Journal of Asthma最新文献

{"title":"Pediatric asthma population risk stratification using k-means clustering.","authors":"Mandana Rezaeiahari, Arina Eyimina, Melanie Boyd, Clare C Brown, Tamara T Perry, Erhan Ararat, J Mick Tilford, Akilah A Jefferson","doi":"10.1080/02770903.2025.2552745","DOIUrl":"10.1080/02770903.2025.2552745","url":null,"abstract":"<p><strong>Objectives: </strong>Incorporating social determinants of health to identify distinct pediatric asthma patient groups can help stratify populations by their risk of adverse events, improving targeted outreach and care.</p><p><strong>Methods: </strong>Insurance claims and enrollment data from the Arkansas All-Payer Claims Database identified 22 169 children aged 5-18 years with an asthma diagnosis in 2018 and continuous Medicaid enrollment in 2018 and 2019. The clustering approach used information on comorbid conditions, asthma controller medication intensity, total controller and reliever medications filled, zip code-level Child Opportunity Index, and rural-urban classification. Binary and categorical variables were first transformed into continuous latent variables using Generalized Low-Rank Models. K-means clustering with Euclidean distance was then applied. The resulting clusters were compared based on asthma-related emergency department (ED) visits and hospitalizations in 2018.</p><p><strong>Results: </strong>K-means clustering identified six clusters. The distribution of ED visits differed significantly across the clusters (<i>p</i> < 0.001) with Cluster 1 having the highest observed percentages (1 ED visit: 9.5%; ≥2 ED visits: 2.6%). This cluster consisted of 65.9% Black and had the highest proportion of children residing in neighborhoods with very low child opportunity scores: 90.5% had very low education scores, 85.5% very low health and environment scores, and 94.4% very low social and economic scores.</p><p><strong>Conclusions: </strong>Interventions to reduce pediatric asthma disparities should address social, economic, and environmental inequities. Clustering identified children from low child opportunity areas in Arkansas, with a high percentage of Black children, as a high-risk group for asthma exacerbations, underscoring the potential of population risk stratification for tailoring interventions.</p>","PeriodicalId":15076,"journal":{"name":"Journal of Asthma","volume":" ","pages":"1-10"},"PeriodicalIF":1.3,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144955138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Asthma endotypes in flux: integrating type 1 and type 2 inflammation for biological therapy advancement.","authors":"Picheswara Rao Polu, Vamsi Krishna Bikki","doi":"10.1080/02770903.2025.2555300","DOIUrl":"10.1080/02770903.2025.2555300","url":null,"abstract":"<p><strong>Objective: </strong>To synthesize current understanding of type 1 (T1) and type 2 (T2) asthma endotypes and evaluate how their integration can advance precision biological therapy selection for improved patient outcomes.</p><p><strong>Data sources: </strong>Comprehensive literature review of peer-reviewed articles from PubMed, Embase, and Cochrane databases focusing on asthma immunopathology, endotype characterization, biomarker development, and biological therapies. Additional sources included clinical trial registries, regulatory agency documents, and recent conference proceedings.</p><p><strong>Study selection: </strong>Studies were selected based on relevance to T1/T2 inflammatory pathways, biomarker validation, biological therapy efficacy, and endotype-guided treatment strategies. Priority was given to randomized controlled trials, systematic reviews, and large observational studies with clear endotype characterization.