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Treatment Approach to Chronic Rhinosinusitis Based on Endotype: Difference Between East and West 基于内型的慢性鼻窦炎治疗方法:东西方差异。
IF 5.2 2区 医学 Q1 ALLERGY Pub Date : 2025-10-02 DOI: 10.1111/cea.70150
Junhai Chen, Linlu Wang, Xinyue Wang, Yana Zhang, Qintai Yang

Heterogeneity among CRSwNP patients in Western and Eastern countries leads to differences in management. Type 2 (T2) inflammation accounts for the majority of CRSwNP patients in Western countries, while non-T2 inflammation is the main endotype in CRSwNP patients in Eastern countries. Precise identification of T2 inflammation holds significant promise for optimising treatment outcomes. The treatment of T2 inflammation-biased CRSwNP primarily involves glucocorticoids, reboot surgery, and T2 biologics, while non-T2 inflammation-dominant CRSwNP is mainly treated with macrolide antibiotics.

东西方国家CRSwNP患者的异质性导致了治疗上的差异。西方国家CRSwNP患者以2型(T2)炎症为主,而东方国家CRSwNP患者以非T2炎症为主。精确识别T2炎症对优化治疗结果具有重要意义。T2炎症偏倚的CRSwNP的治疗主要包括糖皮质激素、重启手术和T2生物制剂,而非T2炎症偏倚的CRSwNP主要使用大环内酯类抗生素治疗。
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引用次数: 0
A Safe and Effective 7 Week Updosing Protocol for Bee and Wasp Venom Immunotherapy 一种安全有效的蜜蜂和黄蜂毒液免疫治疗7周升级方案。
IF 5.2 2区 医学 Q1 ALLERGY Pub Date : 2025-09-30 DOI: 10.1111/cea.70149
Usmaan Ahmed, Yitong Shen, Robert L. Yellon, Jacqui Galloway, Priya Sellaturay, Shuaib Nasser, Padmalal Gurugama
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引用次数: 0
Innovative Approaches to Allergic Disease Characterisation: Comprehensive Antibody Profiling and Non-Invasive Metabolomics 变态反应性疾病表征的创新方法:综合抗体谱分析和非侵入性代谢组学。
IF 5.2 2区 医学 Q1 ALLERGY Pub Date : 2025-09-30 DOI: 10.1111/cea.70152
Mohamed H. Shamji, Robert J. Boyle
<p>In this month's editorial, the Editors of the journal have chosen two interesting studies that are included in this issue. The first article investigates the diversity of circulating food allergen-specific antibodies in eosinophilic esophagitis (EoE), extending the focus beyond IgG4 [<span>1</span>]. EoE is a food-triggered, Th2-mediated inflammatory disease of the oesophagus, characterised by high levels of IgG4 both in tissue and circulation, yet the role of additional antibody isotypes in disease activity has remained unclear. Previous work emphasised IgE or IgG4 alone; however, diet response and disease pathogenesis are not fully explained by these markers.</p><p>The study by Imam et al. [<span>1</span>] delivers key insights, profiling plasma for IgG and IgA subclasses specific to major food allergens in both active and inactive EoE versus non-EoE controls. The results indicate that, in addition to increased IgG4, EoE patients have significantly elevated levels of IgG2, IgA1 and IgA2 targeting allergens like casein, wheat and egg. These antibody signatures differ by disease activity and contrast sharply with non-EoE controls, which suggests a broader and more complex humoral immune landscape. Interestingly, the study found no circulating food-specific B cells, implying antibody production may be mainly tissue-localised in EoE—which aligns with previous research findings that showed the presence of B lymphocytes and plasma cells in the EoE tissue [<span>2-4</span>].</p><p>This study highlights how these diverse antibody responses could reflect sustained antigen exposure and ongoing mucosal inflammation, providing candidate biomarkers for improved dietary and therapeutic strategies. Future studies will need to continue exploring the longitudinal research of these antibodies and their clinical relevance in guiding individualised management and predicting response to diets. Figure 1 represents the graphical abstract illustrating the key findings of this paper.