Departments of Dermatology and Pediatrics, Northwestern University Feinberg School of Medicine and the Ann and Robert H Lurie Children's Hospital of Chicago, Chicago, Ill.
Department of Pediatrics, Division of Allergy and Immunology, the Children's Hospital of Philadelphia, Philadelphia, Pa.
J Allergy Clin Immunol. 2019 Jan;143(1):46-55. doi: 10.1016/j.jaci.2018.11.006. Epub 2018 Nov 17.
The atopic march recognizes the increased occurrence of asthma, allergic rhinitis, or both after atopic dermatitis (AD) onset. Mechanisms for developing atopic comorbidities after AD onset are poorly understood but can involve the impaired cutaneous barrier, which facilitates cutaneous sensitization. The association can also be driven or amplified in susceptible subjects by a systemic T2-dominant immune response to cutaneous inflammation. However, these associations might merely involve shared genetic loci and environmental triggers, including microbiome dysregulation, with the temporal sequence reflecting tissue-specific peak time of occurrence of each disease, suggesting more of a clustering of disorders than a march. Prospective longitudinal cohort studies provide an opportunity to explore the relationships between postdermatitis development of atopic disorders and potential predictive phenotypic, genotypic, and environmental factors. Recent investigations implicate disease severity and persistence, age of onset, parental atopic history, filaggrin (FLG) mutations, polysensitization, and the nonrural environment among risk factors for development of multiple atopic comorbidities in young children with AD. Early intervention studies to repair the epidermal barrier or alter exposure to the microbiome or allergens might elucidate the relative roles of barrier defects, genetic locus alterations, and environmental exposures in the risk and sequence of occurrence of T2 activation disorders.
特应性进行曲（atopic march）认识到特应性皮炎（AD）发病后哮喘、过敏性鼻炎或两者的发生率增加。AD 发病后发生特应性共病的机制尚不清楚，但可能涉及受损的皮肤屏障，这有利于皮肤致敏。易感个体中，全身性 T2 优势免疫反应对皮肤炎症的反应也可能导致或放大这种关联。然而，这些关联可能仅仅涉及共享的遗传位点和环境触发因素，包括微生物组失调，时间序列反映了每种疾病在组织特异性的发生高峰时间，这表明更多的是疾病的聚集而不是进行曲。前瞻性纵向队列研究为探索 AD 后特应性疾病的发展以及潜在的预测表型、基因型和环境因素之间的关系提供了机会。最近的研究表明，疾病严重程度和持续性、发病年龄、父母特应性史、丝聚合蛋白（FLG）突变、多敏化和非农村环境是 AD 患儿发生多种特应性共病的危险因素。早期干预研究修复表皮屏障或改变对微生物组或过敏原的暴露，可能阐明屏障缺陷、基因座改变和环境暴露在 T2 激活障碍的风险和发生顺序中的相对作用。
