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首页> 外文期刊>The Internet Journal of Asthma, Allergy and Immunology >Atopic Dermatitis
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Atopic Dermatitis

机译：特应性皮炎

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Correspondence to:Lynda C. Schneider, M.D.Division of Allergy and ImmunologyChildren Hospital300 Longwood AvenueBoston, MA 02115617-355-6180 Introduction Atopic dermatitis (AD) is a chronic inflammatory skin disorder. Like other allergic diseases, the prevalence of atopic dermatitis appears to be rising. In children, the prevalence of AD has increased from 3 -4% in the 1960’s to 10-15% in the 1980’s. But unlike many other diseases, AD has no primary skin lesions or pathognomenic test. Therefore, the diagnosis of atopic dermatitis has to be made by constellation of physical findings (Table 1). The major features include pruritis, typical morphology and distribution of the lesions. The skin distribution varies with age. In infancy, the face and extensor surfaces of the arms and legs are most commonly affected. Infantile AD may resolve spontaneously or continue into the childhood phase, which is characterized by pruritic papules, xerosis, and lichenification. In the older child and adults, a scaly and lichenified dermatitis on the flexor surfaces of the extremities, neck, and upper trunk is observed. Over 85% of AD presents during the first five years of life, and rarely occurs after 45 years of age . Differential Diagnosis The differential diagnosis of AD includes a number of eczematous dermatitides including contact dermatitis, seborrheic dermatitis, fungal infections, and drug eruptions. In infancy, psoriasis, scabies, Netherton’s syndrome, ectodermal dysplasia, Hyper IgE syndrome, Wiskott-Aldrich syndrome and other immunodeficiencies, and enzyme deficiencies (e.g. phenylketonuria) must also be considered in the differential diagnosis. Histology The histopathologic changes in atopic dermatitis are nonspecific. Acute lesions, characterized by intensely pruritic, erythematous papules, reveal mild epidermal hyperplasia, intercellular edema of the epidermis (spongiosis), and infiltration of lymphocytes and macrophages along the venous plexus in the dermis. In chronic AD, characterized by lichenification and fibrotic papules, there is increased hyperplasia and hyperkeratosis of the epidermis, and a persistent dermal inflammatory cell infiltrate with lymphocytes and macrophages, as well as increased mast cells and Langerhans cells. Even though, there are few eosinophils seen in the lesions, deposition of the eosinophil granular protein major basic protein (MBP) in large quantities has been observed on immunoflourescent staining of chronic AD skin indicating an role for eosinophils in AD. Recent work has further demonstrated that eosinophils undergo cytolytic degeneration leading to release of granule proteins in lesions of AD .Immunohistological analysis of skin lesions in AD reveals a mononuclear cell infiltrate, predominantly in the dermis, consisting of activated memory CD4+ T cells bearing HLA-DR+ and CD45RO+ and of macrophages . The mast cell seen in the lesions are MT-type, which may be dependent on T cell for development. Vascular endothelial cells in AD skin lesions have increased expression of the adhesion molecules E-selectin, VCAM-1 and ICAM-1. These adhesions molecules are important for homing of T cells and eosinophils observed in these lesions. Pathogenesis Genetic and environmental factors induce a complex series of cellular interactions leading to the symptoms and signs of AD. One potential scenario is that Langerhans cells, which are surface IgE positive, present antigen to T cells leading to their activation and release of cytokines, i.e. IL-1, IL-6 and TNF-a. Simultaneously, physical trauma (scratching) causes the keratinocytes to secrete similar cytokines, which in turn attract and activate CD4+ T lymphocytes. Mast cells are also present and upon activation by cross-linking of IgE or other mechanisms, can release histamine and mediators upregulating adhesions molecules, which in turn may recruit additional inflammatory cells including T cells and eosinophils.The T cells appear to play a central role in the proces
机译：对应于：琳达·施耐德（Lynda C.Schneider），医学博士过敏与免疫学儿童医院儿童医院300 Longwood AvenueBoston，MA 02115617-355-6180简介特应性皮炎（AD）是一种慢性炎症性皮肤病。像其他过敏性疾病一样，特应性皮炎的患病率也在上升。在儿童中，AD的患病率从1960年代的3 -4％上升到1980年代的10-15％。但是与许多其他疾病不同，AD没有原发性皮肤病变或病理诊断测试。因此，特应性皮炎的诊断必须通过物理检查结果来确定（表1）。主要特征包括瘙痒，典型形态和病变分布。皮肤分布随年龄而变化。在婴儿期，手臂和腿的面部和伸肌表面最常见。婴幼儿AD可自发消退或持续进入儿童期，其特征是瘙痒性丘疹，干燥症和苔藓化。在较大的儿童和成年人中，在四肢，颈部和上躯干的屈肌表面观察到鳞状和苔藓状的皮炎。超过85％的AD出现在生命的前五年，很少在45岁以后出现。鉴别诊断AD的鉴别诊断包括许多湿疹性皮肤病，包括接触性皮炎，脂溢性皮炎，真菌感染和药疹。在婴儿期，牛皮癣，sc疮，Netherton综合征，外胚层发育不良，Hyper IgE综合征，Wiskott-Aldrich综合征和其他免疫缺陷，以及酶缺乏症（例如苯丙酮尿症）也必须考虑在内。组织学特应性皮炎的组织病理学改变是非特异性的。急性病变的特征是强烈的瘙痒性红斑丘疹，表现出轻度的表皮增生，表皮细胞间水肿（脊椎病）以及沿真皮静脉丛的淋巴细胞和巨噬细胞浸润。在以AD苔藓样化和纤维化性丘疹为特征的慢性AD中，表皮增生和角化过度增加，持续的皮肤炎性细胞渗入淋巴细胞和巨噬细胞，肥大细胞和朗格汉斯细胞增多。即使在病变中几乎看不到嗜酸性粒细胞，但是在慢性AD皮肤的免疫荧光染色中已经观察到大量嗜酸性粒细胞颗粒蛋白主要碱性蛋白（MBP）的沉积，表明嗜酸性粒细胞在AD中的作用。最近的研究进一步表明，嗜酸性粒细胞经历了细胞溶解性变性，导致了AD病变中颗粒蛋白的释放。AD皮肤病变的免疫组织学分析显示，单个核细胞浸润，主要在真皮中，由带有HLA-DR +的活化记忆CD4 + T细胞组成和CD45RO +和巨噬细胞。病变中可见的肥大细胞是MT型的，可能取决于T细胞的发育。 AD皮肤病变中的血管内皮细胞的粘附分子E-选择蛋白，VCAM-1和ICAM-1的表达增加。这些粘附分子对于在这些病变中观察到的T细胞和嗜酸性粒细胞的归巢很重要。发病机理遗传和环境因素诱导一系列复杂的细胞相互作用，导致AD的症状和体征。一种潜在的情况是，表面IgE阳性的朗格汉斯细胞向T细胞呈递抗原，导致它们活化和释放细胞因子，即IL-1，IL-6和TNF-α。同时，身体创伤（刮擦）会导致角质形成细胞分泌相似的细胞因子，进而吸引并激活CD4 + T淋巴细胞。肥大细胞也存在，并且通过IgE的交联或其他机制激活后，可以释放组胺和上调粘附分子的介质，这反过来可能募集其他炎症细胞，包括T细胞和嗜酸性粒细胞.T细胞似乎起着核心作用在过程中

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