</p><p>This issue's second editor's choice article represents untargeted metabolomic analysis of exhaled breath condensate (EBC) to identify disease-specific metabolic signatures in adults with asthma [<span>5</span>]. There are many confounding factors that challenge definitive asthma diagnosis, which requires diagnostic tests with more accuracy and objectivity. Unlike genomic or proteomic markers, metabolites directly indicate cellular biochemical activity and disease states. Metabolomics also provide a highly sensitive approach to uncover small but clinically significant changes in biological pathways. Despite its potential, previous asthma metabolomics research has mostly focused on blood, urine or tissue, where relatively few studies have utilised the non-invasive EBC method to profile airway-derived metabolites [<span>6-8</span>].</p><p>In this study, Zhao et al. [<span>5</span>] utilised advanced mass spectrometry using ultra-performance liquid chromatography to perform untargeted
在本月的社论中,该杂志的编辑们选择了两项有趣的研究。第一篇文章研究了嗜酸性食管炎(EoE)中循环食物过敏原特异性抗体的多样性,将焦点扩展到IgG4[1]以外。EoE是一种食物引发的、th2介导的食道炎症性疾病,其特征是组织和循环中IgG4水平高,但其他抗体同型在疾病活动中的作用仍不清楚。以前的研究只强调IgE或IgG4;然而,这些标志物并不能完全解释饮食反应和疾病发病机制。Imam等人的研究提供了关键的见解,分析了活跃和不活跃EoE与非EoE对照中主要食物过敏原特异性IgG和IgA亚类的血浆。结果表明,除了IgG4升高外,EoE患者针对酪蛋白、小麦和鸡蛋等过敏原的IgG2、IgA1和IgA2水平也显著升高。这些抗体特征因疾病活动而异,与非eoe对照形成鲜明对比,这表明存在更广泛、更复杂的体液免疫格局。有趣的是,该研究没有发现循环中的食物特异性B细胞,这意味着抗体的产生可能主要是在EoE中组织定位的,这与先前的研究结果一致,即EoE组织中存在B淋巴细胞和浆细胞[2-4]。这项研究强调了这些不同的抗体反应如何反映持续的抗原暴露和持续的粘膜炎症,为改善饮食和治疗策略提供了候选生物标志物。未来的研究将需要继续探索这些抗体的纵向研究及其在指导个体化管理和预测饮食反应方面的临床相关性。图1是说明本文主要发现的图形摘要。这期的第二篇编辑选择文章代表了呼气冷凝水(EBC)的非靶向代谢组学分析,以确定成人哮喘bbb的疾病特异性代谢特征。有许多混杂因素挑战明确的哮喘诊断,这需要更准确和客观的诊断测试。与基因组或蛋白质组学标记物不同,代谢物直接指示细胞生化活性和疾病状态。代谢组学还提供了一种高度敏感的方法来发现生物学途径中微小但具有临床意义的变化。尽管其具有潜力,但以往的哮喘代谢组学研究主要集中在血液、尿液或组织中,其中相对较少的研究利用无创EBC方法来分析气道来源的代谢物[6-8]。在这项研究中,Zhao等人利用先进的质谱和超高效液相色谱技术对19名成人哮喘患者和23名健康对照者的EBC样本进行了非靶向代谢组学分析。分析显示,代谢特征(尤其是脂质和氨基酸代谢物)存在明显的疾病特异性变化,从而将哮喘与非哮喘状态区分开来。这些一致的代谢物改变提示了EBC中有价值的诊断和机制生物标志物。这些发现强调了EBC代谢组学如何有助于哮喘表型的准确分类,改善患者风险谱和可行的纵向气道监测。对于未来的研究,作者建议扩大患者队列,整合互补的“组学”数据集,并在前瞻性临床试验中验证EBC代谢物生物标志物,以推动个性化哮喘管理。图2提供了一个图形摘要,总结了成人哮喘中EBC代谢组学分析的主要发现。作者声明无利益冲突。
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引用次数: 0
The Incidence of Addiction and Its Risk Factors in Chinese Chronic Urticaria Patients. 中国慢性荨麻疹患者成瘾发生率及其危险因素分析。
IF 5.2 2区 医学 Q1 ALLERGY Pub Date : 2025-09-29 DOI: 10.1111/cea.70151
Xinyu Shui, Yu Jiang, Cong Peng, Qiaozhi Cao, Jie Li
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引用次数: 0
Optimal ImmunoCAP Aspergillus fumigatus-Specific IgE Threshold for Detecting Allergic Bronchopulmonary Aspergillosis in Adults With Asthma: A Diagnostic Accuracy Study 最佳免疫cap烟曲霉特异性IgE阈值检测成人哮喘变应性支气管肺曲霉病:诊断准确性研究
IF 5.2 2区 医学 Q1 ALLERGY Pub Date : 2025-09-26 DOI: 10.1111/cea.70148
Ritesh Agarwal, Puneet Saxena, Valliappan Muthu, Inderpaul Singh Sehgal, Kuruswamy Thurai Prasad, Sahajal Dhooria, Mani Singh, Mandeep Garg, Ashutosh N. Aggarwal, Shivaprakash M. Rudramurthy, Arunaloke Chakrabarti

Background

Allergic bronchopulmonary aspergillosis (ABPA) requires screening in adults with asthma using Aspergillus fumigatus-specific IgE (Af-IgE). The current Af-IgE threshold of 0.35 kUA/L has low specificity, leading to unnecessary downstream testing.

Objectives

To determine an optimal Af-IgE threshold that maintains high sensitivity while improving specificity for ABPA screening in adults with asthma.

