
Access Level:acceso abierto
Palabra clave:autoinflammatory diseases
interstitial lung disease (ILD)
Janus kinase inhibitors
skin ulcer
STING-associated vasculopathy with onset in infancy (SAVI)
Descripción
Sumario:STING-associated vasculopathy with onset in infancy (SAVI) is caused by pathogenic gain-of-function variants in the gene TMEM173 (also named stimulator of interferon genes, STING1). This report details the case of an 11-year-old girl with SAVI who presented with skin-limited symptoms and discusses the phenotype-genotype correlations of the TMEM173 variant present in our patient. Treatment of SAVI focuses on preventing the development or progression of organ damage by reducing systemic inflammation. We summarize the available treatments for this syndrome.