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特应性皮炎。

Atopic dermatitis.

机构信息

Department of Dermatology and Allergy, University Hospital Schleswig-Holstein, Kiel, Germany.

Department of Dermatology, Medicine and Pathology, University of Rochester Medical Center, Rochester, NY, USA.

出版信息

Nat Rev Dis Primers. 2018 Jun 21;4(1):1. doi: 10.1038/s41572-018-0001-z.

DOI:10.1038/s41572-018-0001-z
PMID:29930242
Abstract

Atopic dermatitis (AD) is the most common chronic inflammatory skin disease, with a lifetime prevalence of up to 20% and substantial effects on quality of life. AD is characterized by intense itch, recurrent eczematous lesions and a fluctuating course. AD has a strong heritability component and is closely related to and commonly co-occurs with other atopic diseases (such as asthma and allergic rhinitis). Several pathophysiological mechanisms contribute to AD aetiology and clinical manifestations. Impairment of epidermal barrier function, for example, owing to deficiency in the structural protein filaggrin, can promote inflammation and T cell infiltration. The immune response in AD is skewed towards T helper 2 cell-mediated pathways and can in turn favour epidermal barrier disruption. Other contributing factors to AD onset include dysbiosis of the skin microbiota (in particular overgrowth of Staphylococcus aureus), systemic immune responses (including immunoglobulin E (IgE)-mediated sensitization) and neuroinflammation, which is involved in itch. Current treatments for AD include topical moisturizers and anti-inflammatory agents (such as corticosteroids, calcineurin inhibitors and cAMP-specific 3',5'-cyclic phosphodiesterase 4 (PDE4) inhibitors), phototherapy and systemic immunosuppressants. Translational research has fostered the development of targeted small molecules and biologic therapies, especially for moderate-to-severe disease.

摘要

特应性皮炎(AD)是最常见的慢性炎症性皮肤病,终生患病率高达 20%,对生活质量有重大影响。AD 的特征是剧烈瘙痒、反复出现的湿疹样病变和波动的病程。AD 具有很强的遗传成分,与其他特应性疾病(如哮喘和过敏性鼻炎)密切相关且常同时发生。几种病理生理机制导致 AD 的发病机制和临床表现。例如,由于结构蛋白丝聚蛋白的缺乏导致表皮屏障功能受损,可促进炎症和 T 细胞浸润。AD 中的免疫反应偏向于辅助性 T 细胞介导的途径,反过来又有利于表皮屏障的破坏。AD 发病的其他促成因素包括皮肤微生物组的失调(特别是金黄色葡萄球菌过度生长)、全身免疫反应(包括 IgE 介导的致敏)和神经炎症,后者与瘙痒有关。AD 的当前治疗方法包括局部保湿剂和抗炎药(如皮质类固醇、钙调神经磷酸酶抑制剂和 cAMP 特异性 3',5'-环磷酸二酯酶 4(PDE4)抑制剂)、光疗和全身免疫抑制剂。转化研究促进了靶向小分子和生物疗法的发展,特别是针对中重度疾病。

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