背景:慢性手部湿疹(CHE)是一种非常普遍的,异质,包括不同病因和临床亚型的皮肤病。没有特应性皮炎的严重CHE与全身性炎症有关;但尚不清楚具体的CHE亚型是否有明显区别。系统性,分子特征。
目的:表征不同病因和临床CHE亚型的炎性血浆特征。
方法:我们评估了51例特征明确的CHE患者和40例健康对照者中266种炎症和心血管疾病风险血浆蛋白的表达水平以及聚丝蛋白基因突变状态。在病因学和临床CHE亚组与对照组之间以及根据临床CHE严重程度比较血浆蛋白表达。生物标志物的相关性分析,对临床变量和自我报告变量进行了分析.
结果:非常严重,与对照组相比,手部慢性过敏性接触性皮炎(ACD)与1型/2型混合全身性免疫激活相关.1型/2型炎症生物标志物的循环水平与ACDCHE患者的临床疾病严重程度呈正相关。没有发现生物标志物,可以区分病因亚型,例如,ACD和刺激性接触性皮炎之间。过度角化CHE表现出明显的,非特应性皮炎样,与1型炎症和肿瘤坏死因子α相关的标志物上调的全身足迹,但不是2型炎症。CCL19和CXCL9/10水平的升高可以将角化过度的CHE与囊泡和慢性裂开的CHE区分开,而在后两种亚型之间没有发现差异。
结论:系统性生物标志物的分析显示出识别某些CHE亚型的潜力。外周血炎性生物标志物水平与手部慢性ACD的临床疾病严重程度相关,强调这是一种系统性疾病。我们质疑过度角化CHE是否应归类为湿疹。
BACKGROUND: Chronic hand eczema (CHE) is a highly prevalent, heterogeneous, skin disease that encompasses different aetiological and clinical subtypes. Severe CHE without atopic dermatitis has been associated with systemic inflammation; yet it remains unknown if specific CHE subtypes leave distinct, systemic, molecular signatures.
OBJECTIVE: To characterize the inflammatory plasma signature of different aetiological and clinical CHE subtypes.
METHODS: We assessed expression levels of 266 inflammatory and cardiovascular disease risk plasma proteins as well as filaggrin gene mutation status in 51 well-characterized CHE patients without concomitant atopic dermatitis and 40 healthy controls. Plasma protein expression was compared between aetiological and clinical CHE subgroups and controls both overall and according to clinical CHE severity. Correlation analyses for biomarkers, clinical and self-reported variables were performed.
RESULTS: Very severe, chronic allergic contact dermatitis (ACD) on the hands was associated with a mixed Type 1/Type 2 systemic immune activation as compared with controls. Circulating levels of Type 1/Type 2 inflammatory biomarkers correlated positively with clinical disease severity among CHE patients with ACD. No biomarkers were found, that could discriminate between aetiological subtypes, for example, between ACD and irritant contact dermatitis. Hyperkeratotic CHE showed a distinct, non-atopic dermatitis-like, systemic footprint with upregulation of markers associated with Type 1 inflammation and tumour necrosis factor alpha, but not Type 2 inflammation. Increased levels of CCL19 and CXCL9/10 could discriminate hyperkeratotic CHE from both vesicular and chronic fissured CHE, whereas no difference was found between the latter two subtypes.
CONCLUSIONS: Profiling of systemic biomarkers showed potential for identifying certain CHE subtypes. Peripheral blood levels of inflammatory biomarkers were associated and correlated with the clinical disease severity of chronic ACD on the hands, underlining that this is a systemic disease. We question whether hyperkeratotic CHE should be classified as eczema.