Clinical and Experimental Allergy最新文献

{"title":"Rhinitis-Related Healthcare Utilization in Colombian Adults, 2015–2024","authors":"Jefferson A. Buendía","doi":"10.1111/cea.70384","DOIUrl":"10.1111/cea.70384","url":null,"abstract":"","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"56 10","pages":"1247-1249"},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148337913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recommended Quantities of Emollients and Topical Corticosteroids for Eczema Management: A Comprehensive UK Survey of Hospital Guidance","authors":"Lucy Mackie, Sorcha O'Sullivan, Marcus Tan, Shahara Ali, Alya Abdul Wahab, Leila Ferguson, Michael R. Perkin","doi":"10.1111/cea.70393","DOIUrl":"10.1111/cea.70393","url":null,"abstract":"<p>Clear guidance on the quantity and regimen of topical treatments is essential for patients with eczema, yet inconsistency persists in clinical practice. We report findings from a UK-wide Freedom of Information request sent to 156 National Health Service (NHS) Trusts on the 17/04/2024 exploring how dermatology services quantify advice on topical corticosteroid and emollient use. An NHS Trust consists of one or more hospitals providing services to a geographical area. The questions were: ‘What advice does your hospital's dermatology department issue to patients with eczema regarding: (1) the amount of moisturiser, and (2) the amount of steroid cream/ointment, that should be applied to patients?’</p><p>We received replies from 133 Trusts, within 20 working days. Three refused the FOI request, 14 did not have a dermatology service, and 4 provided no data, leaving 112 responses for analysis (Table 1). Many respondents emphasised that prescribing is individualised.</p><p>Advice on quantities of topical corticosteroids most commonly referred to finger-tip units (FTUs) [<span>1, 2</span>]. Fifty services explicitly stated that they use FTUs in prescribing, while 19 referenced FTUs within departmental patient information leaflets. Eleven services stated that they follow National Institute for Health and Care Excellence (NICE) or British National Formulary (BNF) guidance, and 12 provided links to external leaflets, most commonly the British Association of Dermatologists (BAD) topical corticosteroid leaflet [<span>3</span>], all of which reference FTUs. Eleven services correctly stated that one FTU equates to approximately 0.5 g [<span>1, 2</span>]. This covers the size of two hand areas (adult palms plus fingers) [<span>4</span>]. Two services explicitly referred to BNF/NICE quantity tables outlining amounts required per body site daily over a two-week period (about half for a child): face and neck 15–30 g, hands 15–30 g, scalp 15–30 g, arms 30–60 g, legs 100 g, trunk 100 g and groin and genitalia 15–30 g [<span>5</span>]. Eleven services provided other specific prescription quantities, which varied considerably. Qualitative descriptors were also used, including to apply treatment until the skin ‘glistens’ (7), ‘shines’ (2), in a ‘thin layer’ (4), or ‘sparingly’ (2). The word ‘sparingly’ is also mentioned in NICE guidance [<span>5</span>].</p><p>Considerable variation was observed in advice regarding frequency and duration of use. NICE guidance supports initial once-daily use on the body for 7–14 days matching potency to severity, application for 48 h after flare resolution, and intermittent or step-down maintenance strategies [<span>5</span>]. Fifteen services recommended once-daily application, 8 advised once or twice daily, and 5 advised twice daily. Eleven described tapering by reducing frequency, 3 by reducing potency, 2 suggested either approach, and 2 suggested both. These regimens were rarely consistent between services. Advice on when to stop t","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"56 10","pages":"1227-1229"},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.70393","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148444768","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}

