RESUMEN
BACKGROUND: Allergic disorders such as atopic dermatitis (AD) are strongly associated with an impairment of the epithelial barrier, in which tight junctions and/or filaggrin expression can be defective. Skin barrier assessment shows potential to be clinically useful for prediction of disease development, improved and earlier diagnosis, lesion follow-up, and therapy evaluation. This study aimed to establish a method to directly assess the in vivo status of epithelial barrier using electrical impedance spectroscopy (EIS). METHODS: Thirty-six patients with AD were followed during their 3-week hospitalization and compared with 28 controls. EIS and transepidermal water loss (TEWL) were measured in lesional and non-lesional skin. Targeted proteomics by proximity extension assay in serum and whole-genome sequence were performed. RESULTS: Electrical impedance spectroscopy was able to assess epithelial barrier integrity, differentiate between patients and controls without AD, and characterize lesional and non-lesional skin of patients. It showed a significant negative correlation with TEWL, but a higher sensitivity to discriminate non-lesional atopic skin from controls. During hospitalization, lesions reported a significant increase in EIS that correlated with healing, decreased SCORAD and itch scores. Additionally, EIS showed a significant inverse correlation with serum biomarkers associated with inflammatory pathways that may affect the epithelial barrier, particularly chemokines such as CCL13, CCL3, CCL7, and CXCL8 and other cytokines, such as IRAK1, IRAK4, and FG2, which were significantly high at admission. Furthermore, filaggrin copy numbers significantly correlated with EIS on non-lesional skin of patients. CONCLUSIONS: Electrical impedance spectroscopy can be a useful tool to detect skin barrier dysfunction in vivo, valuable for the assessment of AD severity, progression, and therapy efficacy.
Asunto(s)
Dermatitis Atópica , Eccema , Citocinas , Dermatitis Atópica/diagnóstico , Espectroscopía Dieléctrica , Proteínas Filagrina , Humanos , Prurito , PielRESUMEN
Cutaneous pruritus can be caused by systemic as well as skin diseases. This paper focuses on differential diagnosis of pruritus and covers therapeutic options.
Asunto(s)
Prurito , Enfermedades de la Piel , Diagnóstico Diferencial , Humanos , Enfermedades de la Piel/diagnósticoRESUMEN
In both clinical experience and molecular genetic studies, atopic diseases (asthma, rhinoconjunctivitis and eczema) have been found to be strongly genetically influenced. The epidermal protein filaggrin seems to play a crucial role and is encoded within the so-called epidermal differentiation complex on chromosome 1. Filaggrin mutations predispose significantly to an increased risk to develop atopic eczema. Apart from filaggrin, other proteins involved in skin barrier functions such as lipid synthesis and metabolism, protease or protease inhibitor functions also seem to play a role. Besides skin barrier function, immune deviation versus a Th2 dominance and increased IgE production is also genetically determined. Polymorphisms have been found in genes encoding IL-4, IL-13 and STAT-6, and recently a polymorphism on the high-affinity IgE receptor gene has been found. Using genome-wide association studies, new genes with yet unknown functions have been determined to be associated with atopy and atopic eczema.
Asunto(s)
Dermatitis Atópica/genética , Dermatitis Atópica/inmunología , Proteínas Filagrina , Estudio de Asociación del Genoma Completo , Humanos , Interleucina-13/genética , Interleucina-13/metabolismo , Interleucina-4/genética , Interleucina-4/metabolismo , Proteínas de Filamentos Intermediarios/genética , Proteínas de Filamentos Intermediarios/metabolismo , Polimorfismo Genético , Receptores de IgE/genética , Receptores de IgE/metabolismo , Factor de Transcripción STAT6/genética , Factor de Transcripción STAT6/metabolismo , Células Th2/inmunología , Células Th2/metabolismoRESUMEN
New ongoing urticarial lesions confined to former injection sites of vaccination and allergy immunotherapy were observed in an 8-year-old boy. This finding can be best explained as an isotopic response phenomenon.