Methods

We performed a diagnostic accuracy study of prospectively collected data using distinct derivation and validation cohorts in a tertiary care setting. The index test was ImmunoCAP Af-IgE at thresholds of 0.35, 0.70 and 0.90 kUA/L. The reference standard was the 2024 ISHAM-ABPA criteria applied by investigators aware of all test results.

Results

We included 543 consecutive asthmatic subjects investigated for possible ABPA in the derivation cohort (July 2017–September 2018) and 375 subjects with established asthma and ABPA in the validation dataset (January 2020–December 2023). ABPA prevalence was 19.5% (106/543) in derivation and 69.6% (261/375) in validation cohorts. Bayesian latent class analysis estimated a 0.3 kUA/L cut-off but did not improve specificity; frequentist analysis showed model misfit. In the validation cohort, increasing the threshold from 0.35 to 0.70 kUA/L improved specificity from 66.7% (95% CI, 57.6–74.7) to 72.8% (95% CI, 64.0–80.1; p = 0.016) without significant sensitivity reduction (100% to 98.9%; 95% CI, 96.7–99.6; p = 0.25). No patients with bronchiectasis were missed. At 0.90 kUA/L, sensitivity significantly decreased (97.7%; 95% CI, 95.1–98.9; p = 0.031).

Conclusions

ImmunoCAP Af-IgE threshold of 0.70 kUA/L optimised diagnostic performance for ABPA screening in adults with asthma, potentially reducing unnecessary confirmatory testing.

背景:过敏性支气管肺曲霉病(ABPA)需要使用烟曲霉特异性IgE (Af-IgE)筛查成人哮喘患者。目前的Af-IgE阈值为0.35 kUA/L,特异性较低,导致不必要的下游检测。目的:确定一个最佳的Af-IgE阈值,在保持高敏感性的同时提高成人哮喘ABPA筛查的特异性。方法:我们在三级医疗机构中使用不同的推导和验证队列对前瞻性收集的数据进行了诊断准确性研究。指标检测为ImmunoCAP Af-IgE,阈值分别为0.35、0.70和0.90 kUA/L。参考标准是2024 ISHAM-ABPA标准,由了解所有测试结果的研究人员应用。结果:我们在衍生队列(2017年7月至2018年9月)中纳入了543名连续哮喘受试者,以调查可能的ABPA,并在验证数据集(2020年1月至2023年12月)中纳入了375名已确诊哮喘和ABPA的受试者。衍生组ABPA患病率为19.5%(106/543),验证组为69.6%(261/375)。贝叶斯潜类分析估计的截止值为0.3 kUA/L,但没有提高特异性;频率分析显示模型不匹配。在验证队列中,将阈值从0.35提高到0.70 kUA/L,特异性从66.7% (95% CI, 57.6-74.7)提高到72.8% (95% CI, 64.0-80.1; p = 0.016),而敏感性没有显著降低(100%至98.9%;95% CI, 96.7-99.6; p = 0.25)。无遗漏支气管扩张患者。在0.90 kUA/L时,敏感性显著降低(97.7%;95% CI, 95.1-98.9; p = 0.031)。结论:0.70 kUA/L的免疫cap Af-IgE阈值优化了成人哮喘ABPA筛查的诊断性能,可能减少不必要的确认性检测。
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引用次数: 0
Changes in Atopic Sensitisation From 1 to 5 Years of Age: Longitudinal Data From the MIS BAIR Trial 1至5岁特应性致敏的变化:来自MIS BAIR试验的纵向数据。
IF 5.2 2区 医学 Q1 ALLERGY Pub Date : 2025-09-22 DOI: 10.1111/cea.70144
Nicole L. Messina, Laure F. Pittet, Emily K. Forbes, Kaya Gardiner, Katie L. Flanagan, Anne-Louise Ponsonby, Roy Robins-Browne, Frank Shann, Mike South, Peter Vuillermin, Susan Donath, Dan Casalaz, Nigel Curtis, the Melbourne Infant Study: BCG for Allergy and Infection Reduction (MIS BAIR) Group
<p>Vaccination with BacilleCalmette-Guérin (BCG) has off-target effects on the immune system which may influence the risk of developing allergic disease in later life. The Melbourne Infant Study: BCG for Allergy and Infection Reduction (MIS BAIR) randomised controlled trial (NCT01906853) investigated whether neonatal BCG vaccination reduces the incidence of allergy, eczema and infections at 1 and 5 years of age, and asthma at 5 years of age [<span>1</span>]. In the trial, neonatal BCG vaccination reduced the incidence of eczema at 1 year [<span>2</span>], particularly in children of parents with a history of eczema, but did not significantly reduce lower respiratory tract infections [<span>3</span>] or food allergy [<span>4</span>] at 1 year of age. At 5 years of age, neonatal BCG vaccination reduced the risk of more severe forms of asthma but had minimal effect on the overall incidence of asthma [<span>5</span>].