Allergic Rhinitis-猫眼课题宝

DOI：

10.1093/med/9780199683956.003.0028

发表时间：

2015-08

期刊：

Succinct Pediatrics: Evaluation and Management for Common and Critical Care

影响因子：

通讯作者：

中科院分区：

其他

文献类型：

作者：

Christine B. Cho;David Goff;Amber M. Patterson

一名35岁的女性在一年中的大部分时间都有鼻塞史，可以追溯到她十几岁的时候。她有慢性鼻引流，这是明确和厚。她的充血在夏末秋初和早春时最严重;在这些时候，她也会打喷嚏，鼻痒和咳嗽。五年前，她在鼻部症状严重的一天出现了呼吸急促伴喘息的发作，但这一发作自行消退，没有复发。她的眼睛并不困扰她，非处方的口服抗组胺药对她的症状有一点帮助，偶尔使用的鼻腔减充血剂也有帮助。她6岁的儿子也有类似症状。这种情况应该如何处理？临床问题过敏性鼻炎被定义为打喷嚏、鼻瘙痒、气流阻塞和主要由IgE介导的针对吸入的过敏原的反应引起的清鼻涕的症状，并且涉及由2型辅助性T（Th 2）细胞驱动的粘膜炎症。1重要的过敏原包括季节性花粉和霉菌，以及常年性室内过敏原，如尘螨、宠物、害虫和一些霉菌。主要过敏原的模式取决于地理区域和城市化程度，但过敏原致敏的总体患病率在美国的人口普查区之间没有变化。2吸入性过敏原致敏开始于生命的第一年;室内过敏原致敏先于花粉致敏。由于病毒性呼吸道感染经常发生在幼儿身上，并产生类似的症状，因此在生命的前2或3年诊断过敏性鼻炎非常困难。过敏性鼻炎的患病率在生命的第二至第四个十年达到高峰，然后逐渐减少。3，4版权所有© 2015马萨诸塞州医学会。地址重印要求博士惠特利在美国国立卫生研究院，5601费舍尔Ln，RM. 6 B56，贝塞斯达，马里兰州20892-9827，或在丽莎.惠特利@nih. gov.。这篇文章的音频版本可在NEJM.org上找到，没有与这篇文章相关的潜在利益冲突的报道。作者提供的披露表格可在NEJM.org上查阅这篇文章的全文。然后提出支持各种战略的证据，然后审查现有的正式准则。文章最后给出了作者的临床建议。NIH Public Access Author Mandarin pt N Engl J Med. Author manuscript; available in PMC 2015 July 29.以最终编辑形式发表：N Engl J Med. 2015年1月29日; 372（5）：456-463。doi：10.1056/NEJMcp1412282。吸入性过敏原致敏的频率正在增加，现在在美国和欧洲的许多人群中超过40%。6根据医生诊断，美国过敏性鼻炎的患病率约为15% 7，3过敏性鼻炎导致工作和学习时间的缺失或无效率，睡眠问题，以及受影响的儿童参与户外活动的减少。7此外，与正常儿童相比，过敏性鼻炎儿童更有可能接受鼓膜切开插管，并切除扁桃体和腺样体。7控制哮喘的能力在哮喘和过敏性鼻炎患者中，这种治疗方法与控制过敏性鼻炎有关。大多数哮喘患者患有鼻炎。过敏性鼻炎的症状有哪些（季节性或常年性）显著增加哮喘的可能性：高达40%的过敏性鼻炎患者患有或将患有哮喘。9，10特应性湿疹经常先于过敏性鼻炎。11过敏性鼻炎患者通常也有过敏性结膜炎。12决定个体发生特应性疾病的因素以及某些人发生特应性疾病的原因只有鼻炎和其他鼻炎后湿疹或与哮喘仍不清楚。有一个过敏性鼻炎的父母超过一倍的风险。13有多个哥哥姐姐和在农业环境中长大与过敏性鼻炎的风险降低14，15;据推测，这些明显的保护因素可能反映了生命早期的微生物暴露，使免疫系统远离Th 2极化和过敏。14，15当人暴露于过敏原时，过敏原与粘膜肥大细胞结合的IgE交联，在几分钟内导致鼻部症状（图1）。这是由于神经活性和血管活性物质的释放，如组胺、前列腺素D2和半胱氨酰白三烯。16在接下来的几个小时内，通过肥大细胞、上皮细胞、树突细胞、T细胞、先天性淋巴细胞、嗜酸性粒细胞和嗜碱性粒细胞的复杂相互作用，Th 2炎症在鼻粘膜中发展，由这些细胞产生的多种趋化因子和细胞因子参与。16，17由于粘膜炎症，鼻症状可在过敏原暴露后持续数小时，粘膜对沉淀过敏原（引发）以及其他过敏原和非过敏性刺激（如强烈气味和其他刺激物）更具反应性（非特异性鼻高反应性）。18，19过敏性鼻炎应被视为这些机制的一个星座，而不是对过敏原暴露的简单急性反应。战略和证据

