Rybojad M
Hôpital Saint-Louis, 1, avenue Claude-Vellefaux, 75010 Paris, France.
Arch Pediatr. 2012 Aug;19(8):882-5. doi: 10.1016/j.arcped.2012.05.020. Epub 2012 Jul 15.
Atopic dermatitis (AD), or atopic eczema, is a pruriginous inflammatory dermatosis with a genetic predisposition evolving in recurrent flare-ups on a background of chronicity, affecting essentially infants and small children. The clinical phenotype of AD results from interactions between genes and susceptibility, a defect in the cutaneous barrier function (abnormalities in filaggrin and the proteins of the epidermic differentiation complex) and dysfunction of the innate and/or adaptive immune response. With its multifactorial origin, it is dependent on the TH2 lymphocyte system, with a tendency to produce immunoglobulin E (IgE) and the risk of asthma, rhinitis, or allergic conjunctivitis define an atopic susceptibility. Staphylococcus aureus colonization plays a vital role in the perpetuation of the inflammatory phenomena. The disease often regresses in older children. Its prevalence is on the rise in industrialized countries. Diagnosis is clinical, facilitated by certain criteria initially proposed by Hanifin and Rajka and then simplified by Williams. The allergological investigation is reserved for cases that are stubborn, severe, or associated with respiratory symptoms. AD is a dermatosis that evolves in erratic and often unpredictable flare-ups. AD flare-up treatment is based on local corticosteroid therapy. Maintenance therapy attempts to correct the cutaneous dryness with hydrating products whose efficacy has now been proven. Optimal management includes the family's and/or the child's comprehension of the treatment, explaining to them that the goal to reach is not only to relieve the child, but also to attempt to modify the course of the disease. AD is thus a star disease and a public health problem. The major progress made in the comprehension of the physiopathological mechanisms of AD promise targeted therapies from new biotechnologies.
特应性皮炎(AD),又称特应性湿疹,是一种具有遗传易感性的瘙痒性炎症性皮肤病,在慢性病程背景下反复发作,主要影响婴幼儿。AD的临床表型是由基因与易感性之间的相互作用、皮肤屏障功能缺陷(丝聚合蛋白和表皮分化复合体蛋白异常)以及先天性和/或适应性免疫反应功能障碍所致。由于其多因素起源,它依赖于TH2淋巴细胞系统,有产生免疫球蛋白E(IgE)的倾向以及哮喘、鼻炎或过敏性结膜炎的风险,这些定义了一种特应性易感性。金黄色葡萄球菌定植在炎症现象的持续存在中起着至关重要的作用。该病在大龄儿童中常自行消退。其患病率在工业化国家呈上升趋势。诊断主要依靠临床,Hanifin和Rajka最初提出的某些标准有助于诊断,随后Williams对其进行了简化。变应性检查仅适用于顽固、严重或伴有呼吸道症状的病例。AD是一种病情发展不稳定且往往不可预测的皮肤病。AD发作期的治疗以局部使用皮质类固醇激素为主。维持治疗试图用现已证实有效的保湿产品纠正皮肤干燥。最佳管理包括让家庭和/或儿童理解治疗方法,向他们解释治疗目标不仅是缓解患儿症状,还要试图改变疾病进程。因此,AD是一种备受关注的疾病和公共卫生问题。在理解AD生理病理机制方面取得的重大进展有望带来基于新型生物技术的靶向治疗。