</p><p><strong>Results: </strong>T2 inflammation, characterized by interleukin-4 (IL-4), IL-5, and IL-13 pathways with eosinophilic involvement, has well-established biomarkers (blood eosinophils, fractional exhaled nitric oxide (FeNO), periostin) and successful targeted biologics (anti-IL-5, anti-IL-4 receptor alpha (anti-IL-4Rα), anti-immunoglobulin E (anti-IgE)). T1 inflammation, involving interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), and IL-17 with neutrophilic predominance, lacks validated biomarkers and effective therapeutics. Emerging evidence demonstrates significant T1/T2 overlap in severe asthma, challenging traditional dichotomous classification. Multi-pathway targeting strategies and upstream cytokine inhibition show promise for mixed endotypes.</p><p><strong>Conclusion: </strong>Integration of T1 and T2 endotype characterization through validated biomarkers and multi-omics approaches is essential for advancing precision medicine in asthma. Future therapeutic strategies must address endotype plasticity and mixed inflammatory patterns to optimize biological therapy selection and improve treatment outcomes in heterogeneous asthma populations.</p>","PeriodicalId":15076,"journal":{"name":"Journal of Asthma","volume":" ","pages":"1-21"},"PeriodicalIF":1.3,"publicationDate":"2025-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144955183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oscillometry-defined small airway dysfunction in steroid-naïve adult bronchial asthma: association with eosinophilic and non-eosinophilic phenotypes.","authors":"Aditi Maheshwari, Sajal De","doi":"10.1080/02770903.2025.2552737","DOIUrl":"https://doi.org/10.1080/02770903.2025.2552737","url":null,"abstract":"<p><strong>Objective: </strong>Small airway dysfunction (SAD) is a common feature of bronchial asthma. However, its association with asthma phenotypes remains poorly understood. This study aimed to assess the prevalence of oscillometry-defined SAD in steroid-naïve adult bronchial asthma and to explore its association with asthma phenotypes based on peripheral blood eosinophil count (BEC).</p><p><strong>Methods: </strong>A total of 320 consecutive cases of bronchial asthma patients were enrolled. The severity of impairment in oscillometry parameters was expressed in <i>z</i>-scores. SAD in oscillometry was defined as R5-19 > upper limit of normal and/or X5 < lower limit of normal. The cohort was categorized into eosinophilic asthma (EA) and non-eosinophilic asthma (NEA) using a BEC cutoff of 300 cells/µL.</p><p><strong>Results: </strong>The mean age of the cohort was 37.5 ± 12.5 years, and 58.1% were male. The median BEC was 350 cells/µL. The mean FEV₁ was 66.7 ± 18.4 %predicted. Oscillometry-defined SAD was observed in 54.4% (95% CI: 48.1-59.4). Patients with SAD exhibited significantly lower spirometric indices compared to those without SAD. The proportion of EA was 58.4% (95% CI: 53.4-64.7). Spirometric parameters did not differ significantly between the EA and NEA. The severity of impairment in R5 and X5 was less in EA compared to NEA, though the difference was not statistically significant. The proportion of impaired R5-19 was significantly less in EA than NEA (47.6% vs. 57.9%; <i>p</i> = .04).</p><p><strong>Conclusions: </strong>Half of steroid-naïve bronchial asthma patients exhibited SAD at the time of diagnosis. NEA phenotypes are associated with higher impairment in oscillometry.</p>","PeriodicalId":15076,"journal":{"name":"Journal of Asthma","volume":" ","pages":"1-7"},"PeriodicalIF":1.3,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145006194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the causal role of plasma metabolites in pediatric asthma: a Mendelian randomization study.","authors":"Shaojie Ma, Wenjuan Hu, Yingwei Bi, Ying Han, Wei Wang, Deli Xin","doi":"10.1080/02770903.2025.2552748","DOIUrl":"10.1080/02770903.2025.2552748","url":null,"abstract":"<p><strong>Background: </strong>Pediatric asthma (PA) is the prevailing chronic respiratory ailment in childhood. A better understanding of plasma metabolites is the goal for elucidating the molecular pathological mechanisms of PA and investigating novel therapeutic approaches.