A 35-year-old woman has a history of nasal congestion on most days of the year, dating back to her late teens. She has chronic nasal drainage, which is clear and thick. Her congestion is worst in the late summer and early fall and again in the early spring; at these times, she also has sneezing, nasal itching, and cough. Five years ago, she had an episode of shortness of breath with wheezing on a day when her nasal symptoms were severe, but this episode resolved spontaneously and has not recurred. Her eyes do not bother her. Over-the-counter oral antihistamines help her symptoms a little, as do nasal decongestants, which she uses occasionally. Her 6-year-old son has similar symptoms. How should this case be managed? THE CLINICAL PROBLEM Allergic rhinitis is defined as symptoms of sneezing, nasal pruritus, airflow obstruction, and mostly clear nasal discharge caused by IgE-mediated reactions against inhaled allergens and involving mucosal inflammation driven by type 2 helper T (Th2) cells.1 Allergens of importance include seasonal pollens and molds, as well as perennial indoor allergens, such as dust mites, pets, pests, and some molds. The pattern of dominant allergens depends on the geographic region and the degree of urbanization, but the overall prevalence of sensitization to allergens does not vary across census tracts in the United States.2 Sensitization to inhaled allergens begins during the first year of life; sensitization to indoor allergens precedes sensitization to pollens. Because viral respiratory infections occur frequently in young children and produce similar symptoms, it is very difficult to diagnose allergic rhinitis in the first 2 or 3 years of life. The prevalence of allergic rhinitis peaks in the second to fourth decades of life and then gradually diminishes.3,4 Copyright © 2015 Massachusetts Medical Society. Address reprint requests to Dr. Wheatley at the National Institutes of Health, 5601 Fishers Ln., Rm. 6B56, Bethesda, MD 20892-9827, or at lisa.wheatley@nih.gov.. An audio version of this article is available at NEJM.org No potential conflict of interest relevant to this article was reported. Disclosure forms provided by the authors are available with the full text of this article at NEJM.org. This Journal feature begins with a case vignette highlighting a common clinical problem. Evidence supporting various strategies is then presented, followed by a review of formal guidelines, when they exist. The article ends with the authors’ clinical recommendations. NIH Public Access Author Manuscript N Engl J Med. Author manuscript; available in PMC 2015 July 29. Published in final edited form as: N Engl J Med. 2015 January 29; 372(5): 456–463. doi:10.1056/NEJMcp1412282. N IH -P A A uhor M anscript N IH -P A A uhor M anscript N IH -P A A uhor M anscript The frequency of sensitization to inhalant allergens is increasing and is now more than 40% in many populations in the United States and Europe.2,5,6 The prevalence of allergic rhinitis in the United States is approximately 15% on the basis of physician diagnoses7 and as high as 30% on the basis of self-reported nasal symptoms.3 Allergic rhinitis contributes to missed or unproductive time at work and school, sleep problems, and among affected children, decreased involvement in outdoor activities.7 In addition, children with allergic rhinitis are more likely than unaffected children to have myringotomy tubes placed and to have their tonsils and adenoids removed.7 The ability to control asthma in people with both asthma and allergic rhinitis has been linked to the control of allergic rhinitis.8 Most people with asthma have rhinitis. The presence of allergic rhinitis (seasonal or perennial) significantly increases the probability of asthma: up to 40% of people with allergic rhinitis have or will have asthma.9,10 Atopic eczema frequently precedes allergic rhinitis.11 Patients with allergic rhinitis usually have allergic conjunctivitis as well.12 The factors determining which atopic disease will develop in an individual person and the reasons why some people have only rhinitis and others have rhinitis after eczema or with asthma remain unclear. Having a parent with allergic rhinitis more than doubles the risk.13 Having multiple older siblings and growing up in a farming environment are associated with a reduced risk of allergic rhinitis14,15; it is hypothesized that these apparently protective factors may reflect microbial exposures early in life that shift the immune system away from Th2 polarization and allergy.14,15 When persons are exposed to an allergen against which they are sensitized, cross-linking by the allergen of IgE bound to mucosal mast cells results in nasal symptoms within minutes (Fig. 1). This is due to the release of neuroactive and vasoactive substances such as histamine, prostaglandin D2, and cysteinyl leukotrienes.16 During the next hours, through a complex interaction of mast cells, epithelial cells, dendritic cells, T cells, innate lymphoid cells, eosinophils, and basophils, Th2 inflammation develops in the nasal mucosa with the participation of a wide array of chemokines and cytokines produced by these cells.16,17 As a consequence of mucosal inflammation, nasal symptoms can persist for hours after allergen exposure and the mucosa becomes more reactive to the precipitating allergen (priming) as well as to other allergens and to nonallergenic stimuli, such as strong odors and other irritants (nonspecific nasal hyperresponsiveness).18,19 Allergic rhinitis should be viewed as a constellation of these mechanisms and not as a simple acute reaction to allergen exposure. STRATEGIES AND EVIDENCE

Allergic Rhinitis

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