</p><p>The MIS BAIR trial also aimed to investigate atopic sensitisation to a range of common allergens at 5 years of age. This required participants to attend a clinic visit for skin prick testing (SPT) at 5 years of age [<span>1, 4</span>]. In March 2020, COVID-19 pandemic ‘lockdown’ measures in Melbourne (which included stay-at-home orders [<span>6, 7</span>]) prevented 5-year SPT clinic visits being done for the following 12 months. During this period, 1124 (88%) of participants were eligible for their SPT clinic visit, with 62.7% (798/1272) only eligible after March 2020. To provide an opportunity for these participants to attend their SPT clinic visit after lockdown restrictions had eased, the age of eligibility for the SPT clinic visit was extended to 7 years of age. However, participants' families remained reluctant to visit a hospital setting during the pandemic and consequently, overall, only 34.2% (435/1272) attended a school-age (5–7 years of age) SPT clinic visit (Figure 1A).</p><p>In addition to the low follow-up rate, there was a difference between the randomisation groups in the proportion of participants who did not attend an SPT clinic visit (58.6% (373/637) in the BCG group vs. 73.1% (464/635) in the Control group) (Figure 1A). This might be attributable to disappointment in being randomised to the Control group [<span>8</span>] as participants' families were not blinded to the randomisation group due to BCG vaccination site scarring. Despite the large proportion of missing data, the available SPT results and longitudinal testing provide valuable information in relation to the progression of atopic sensitisation in early life.</p><p>Among the 435 participants who attended, the median age at the SPT clinic visit was 64 months (IQR 61–68 months; range 60–87 months). Of these, 99.1% (431/435) had a valid SPT, and 90.6% (394/435) were tested against all the pre-specified food (peanut, cashew nuts, hazelnut, walnut, raw egg, cow's milk, sesame and shellfish) and aero (dog, cat, house dust mite, rye grass and <i>Alternaria t
接种卡介苗(BCG)对免疫系统有脱靶作用,可能影响日后患过敏性疾病的风险。墨尔本婴儿研究:减少卡介苗过敏和感染(MIS BAIR)随机对照试验(NCT01906853)调查了新生儿接种卡介苗是否能降低1岁和5岁时过敏、湿疹和感染的发生率,以及5岁时哮喘的发生率。在试验中,新生儿接种卡介苗降低了1岁时湿疹的发病率,特别是在父母有湿疹史的儿童中,但没有显著降低1岁时下呼吸道感染[3]或食物过敏[4]。在5岁时,新生儿接种卡介苗降低了更严重哮喘形式的风险,但对哮喘bbb的总体发病率影响甚微。MIS BAIR试验还旨在调查5岁儿童对一系列常见过敏原的特应性致敏。这要求参与者在5岁时去诊所进行皮肤点刺试验(SPT)[1,4]。2020年3月,墨尔本的COVID-19大流行“封锁”措施(包括居家令[6,7])阻止了接下来12个月的5年SPT诊所就诊。在此期间,1124(88%)的参与者有资格参加他们的SPT诊所就诊,62.7%(798/1272)的参与者只有在2020年3月之后才有资格。为了让这些参与者有机会在封锁限制放松后参加防范小组委员会诊所就诊,防范小组委员会诊所就诊的资格年龄延长至7岁。然而,在大流行期间,参与者的家庭仍然不愿意去医院就诊,因此,总体而言,只有34.2%(435/1272)参加了学龄(5-7岁)SPT诊所就诊(图1A)。除了低随访率外,随机分组之间未参加SPT门诊就诊的参与者比例也存在差异(BCG组为58.6%(373/637),对照组为73.1%(464/635))(图1A)。这可能是由于被随机分配到对照组[8]的失望,因为参与者的家庭没有因为卡介苗接种部位疤痕而对随机分组视而不见。尽管有很大比例的数据缺失,但现有的SPT结果和纵向测试提供了与生命早期特应性致敏的进展有关的有价值的信息。