</p><p><strong>Methods: </strong>Data for PA from Genome-Wide Association Studies (GWAS) was derived from the IEU-OpenGWAS project, featuring a collection of 1400 plasma metabolites. The inverse-variance weighting (IVW) method assessed causal relationships between plasma metabolites and PA, with measures taken to mitigate horizontal pleiotropy and heterogeneity. To select instrumental variables, a genome-wide significance threshold (<i>p</i> < 5 × 10-8) was applied to ensure robust genetic instruments. A Bonferroni correction controlled for multiple testing, with statistical significance defined as <i>p</i> < 3.57 × 10-5) (0.05/1400). To further substantiate outcomes, a reverse Mendelian randomization analysis was conducted.</p><p><strong>Results: </strong>Research found 91 plasma metabolites linked to PA, ten of which showed significant associations. Of note, 20:4n6 levels (IVW: OR (95% CI) = 1.062 (1.030 to 1.094) and G/C16 (IVW: OR (95% CI) = 0.886 (0.832 to 0.943) were identified as pivotal exposure factors for PA.</p><p><strong>Conclusions: </strong>This study highlights 10 plasma metabolites that may have significant associations with PA incidence, with 20:4n6 levels and G/C16 potentially serving as valuable biomarkers for the early detection and management of PA.</p>","PeriodicalId":15076,"journal":{"name":"Journal of Asthma","volume":" ","pages":"1-14"},"PeriodicalIF":1.3,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144992655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence and Risk Factors of Asthma in Children: A Systematic Review and Meta-analysis.","authors":"Li Yin, Feifei Zhang, Xue Wang, Mimi Gao, Anna Liu, Fang Li","doi":"10.1080/02770903.2025.2552749","DOIUrl":"10.1080/02770903.2025.2552749","url":null,"abstract":"<p><strong>Objective: </strong>The present study aims to evaluate the prevalence and risk factors of asthma in children through a meta-analysis.</p><p><strong>Data sources: </strong>The PubMed, Embase, Cochrane, and Web of Science databases were comprehensively retrieved for studies on the prevalence and risk factors of childhood asthma (CA) published between January 1, 2015, and July 8, 2024. Studies were screened and selected based on predefined eligibility criteria, and pertinent data were extracted. The quality of eligible studies was evaluated through the Newcastle-Ottawa Scale (NOS). Statistical analyses were undertaken via Stata 16 and R 4.4.1.</p><p><strong>Study selection: </strong>45 studies comprising 647,414 participants were included.</p><p><strong>Results: </strong>The pooled prevalence of CA was 11.9% (95% CI: 8.8-15.8%). The meta-analysis identified several risk factors for CA, including prenatal exposure to per- and polyfluoroalkyl substances (PFAS) (OR = 0.89, 95% CI: 0.80-0.98, P = 0.021), prenatal exposure to acid-suppressive medications (OR = 1.11, 95% CI: 1.04-1.19, P = 0.002), maternal folic acid supplementation during pregnancy (OR = 1.18, 95% CI: 1.10-1.27, <i>p</i> < 0.001), as well as <i>Helicobacter pylori</i> infection in childhood (OR = 2.07, 95% CI: 1.35-3.15, <i>p</i> = 0.001).</p><p><strong>Conclusions: </strong>The prevalence rate of asthma among children was approximately 11.9%. Prenatal exposure to PFAS and acid-suppressive medications, <i>Helicobacter pylori</i> infection in childhood were proved to be risk factors for asthma. Folic acid supplementation during pregnancy is positively associated with a reduced risk of asthma in children. Further large-scale prospective research is warranted to unveil the roles and significance of these factors.</p>","PeriodicalId":15076,"journal":{"name":"Journal of Asthma","volume":" ","pages":"1-12"},"PeriodicalIF":1.3,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144955176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New insights into causal relationship between serum lipids, obesity, and asthma: a Mendelian randomization study.","authors":"Jialiang Sun, Lanlan Chen, Peiliang Zhao, Xinquan Bai, Shu Nie, Yanan Li","doi":"10.1080/02770903.2025.2493177","DOIUrl":"10.1080/02770903.2025.2493177","url":null,"abstract":"<p><strong>Objective: </strong>To identify causal risk factors for asthma using a Mendelian randomization (MR) approach.