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从特应性皮炎到哮喘:特应性进行曲。

From atopic dermatitis to asthma: the atopic march.

机构信息

Division of Allergy and Immunology, The Children's Hospital of Philadelphia, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104-4399, USA.

出版信息

Ann Allergy Asthma Immunol. 2010 Aug;105(2):99-106; quiz 107-9, 117. doi: 10.1016/j.anai.2009.10.002. Epub 2010 Jan 22.

Abstract

OBJECTIVE

To examine the mechanisms whereby allergen exposure through the epidermis could initiate systemic allergy and predispose individuals to the development of 1 or more atopic diseases via the so-called atopic march.

DATA SOURCES

PubMed databases from 1950 to the present were searched for relevant articles pertaining to epidemiologic and genetic evidence of the progression of the atopic march.

STUDY SELECTION

Articles concerning pathophysiologic conditions that link atopic dermatitis, allergic rhinitis, and asthma were examined.

RESULTS

The data suggest that a sequence of atopic manifestations occurs, typically atopic dermatitis in infancy followed by allergic rhinitis and/or asthma in later stages. Reduced filaggrin expression is implicated as a major predisposing factor for atopy in multiple lines of evidence, including genome-wide analysis and microarray investigations. Other gene products have an important role. Cross-sectional and longitudinal studies provide preliminary epidemiologic support for the sequential development of allergic diseases.

CONCLUSION

The mechanisms by which allergen exposure through the epidermis can initiate systemic allergy and predispose individuals to atopic dermatitis, allergic rhinitis, and asthma have become clearer in recent years. Longitudinal studies of individuals carrying loss-of-function filaggrin gene mutations are needed to further define the risks associated with epidermal barrier dysfunction and potentially identify specific targets for barrier repair and prevention of atopic dermatitis and other atopic disease. The effects of preventive and treatment strategies have been inconsistent across studies, and further research is warranted before any definitive recommendations can be made.

摘要

目的

探讨过敏原通过表皮暴露引发全身性过敏,并通过所谓的特应性进行曲使个体易患 1 种或多种特应性疾病的机制。

资料来源

从 1950 年至今,在 PubMed 数据库中搜索了与特应性进行曲的进展相关的流行病学和遗传证据的相关文章。

研究选择

检查了与特应性皮炎、过敏性鼻炎和哮喘相关的病理生理条件的文章。

结果

数据表明,特应性表现的序列发生,通常是婴儿期的特应性皮炎,随后是后期的过敏性鼻炎和/或哮喘。多项证据表明,减少丝聚蛋白的表达是特应性的主要易感因素,包括全基因组分析和微阵列研究。其他基因产物也有重要作用。横断面和纵向研究为过敏性疾病的序贯发展提供了初步的流行病学支持。

结论

近年来,过敏原通过表皮暴露引发全身性过敏并使个体易患特应性皮炎、过敏性鼻炎和哮喘的机制变得更加清晰。需要对携带丝聚蛋白基因突变的个体进行纵向研究,以进一步确定与表皮屏障功能障碍相关的风险,并可能确定针对屏障修复和预防特应性皮炎和其他特应性疾病的特定靶点。预防和治疗策略的效果在研究中不一致,需要进一步研究才能提出任何明确的建议。

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