在参加的435名参与者中,SPT诊所就诊时的中位年龄为64个月(IQR为61-68个月;范围为60-87个月)。其中,99.1%(431/435)具有有效的SPT, 90.6%(394/435)针对所有预先指定的食物(花生、腰果、榛子、核桃、生鸡蛋、牛奶、芝麻和贝类)和空气(狗、猫、屋螨、黑麦草和狐猸子)过敏原进行了测试。在有效SPT的参与者中,37.4%(161/431)对至少一种过敏原有特应性致敏(比阴性对照≥2mm)。这些参与者中的大多数对黑麦草(62.1%,100/161)和/或屋尘螨(52.8%,85/161)敏感(图1B)。对多种过敏原有有效SPT的参与者中有19.0%(81/426)发现对一种以上过敏原敏感,其中48名参与者对2,16至3,10至4和7至5种或更多过敏原敏感,主要是草(7/7),屋尘螨(6/7),花生(5/7)和鸡蛋(5/7)。与先前的研究一致,对食物过敏原的致敏性随着时间的推移从1岁时的18.2%(198/1089)下降到5-7岁(学龄)时的10.9%(47/431)。这是由于先前食物致敏的减少和解决(图1B)。一岁和学龄儿童的食物过敏原致敏持续时间因食物而异。卵子致敏从1年的9.9%下降到5-7年的2.3%,只有13.3%的参与者持续致敏。同样,榛子过敏只持续了6.3%的参与者。对于其他食物过敏原,在一年和学龄期间,23%-37%的参与者持续致敏(牛奶23.1%,腰果29.2%,芝麻33.3%,贝类33.3%和花生37.1%)。相比之下,对空气过敏原(黑麦草、室内尘螨、狗和猫)的致敏率从1岁时的5.0%(54/1089)增加到5-7岁时的34.8%(150/431)(图1B)。BCG组对任何核心过敏原的特应性致敏率为38.8%(95/245),对照组为42.0%(66/157)(图1C)。由于数据缺失的比例较大,且干预组之间的不平衡,统计比较卡介苗接种对5-7岁儿童特应性致敏的影响是不可行的。我们调查了与未参加学龄儿童访视相关的因素,如预期的那样,发现未参加学龄儿童访视与2020年3月1日后的访视有关(χ2 p &lt; 0。 001)并随机分配到对照组(χ2 p &lt; 0.001)。它还与母亲受教育程度较低(χ2 p &lt; 0.001)、出生后第一年接受托儿服务(χ2 p = 0.005)以及居住地距离诊所超过30公里(χ2 p = 0.02)有关。未参加学龄访问与测试的其他变量无关,包括1岁时的特应性致敏或湿疹、过敏性疾病家族史(过敏、湿疹、花粉热或哮喘)或父母出生在海外(数据未显示)。这些数据为墨尔本儿童早期对食物和空气过敏原的致敏演变提供了有价值的见解,这是一个过敏性疾病高发的环境。担任首席研究员,负责研究构思、设计和获得资金。北卡罗来纳和sd制定了最终的科学方案和伦理申请,所有其他作者都提供了关键的评估和修改。K.G.负责协调,n.c.、d.c.、P.V.和N.L.M.参与实施。E.K.F.和N.L.M.参与了研究,n.c.、s.d.、L.F.P.和M.S.参与了分析计划。E.K.F.领导,N.L.M.监督,L.F.P.负责数据的清理和准备。N.L.M.起草了手稿,并协调了手稿的准备和修改。所有作者都对稿件进行了批判性的评价和修改。作者声明无利益冲突。支持本研究结果的数据可根据通讯作者的合理要求提供。
{"title":"Changes in Atopic Sensitisation From 1 to 5 Years of Age: Longitudinal Data From the MIS BAIR Trial","authors":"Nicole L. Messina,&nbsp;Laure F. Pittet,&nbsp;Emily K. Forbes,&nbsp;Kaya Gardiner,&nbsp;Katie L. Flanagan,&nbsp;Anne-Louise Ponsonby,&nbsp;Roy Robins-Browne,&nbsp;Frank Shann,&nbsp;Mike South,&nbsp;Peter Vuillermin,&nbsp;Susan Donath,&nbsp;Dan Casalaz,&nbsp;Nigel Curtis,&nbsp;the Melbourne Infant Study: BCG for Allergy and Infection Reduction (MIS BAIR) Group","doi":"10.1111/cea.70144","DOIUrl":"10.1111/cea.70144","url":null,"abstract":"&lt;p&gt;Vaccination with BacilleCalmette-Guérin (BCG) has off-target effects on the immune system which may influence the risk of developing allergic disease in later life. The Melbourne Infant Study: BCG for Allergy and Infection Reduction (MIS BAIR) randomised controlled trial (NCT01906853) investigated whether neonatal BCG vaccination reduces the incidence of allergy, eczema and infections at 1 and 5 years of age, and asthma at 5 years of age [&lt;span&gt;1&lt;/span&gt;]. In the trial, neonatal BCG vaccination reduced the incidence of eczema at 1 year [&lt;span&gt;2&lt;/span&gt;], particularly in children of parents with a history of eczema, but did not significantly reduce lower respiratory tract infections [&lt;span&gt;3&lt;/span&gt;] or food allergy [&lt;span&gt;4&lt;/span&gt;] at 1 year of age. At 5 years of age, neonatal BCG vaccination reduced the risk of more severe forms of asthma but had minimal effect on the overall incidence of asthma [&lt;span&gt;5&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;The MIS BAIR trial also aimed to investigate atopic sensitisation to a range of common allergens at 5 years of age. This required participants to attend a clinic visit for skin prick testing (SPT) at 