</p><p><strong>Methods: </strong>Genetic variants associated with the exposures at the genome-wide significance level (<i>p</i> < 5 × 10 - 8) were obtained from corresponding genome-wide association studies. Summary-level statistical data for asthma were obtained from the UK Biobank (UKB) and the FinnGen Consortia. Univariate and multivariate MR analyses were performed to clarify causal relationships among obesity, serum lipids, and asthma. Meta-analyses were performed to combine UKB and FinnGen results using a fixed-effects model.</p><p><strong>Results: </strong>In FinnGen, the odds for asthma increased for every 1-SD increase in body mass index (BMI; odds ratio [OR] 1.292, <i>p</i> = 1.34 × 10^-7), together with body fat percentage (BF%; OR 1.449, <i>p</i> = 4.90×10^-3), and total cholesterol level (OR = 0.949, <i>p</i> = 0.027). However, higher BMI and BF% were found to increase the risk for asthma in the multivariate MR analysis. In the UKB, the BMI results were replicated. Meta-analysis revealed that high-density lipoprotein cholesterol could also increase the risk for asthma, although there were no associations with other risk factors included in this study.</p><p><strong>Conclusion: </strong>This MR study found that genetically predicted higher BF% and BMI could increase the risk for asthma and corroborated some risk factors for asthma from previous MR studies. Moreover, the results suggest that higher BMI and BF% could serve as independent risk factors for asthma.</p>","PeriodicalId":15076,"journal":{"name":"Journal of Asthma","volume":" ","pages":"1525-1536"},"PeriodicalIF":1.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144020286","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Causal relationship between serum urate and asthma: a Mendelian randomization study.","authors":"Guobing Jia, Tao Guo, Lei Liu, Chengshi He","doi":"10.1080/02770903.2025.2495734","DOIUrl":"10.1080/02770903.2025.2495734","url":null,"abstract":"<p><strong>Background: </strong>Previous studies have suggested that elevated urate levels may increase the risk of asthma; however, the nature of this association remains debated. To clarify this uncertainty, we conducted a Mendelian randomization (MR) study to investigate the potential causal relationship.</p><p><strong>Methods: </strong>Summary statistics for urate were sourced from the Global Urate Genetics Consortium (GUGC), and those for asthma were obtained from the FinnGen database. Genetic variants strongly associated with urate were selected as instrumental variables (IVs). Univariable and multivariable MR analyses were conducted to investigate the causal relationship between urate and asthma. Subsequently, network MR analyses were performed to reveal the mediating role of urate in the relationship between body mass index (BMI) and asthma.</p><p><strong>Results: </strong>The univariable MR analysis showed that urate was associated with an increased risk of asthma (IVW OR = 1.13, 95%CI = 1.04-1.23, <i>p</i> = 0.004). This causal relationship remained consistent in multivariable MR analyses, even after adjusting for potential confounders, including smoking initiation, cigarettes per day, alcohol intake frequency, BMI, allergic rhinitis, and gastroesophageal reflux disease (GERD). Furthermore, network MR analyses demonstrated that the proportion of causal effect between BMI and asthma mediated by urate was 18.05% (95%CI = 6.23%-29.88%).</p><p><strong>Conclusion: </strong>Our study confirms that serum urate is associated with an increased risk of asthma, suggesting its potential as a target for both prevention and treatment. Additionally, our findings indicate that urate partially mediates the relationship between BMI and asthma, emphasizing its role in the mechanism underlying BMI-induced asthma.