IgE Sensitization Drives the Atopic March.
IgE Sensitization Drives the Atopic March.
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IgE 致敏推动特应性发作。
DOI：
10.1164/rccm.202210-2022le
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发表时间：
2023
影响因子：
24.7
通讯作者：
Järvinen,KirsiM
中科院分区：
文献类型：
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作者：
Beck,LisaA;Pesonen,Maria;Thakar,Juilee;Georas,SteveN;Järvinen,KirsiM
我们饶有兴趣地阅读了 Haider 及其同事的报告，他们根据对四个英国出生队列的研究得出的结论是，“没有证据表明特应性病会连续进展”(1)。他们研究了生命早期的湿疹、喘息或遗传因素是否会增加特应性多发病的风险。我们想强调这项研究设计、方法和结果解释的局限性，我们认为这些局限性与其他评估特应性进展的研究很常见。特应性的定义意味着产生过敏原特异性 IgE 的倾向。因此，有可能仅在有过敏原致敏的参与者中考虑特应性行军，不包括非 IgE 相关的特应性皮炎和非特应性短暂性喘息。尽管最初的报告并未将食物过敏 (FA) 纳入特应性游行的定义中 (2)，但我们与国家过敏和传染病研究所特应性游行共识报告一样，认为需要将其包括在内 (3)。然而，这里的四个队列中只有一个评估了 FA，仅限于花生过敏。我们认为 IgE 致敏（有或没有屏障功能障碍）驱动特应性进展，如果没有 IgE 致敏，则不存在特应性或进展。尽管从这些出生队列中前瞻性收集的大量数据是一项了不起的成就，但在评估特应性进展方面存在一些方法学问题。基于问卷的研究不能准确反映真正的特应性疾病，并且存在诊断不足和过度诊断的偏差 (4)。为了更准确地估计特应性疾病，需要医生诊断，我们在 200 名婴儿的出生队列中进行了这项研究，随后进入成年期 (2)。特应性皮炎、过敏性鼻结膜炎和复发性喘息的诊断是由同一位医生在出生后第一年内以及在 5、11 和 20 岁时反复进行的临床检查得出的。对食物过敏进行了评估，并根据家长和参与者的访谈报告了食物过敏的症状。在我们的研究中，早发型（12 个月大）特应性皮炎是后来发展为过敏性呼吸道疾病的一个重要危险因素，而患有 AD 和食物过敏的患者进展风险最高。我们认为其他一些方法学问题值得强调。参与者在每个时间点被分配当前疾病状态（即，无疾病；单一疾病：仅湿疹、仅喘息或仅鼻炎；两种疾病的组合；以及定义为湿疹加喘息加特应性多发病）
We read with interest the report by Haider and colleagues, who concluded from the study of four UK birth cohorts that there is “no evidence for a sequential atopic march progression”(1). They investigated whether early-life eczema, wheeze, or genetic factors increased the risk of atopic multimorbidity. We would like to highlight limitations in this study design, methodology, and interpretation of the results, which we think are common to other studies evaluating the atopic march. The definition of atopy implies predisposition toward development of allergen-specific IgE. Therefore, it is possible that the atopic march should only be considered in participants with allergen sensitization excluding non–IgE-associated atopic dermatitis and nonatopic transient wheezers. Although the initial reports did not include food allergy (FA) in the definition of atopic march (2), we, like the National Institute of Allergy and Infectious Diseases Atopic March Consensus report, believe it needs to be included (3). However, only one of the four cohorts here assessed FA, limited to peanut allergy. We propose that it is IgE sensitization (with or without barrier dysfunction) that drives atopic march, and without IgE sensitization, there is no atopy or march. Although the large and prospectively collected pool of data from these birth cohorts is a remarkable achievement, there were some methodological concerns as they relate to evaluating the atopic march. Questionnaire-based studies do not accurately reflect true atopic diseases and are biased with both under-and overdiagnosis (4). Physician diagnosis is needed for more accurate estimates of atopic conditions, which we did in a birth cohort of 200 infants followed into young adulthood (2). Diagnoses of atopic dermatitis, allergic rhinoconjunctivitis, and recurrent wheeze were rendered based on clinical exams by the same physician repeatedly within the first year of life and again at 5, 11, and 20 years of age. Food sensitization was assessed, and symptoms of food hypersensitivity were reported based on parental and participant interviews. In our study, early-onset (, 12 months of age) atopic dermatitis was a significant risk factor for later development of allergic respiratory disease, and those with AD and food hypersensitivity had the highest risk for progression.We believe a few other methodologic concerns are worth highlighting. Participants were assigned a current disease state at each time point (ie, no disease; single disease: only eczema, only wheeze, or only rhinitis; combinations of two diseases; and atopic multimorbidity defined as eczema plus wheeze plus