2008年的特应性皮炎。

Lawrence S Chan
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引用次数: 30

摘要

特应性皮炎(也称为特应性湿疹和婴儿湿疹)是一种慢性、发痒、炎症性皮肤病,发生于婴儿期或幼儿期,在世界各地,特别是发达国家的发病率越来越高。虽然还没有足够的证据将其定义为一种典型的自身免疫性疾病,但已经发现了自身抗原。在人类患者和动物模型中对特应性皮炎的研究表明,这种疾病是由细胞因子、趋化因子、T细胞、抗原呈递细胞和其他炎症细胞的作用引发、维持和延续的;也有证据表明皮肤屏障缺损和血管生成。最近发现的表皮屏障蛋白聚丝蛋白(由FLG编码)突变存在于约9%的欧洲人中,其中70%的FLG零等位基因纯合或复合杂合的个体发展为特应性皮炎,这表明表皮屏障缺陷容易使病原体/过敏原通过皮肤渗透,并且对渗透的病原体/过敏原产生全身过度活跃的免疫反应。新引入的“内在”和“外在”特应性皮炎的概念引发了学术皮肤科医生关于如何定义“特应性”特应性皮炎的争论。本文还讨论了特应性皮炎治疗方法的最新进展。
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Atopic dermatitis in 2008.

Atopic dermatitis (also termed atopic eczema and infantile eczema), a chronic, itchy, inflammatory skin disease that sets on at infancy or early childhood, is observed with increasing prevalence around the world, particularly in developed nations. Although sufficient evidences are not yet available to define it as a classical autoimmune disease, autoantigens have been identified. Investigations of atopic dermatitis in human patients and animal models suggest that this disease is initiated, maintained and perpetuated by the actions of cytokines, chemokines, T cells, antigen-presenting cells and other inflammatory cells; there is also evidence of skin barrier defect and angiogenesis. Recent identification of mutations of the epidermal barrier protein filaggrin (encoded by FLG), present in about 9% of people of European origin, with 70% of individuals homozygous or compound heterozygous for FLG null alleles developing atopic dermatitis, provides a strong link between a defect of the epidermal barrier that allows easy penetration of pathogen/allergen through the skin and a systemic hyperactive immune response to the penetrated pathogen/allergen. The newly introduced concept of 'intrinsic' and 'extrinsic' atopic dermatitis has fueled the debate among academic dermatologists as to how 'atopic' atopic dermatitis should be defined. Some recent advancements on the management options for atopic dermatitis are also discussed.

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