</p>","PeriodicalId":15076,"journal":{"name":"Journal of Asthma","volume":" ","pages":"1575-1583"},"PeriodicalIF":1.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Severe asthma, biologic hypersensitivity and inefficacy: overcoming treatment barriers with tezepelumab.","authors":"Maria Bragança, Inês Barreto, Henrique Rodrigues, Ana Mendes, Carlos Lopes","doi":"10.1080/02770903.2025.2552744","DOIUrl":"https://doi.org/10.1080/02770903.2025.2552744","url":null,"abstract":"<p><p>Severe asthma is a heterogeneous disease involving multiple inflammatory pathways, with significant therapeutic challenges. Biologic therapies targeting T2 inflammation improve outcomes but may, in rare cases, trigger hypersensitivity reactions due to anti-drug antibodies, excipients, or protein structure. Additionally, some patients exhibit suboptimal or no response. Tezepelumab, a thymic stromal lymphopoietin inhibitor, offers a novel upstream approach, addressing diverse endotypes.</p><p><p>We present a 30-year-old female with severe T2-high asthma, multiple allergies, and poor disease control despite optimal therapy. She experienced an allergic reaction with omalizumab and dupilumab and had inadequate response to benralizumab. Enrolled in an early access program for tezepelumab, she showed remarkable clinical improvement, with significant FEV1 increase and FeNO reduction, allowing discontinuation of systemic corticosteroids and supplemental oxygen.</p>","PeriodicalId":15076,"journal":{"name":"Journal of Asthma","volume":" ","pages":"1-5"},"PeriodicalIF":1.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144955168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct characteristics of asthma overlap phenotypes: Insights from the Turkish adult asthma registry.","authors":"Secil Kepil Ozdemir, Bilun Gemicioglu, Fusun Yildiz, Serhat Hayme, Gulistan Alpagat, Nurgul Bozkurt, Ismet Bulut, Munevver Erdinc, Gul Karakaya, Metin Keren, Gulden Pacaci Cetin, Insu Yilmaz, Arzu Yorgancioglu, Omur Aydin, Derya Gokmen, Gozde Koycu Buhari, Zeynep Celebi Sozener, Sengul Beyaz, Cihan Orcen, Ebru Damadoglu, Tugce Yakut, Ayse Fusun Kalpaklioglu, Ayse Baccioglu, Sumeyra Alan Yalim, Ilkay Koca Kalkan, Mehmet Atilla Uysal, Elif Yelda Ozgun Niksarlioglu, Ali Fuat Kalyoncu, Muge Erbay, Sibel Nayci, Fatma Merve Tepetam, Aslı Gelincik, Hulya Dirol, Ozlem Goksel, Selen Karaoglanoglu, Ferda Oner Erkekol, Sacide Rana Isik, Yasemin Yavuz, Dilek Karadogan, Ummuhan Seker, Ipek Kivilcim Oguzulgen, Ilknur Basyigit, Serap Argun Baris, Elif Yilmazel Ucar, Tuba Erdogan, Mehmet Polatli, Dane Ediger, Fatma Esra Gunaydin, Murat Turk, Leyla Pur, Zeynep Yegin Katran, Yonca Sekibag, Enes Furkan Aykac, Dilsad Mungan, Ozcan Gul, Ali Cengiz, Bulent Akkurt, Seyma Ozden, Semra Demir, Derya Unal, Ayse Feyza Aslan, Ali Can, Reyhan Gumusburun, Gulhan Bogatekin, Hatice Serpil Akten, Sinem Inan, Aliye Candan Ogus, Murat Kavas, Demet Polat Yulug, Mehmet Erdem Cakmak, Saltuk Bugra Kaya, Eylem Sercan Ozgur, Oguz Uzun, Sule Tas Gulen, Gulseren Pekbak, Deniz Kizilirmak, Yavuz Havlucu, Halil Donmez, Bahar Arslan, Sadan Soyyigit, Bilge Yilmaz Kara, Gulden Pasaoglu Karakis, Adile Berna Dursun, Resat Kendirlinan, Ayse Bilge Ozturk, Can Sevinc, Gokcen Omeroglu Simsek, Oznur Abadoglu, Pamir Cerci, Taskin Yucel, Irfan Yorulmaz, Zahide Ciler Tezcaner, Emel Cadalli Tatar, Ahmet Emre Suslu, Serdar Ozer, Engin Dursun, Gulfem Elif Celik","doi":"10.1080/02770903.2025.2493134","DOIUrl":"10.1080/02770903.2025.2493134","url":null,"abstract":"<p><strong>Introduction: </strong>Considerable overlaps exist between asthma phenotypes and the clinical significance of these overlaps remains undetermined. The objective of this study is to analyze the characteristics of asthma overlap phenotypes using data from the Turkish Adult Asthma Registry (TAAR).</p><p><strong>Methods: </strong>This cross-sectional registry study included 2053 adult patients (74.8% female) with asthma.