5 years of age [&lt;span&gt;1, 4&lt;/span&gt;]. In March 2020, COVID-19 pandemic ‘lockdown’ measures in Melbourne (which included stay-at-home orders [&lt;span&gt;6, 7&lt;/span&gt;]) prevented 5-year SPT clinic visits being done for the following 12 months. During this period, 1124 (88%) of participants were eligible for their SPT clinic visit, with 62.7% (798/1272) only eligible after March 2020. To provide an opportunity for these participants to attend their SPT clinic visit after lockdown restrictions had eased, the age of eligibility for the SPT clinic visit was extended to 7 years of age. However, participants' families remained reluctant to visit a hospital setting during the pandemic and consequently, overall, only 34.2% (435/1272) attended a school-age (5–7 years of age) SPT clinic visit (Figure 1A).&lt;/p&gt;&lt;p&gt;In addition to the low follow-up rate, there was a difference between the randomisation groups in the proportion of participants who did not attend an SPT clinic visit (58.6% (373/637) in the BCG group vs. 73.1% (464/635) in the Control group) (Figure 1A). This might be attributable to disappointment in being randomised to the Control group [&lt;span&gt;8&lt;/span&gt;] as participants' families were not blinded to the randomisation group due to BCG vaccination site scarring. Despite the large proportion of missing data, the available SPT results and longitudinal testing provide valuable information in relation to the progression of atopic sensitisation in early life.&lt;/p&gt;&lt;p&gt;Among the 435 participants who attended, the median age at the SPT clinic visit was 64 months (IQR 61–68 months; range 60–87 months). Of these, 99.1% (431/435) had a valid SPT, and 90.6% (394/435) were tested against all the pre-specified food (peanut, cashew nuts, hazelnut, walnut, raw egg, cow's milk, sesame and shellfish) and aero (dog, cat, house dust mite, rye grass and &lt;i&gt;Alternaria t","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"56 1","pages":"79-81"},"PeriodicalIF":5.2,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.70144","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Remission and Recurrence of Food Protein–Induced Enterocolitis Syndrome: Insights From Oral Food Challenge Outcomes 食物蛋白诱导的小肠结肠炎综合征的缓解和复发:来自口服食物挑战结果的见解。
IF 5.2 2区 医学 Q1 ALLERGY Pub Date : 2025-09-19 DOI: 10.1111/cea.70146
Kotaro Umezawa, Kiwako Yamamoto-Hanada, Miori Sato, Mami Shimada, Daichi Suzuki, Fumi Ishikawa, Seiko Hirai, Mayako Saito-Abe, Kenji Toyokuni, Ichiro Nomura, Tatsuki Fukuie, Yukihiro Ohya
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引用次数: 0
Systemic N-Acylethanolamines and Other Lipid Mediators Are Associated With NSAID-Exacerbated Respiratory Disease 系统性n -酰基乙醇胺和其他脂质介质与非甾体抗炎药加重的呼吸系统疾病有关
IF 5.2 2区 医学 Q1 ALLERGY Pub Date : 2025-09-18 DOI: 10.1111/cea.70145
Viljami E. Salmi, Annina Lyly, Mikko Neuvonen, Elmo Saarentaus, Mikko Niemi, Sanna Toppila-Salmi
<p>Nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) is a common chronic airway inflammatory disease characterised by asthma, chronic rhinosinusitis with nasal polyps (CRSwNP) and hypersensitivity to NSAIDs, including acetylsalicylic acid (ASA, aspirin), posing a significant burden on respiratory health [<span>1</span>]. N-ERD currently lacks reliable clinical laboratory tests, yet early diagnosis and management are essential to prevent disease progression [<span>2</span>]. The pathogenesis of N-ERD has been linked to dysregulation of arachidonic acid (AA) metabolism, which affects levels of pro-inflammatory lipid mediators such as leukotrienes and prostaglandins [<span>1, 3</span>]. ASA alters AA metabolism by inhibiting cyclooxygenase (COX) enzymes and redirecting lipid synthesis towards pro-inflammatory leukotrienes [<span>1</span>]. Despite extensive research into eicosanoids in N-ERD, the full spectrum of lipid mediators involved remains incompletely understood. In this study, we investigated the effect of a low dose of ASA (25 mg) on plasma and urine lipid mediator concentrations in N-ERD patients compared with healthy controls, aiming to identify novel biomarkers and deepen understanding of disease mechanisms.</p><p>This study included eight consecutively recruited N-ERD patients and seven age-matched healthy controls (25–62 years). All subjects were Finnish females, selected to minimise demographic variability. N-ERD was diagnosed based on typical symptoms after NSAID intake and confirmed with ASA challenge, lung function testing and clinical examination [<span>1</span>]. All patients had asthma and CRSwNP. Ethics approval and informed consent were obtained as part of the AirGOs-Medical clinical trial (NCT03825757) [<span>4</span>].</p><p>Blood plasma and urine samples were collected after overnight fasting at baseline and 2 h after ingestion of 25 mg ASA (Primaspan, 50 mg tablet, Orion, Espoo, Finland). Although this initial dose did not provoke symptoms in all patients, it was part of a broader challenge that ultimately confirmed N-ERD in each case (Figure 1A). Our aim was to detect metabolic changes while minimising the risk of severe respiratory reactions. Lipid mediators were quantified using liquid chromatography–tandem mass spectrometry, targeting 158 eicosanoids and related compounds, with 30 analytes quantified. Urine concentrations were normalised to creatinine levels.</p><p>Linear mixed-effects models were used to evaluate the effects of group (N-ERD vs. control), ASA intake (before vs. after) and their interaction (different ASA effects between groups) on individual lipid concentrations. Lipids with a significant <i>p</i> value (<i>p</i> < 0.05) in the group comparison were considered main findings and are presented in this letter.</p><p>Reduced plasma concentrations of the endocannabinoid-related lipids arachidonoylethanolamide (AEA) and oleoylethanolamide (OEA) were associated with N-ERD
非甾体抗炎药(NSAID)加重呼吸系统疾病(N-ERD)是一种常见的慢性气道炎症性疾病,其特征为哮喘、慢性鼻窦炎伴鼻息肉(CRSwNP)和对非甾体抗炎药(包括乙酰水杨酸(ASA,阿司匹林))的超敏反应,对呼吸系统健康造成重大负担。N-ERD目前缺乏可靠的临床实验室检测,但早期诊断和管理对于预防疾病进展至关重要。N-ERD的发病机制与花生四烯酸(AA)代谢失调有关,后者会影响促炎脂质介质如白三烯和前列腺素的水平[1,3]。ASA通过抑制环氧合酶(COX)酶和重定向脂质合成促炎白三烯[1]来改变AA代谢。尽管对N-ERD中的类二十烷酸进行了广泛的研究,但所涉及的脂质介质的全谱仍未完全了解。在这项研究中,我们研究了低剂量ASA (25mg)对N-ERD患者血浆和尿脂质介质浓度的影响,并与健康对照组进行了比较,旨在发现新的生物标志物并加深对疾病机制的理解。本研究包括8名连续招募的N-ERD患者和7名年龄匹配的健康对照(25-62岁)。所有的研究对象都是芬兰女性,选择她们是为了尽量减少人口统计学上的差异。N-ERD是根据服用非甾体抗炎药后的典型症状诊断的,并通过ASA激发、肺功能测试和临床检查[1]证实。所有患者均有哮喘和CRSwNP。