</p><p><strong>Results: </strong>Overall, 39.3% (<i>n</i> = 697) had allergic-eosinophilic (AE), 26.0% (<i>n</i> = 461) had allergic-non-eosinophilic (ANE), 21.3% (<i>n</i> = 377) had non-allergic-eosinophilic (NAE), and 13.4% (<i>n</i> = 237) had non-allergic-non-eosinophilic (NANE) asthma. Severe asthma exacerbations and emergency department (ED) visits were more frequent in the AE (28.3%, 31.2%, respectively) and NAE groups (36.0%, 34.0%, respectively) than in the ANE (14.3%, 20.6%, respectively) and NANE groups (12.6%, 16.7%, respectively) (<i>p</i> < 0.001). FEV1 values were significantly lower in the AE group than in the ANE and NANE groups (<i>p</i> < 0.001, <i>p</i> = 0.048, respectively) and in the NAE group than in the ANE group (<i>p</i> < 0.001). Risk factors for poor asthma control included living in rural areas, asthma-related ED visits, FEV1 < 60% in the NAE; being overweight, chronic rhinosinusitis, oral corticosteroids use, age < 40 years in the NANE; FEV1 < 80% in the AE; and severe asthma exacerbations, ED visits for AE and ANE groups.</p><p><strong>Conclusion: </strong>The considerable overlap between allergic and eosinophilic asthma phenotypes has clinical implications as increased rates of asthma exacerbations and healthcare utilization. The clinical heterogeneity among asthma phenotypes based on a single biomarker highlights the importance of multidimensional asthma phenotyping.</p>","PeriodicalId":15076,"journal":{"name":"Journal of Asthma","volume":" ","pages":"1512-1524"},"PeriodicalIF":1.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bibliometric perspectives on inflammatory and immunological research in pediatric asthma.","authors":"Danqing Hu, Ling Mei, Dongyang An, Zengyu Zhang, Yugen Sha, Wei Zhou","doi":"10.1080/02770903.2025.2494231","DOIUrl":"10.1080/02770903.2025.2494231","url":null,"abstract":"<p><strong>Objective: </strong>Pediatric bronchial asthma, a prevalent chronic inflammatory respiratory disease, significantly affects children globally. However, bibliometric analyses focused on its inflammatory and immunological aspects are limited. This study aims to provide an overview of the field, identify key focus areas, and predict emerging trends.</p><p><strong>Methods: </strong>We collected and analyzed relevant literature published from January 1, 2000, to May 31, 2024, from the Web of Science Core Collection. Collaborative network analysis was conducted using CiteSpace 5.8.R3, VOSviewer 1.6.20, and Bibliometrix.</p><p><strong>Results: </strong>A total of 911 papers were retrieved, showing growth in research output since 2006, with the United States leading in publications. The University of Western Australia ranks first in publication count, while the University of Wisconsin-Madison has the highest average citations per paper. Among 5,059 authors, 146 core authors contributed to 592 articles, accounting for 64.98% of total publications, with Anne M. Fitzpatrick as the leading author. The journal \"Allergy, Asthma & Immunology Reviews\" is the most influential, and \"asthma\" is the most cited keyword. Co-citation analysis reveals 20 keyword clusters, with hotspots including \"efficacy\" and \"allergic rhinitis.\" The most cited paper is by D. P. Strachan in the \"British Medical Journal.\"</p><p><strong>Conclusion: </strong>This study reveals a significant increase in pediatric asthma research from 2000 to 2024, with the U.S. leading in scholarly contributions. Key findings highlight allergic airway inflammation and type 2 inflammation as primary mechanisms underlying the disease. Inhaled corticosteroids and biologics are identified as effective treatments. These insights emphasize the importance of global collaboration and ongoing research efforts to advance understanding of pathogenic mechanisms and clinical management in pediatric asthma patients.</p>","PeriodicalId":15076,"journal":{"name":"Journal of Asthma","volume":" ","pages":"1547-1559"},"PeriodicalIF":1.3,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144035919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}