作为AirGOs-Medical临床试验(NCT03825757) bbb的一部分,获得了伦理批准和知情同意。在基线禁食过夜和摄入25 mg ASA (Primaspan, 50 mg片剂,Orion, Espoo, Finland)后2小时采集血浆和尿液样本。虽然这个初始剂量并没有在所有患者中引起症状,但它是一个更广泛挑战的一部分,最终证实了每个病例的N-ERD(图1A)。我们的目的是检测代谢变化,同时尽量减少严重呼吸反应的风险。采用液相色谱-串联质谱法对脂质介质进行定量,针对158种二十烷类化合物及相关化合物,对30种分析物进行定量。尿浓度恢复正常至肌酐水平。使用线性混合效应模型来评估各组(N-ERD vs.对照组)、ASA摄入(前后)及其相互作用(组间不同的ASA效应)对个体脂质浓度的影响。在组比较中p值显著(p &lt; 0.05)的脂质被认为是主要发现,并在这封信中提出。与对照组相比,内源性大麻素相关脂质花生四烯醇乙醇酰胺(AEA)和油基乙醇酰胺(OEA)在基线和ASA摄入后的血浆浓度降低与N-ERD相关(两者的p &lt; 0.01)(图1B)。AEA和OEA是n -酰基乙醇胺(NAEs),是来源于膜磷脂的脂质介质,其中AA也可以通过磷脂酶A2 (PLA2)释放(图1C)。AEA和OEA通过不同的途径发挥抗炎作用:AEA通过大麻素2型受体(CB2R)减少促炎细胞因子,OEA通过过氧化物酶体增殖物激活受体α (PPAR-α)抑制细胞因子产生、嗜酸性粒细胞募集和氧化应激。这两种NAEs进一步被COX-2、脂氧合酶(LOX)和细胞色素P450 (CYP450)酶代谢为免疫调节代谢物[5]。N-ERD患者血浆AEA和OEA水平降低,提示NAE代谢失调,CB2R-和PPAR-α-介导的抗炎信号传导受损,ASA后水平不变,提示合成或下游转化受损。内源性大麻素系统是一个保守的信号网络,调节二十烷类细胞驱动的炎症。CB2R激活可降低2型炎症和AA水平,其在N-ERD患者鼻息肉组织[6]中的表达上调,提示其存在代偿机制。因此,AEA和OEA水平的降低可能反映了负反馈,解释了症状严重、对传统治疗的不良反应[7]以及生物制剂在N-ERD[2]中的潜在作用。N-ERD组血浆白三烯E4 (LTE4)水平在两个时间点均显著升高(p &lt; 0.01)。服用ASA后,N-ERD组LTE4显著升高,而对照组LTE4仍低于定量(组× ASA相互作用p &lt; 0.05)(图1B)。作为通过5-LOX途径产生的促炎介质(图1C),升高的LTE4支持其在N-ERD病理生理中的作用和作为生物标志物的效用,如先前所示[3]。N-ERD组在两个时间点血浆12-羟基庚二烯酸(12-HHT)均显著升高(p &lt; 0.05)(图1B)。 12-HHT是一种aa衍生的介质,通过激活白三烯B4受体2 (BLT2)来抑制过敏性气道炎症(图1C)[8]。升高的水平可能反映了N-ERD中持续的慢性气道炎症,并具有诊断潜力。N-ERD组血浆二十碳五烯酸(EPA)持续显著降低(p &lt; 0.05)(图1B)。EPA是由α -亚麻酸通过脂肪酸去饱和酶2 (FADS2)产生的一种omega-3脂肪酸(图1C),它是促溶解介质的前体,与AA竞争COX酶并抑制炎症细胞因子。EPA水平的降低可能反映了饮食不足或ω -3代谢的改变,可能导致N-ERD的过敏性气道炎症,因为EPA对哮喘和过敏性疾病的发展具有保护作用。在组间比较中,尿液中测量的脂质介质均无统计学意义的p值。其他分析脂质的详细结果也可在以下存储库中获得:https://osf.io/eazn6/?view_only=6b8eff58edfc4c43a76d811680f93732.To据我们所知,这是第一份证明内源性大麻素相关脂质AEA和OEA血浆浓度降低与N-ERD之间存在关联的报告。在N-ERD患者中,AEA或OEA信号受损可能导致疼痛感知增强,提示潜在的诊断和治疗意义。我们还发现了其他可能具有N-ERD代谢特征的脂质。需要更多的研究来证实这些发现。和a.l.:招募受试者、测试受试者、抽样。M.Ni。m.n .:实验室实验,数据准备。v.e.s.:数据分析,撰写稿件,准备数据和表格。所有作者都对论文的构思和设计,或对数据的解释做出了实质性的贡献,并参与了对稿件的严格修改,并最终批准了即将出版的版本。该研究已获得国家药品管理局(Eudra CT 2017-0015070-42, KL/41/2018)、赫尔辛基医院区伦理委员会和Uusimaa (HUS/1801/2017)的批准。所有受试者均获得书面知情同意。报告咨询ALK-Abelló、阿斯利康、Clario、ERT、葛兰素史克、诺华、赛诺菲制药、Orion制药、罗氏产品以及葛兰素史克和赛诺菲的资助。都在提交的作品之外。A.L.为阿斯利康(AstraZeneca)提供咨询服务,并从芬兰肺部健康协会(Finnish Lung Health Association)收取讲课费。都在提交的作品之外。所有其他作者声明无利益冲突。有关研究方法和结果的更多信息可在以下存储库中获得:https://osf.io/eazn6/?view_only=6b8eff58edfc4c43a76d811680f93732。支持本研究结果的数据可根据通讯作者的要求提供。
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引用次数: 0
Quality of Life in Paediatric Food Allergy: Diverging Influences on Parent and Child Reports in the ROAD Study 儿童食物过敏的生活质量:ROAD研究中对父母和儿童报告的不同影响
IF 5.2 2区 医学 Q1 ALLERGY Pub Date : 2025-09-16 DOI: 10.1111/cea.70143
Chisato Jimbo, Sayaka Hamaguchi, Kenji Toyokuni, Miori Sato, Ai Kishino, Mami Shimada, Tomoki Yaguchi, Kouhei Hagino, Daisuke Harama, Marei Omori, Daichi Suzuki, Kotaro Umezawa, Fumi Ishikawa, Seiko Hirai, Mayako Saito-Abe, Tatsuki Fukuie, Yukihiro Ohya, Kiwako Yamamoto-Hanada
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引用次数: 0
British Society for Allergy and Immunology Abstracts From the 2025 Annual Conference 英国过敏和免疫学会2025年年会摘要。
IF 5.2 2区 医学 Q1 ALLERGY Pub Date : 2025-09-08 DOI: 10.1111/cea.70139
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引用次数: 0
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Clinical and Experimental Allergy
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