{"title":"Maternal Diabetes and Subsequent Risk of Asthma and Atopic Dermatitis in Offspring: A Binational Birth Cohort Study in South Korea and Japan","authors":"Yoon Lee, Hyunjee Kim, Hyesu Jo, Sooji Lee, Dongjin Yeo, Kyeongmin Lee, Tae Hyeon Kim, Jaeyu Park, Young Chan Lee, Seong H. Cho, Hayeon Lee, Dong Keon Yon, Nikolaos G. Papadopoulos","doi":"10.1111/cea.70385","DOIUrl":"10.1111/cea.70385","url":null,"abstract":"","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"56 10","pages":"1243-1246"},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GWAS of Second-Generation Antihistamine Use: Locus Specificity and Highlighted Signalling Pathways","authors":"M. Niemi, S. Ruotsalainen, E. Saarentaus, I. Vähätalo, F. FinnGen, I. Starskaia, T. Harju, M. Pelkonen, T. Feuth, P. Kauppi, J. Partanen, R. Lahesmaa, V. Hytönen, A. Palotie, H. Kankaanranta, T. Laitinen","doi":"10.1111/cea.70382","DOIUrl":"10.1111/cea.70382","url":null,"abstract":"<p>Histamine is a central mediator of inflammatory responses released predominantly from mast cells and basophils following IgE-dependent and independent activation [<span>1</span>]. Second-generation H1-antagonists (sgAHs) are first-line therapy for allergic rhino-conjunctivitis and urticaria and are widely used in asthma, atopic dermatitis and chronic rhinosinusitis [<span>2</span>]. Although sgAHs differ structurally, they share selective antagonism of the H1 receptor and a favourable safety profile compared with first-generation antihistamines. Genome-wide association studies (GWAS) of medication use may provide insights into disease mechanisms and pharmacologically responsive biological pathways beyond conventional diagnostic boundaries. We therefore performed a GWAS of long-term, non-seasonal sgAH use to identify genetic determinants associated with sustained treatment benefit and to distinguish loci reflecting medication use from those associated with underlying inflammatory diseases.</p><p>We analysed 392,000 participants from FinnGen Data Freeze 9 [<span>3</span>]. Cases were defined as individuals with > 10 systemic sgAH purchases, also outside pollen season, thereby enriching for long-term and year-round use (<i>N</i> = 39,804). Controls had no recorded sgAH purchases (<i>N</i> = 209,106), while individuals with 1–9 purchases were excluded. Medication use was identified from the nationwide drug purchase register (data available1995-2021). Disease phenotypes were derived from linked nationwide healthcare registries. Genome-wide association analyses of approximately 17 million variants were conducted using REGENIE v2.2.4 adjusted for age, sex, genotyping batch, ancestry principal components and relatedness. Fine-mapping, HLA imputation and pathway analyses used SuSiE, HIBAG and MAGMA, respectively.</p><p>Cases had a mean age of 58 years, mean follow-up of 20.4 years and 28.5 sgAH purchases; cetirizine was the most frequently used drug. Cases were more often female than controls (73.5% vs. 46.7%) and had as expected substantially higher prevalence of inflammatory mucosal and skin diseases, including asthma, allergic or vasomotor rhinitis, chronic sinusitis, conjunctivitis, atopic dermatitis and urticaria (65.4% vs. 18.3% among controls, <i>p</i> < 2.2 × 10<sup>−16</sup>). Disease-specific corticosteroids were used by almost everybody among cases (95.5% vs. 65.3% among controls, <i>p</i> < 2.0 × 10<sup>−16</sup>), further supporting chronic inflammatory disease burden.</p><p>GWAS identified 66 independent loci (100 credible sets) and the HLA region associated with sgAH use at genome-wide significance (<i>p</i> < 10<sup>−8</sup>) (Figure 1). Two of the identified lead variants were highly Finnish-enriched missense variants in <i>IL4RA</i> and <i>TESPA1</i>. Additional coding signals included lead variants in <i>IL6RA</i> and <i>C17orf58</i> and a premature stop codon in <i>FLG</i>. Structural prediction suggested the <i>TESPA1</","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"56 10","pages":"1224-1226"},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.70382","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148367510","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}

{"title":"Prevalence and Sociodemographic Variation of Allergic Diseases in Australia: Findings From the Australian National Health Survey","authors":"Yichao Wang,&nbsp;Jennifer J. Koplin,&nbsp;Janet M. Davies,&nbsp;Constance H. Katelaris,&nbsp;Debra J. Palmer,&nbsp;Jason A. Trubiano,&nbsp;Joy Lee,&nbsp;Michaela Lucas,&nbsp;Michael O′Sullivan,&nbsp;Sandra Vale,&nbsp;Sheryl van Nunen,&nbsp;Troy Wanandy,&nbsp;Dianne E. Campbell,&nbsp;Kirsten P. Perrett,&nbsp;Rachel L. Peters","doi":"10.1111/cea.70288","DOIUrl":"10.1111/cea.70288","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>The prevalence of allergic diseases across the Australian population, in all regions and age groups, is not well documented. This study aimed to describe the prevalence and distribution of five allergic diseases (allergic rhinitis, asthma, drug allergy, eczema, and food allergy) and examine differences by sociodemographic factors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This study used data from the 2022 cross-sectional Australian National Health Survey. The survey randomly selected a sample of 13,095 households (with 17,093 participants) living in private dwellings in all Australian states and territories. Questionnaires were completed via face-to-face interviews. Allergic rhinitis, asthma, drug allergy, eczema, and food allergy were captured as self- or parent-reported long-term health conditions. Weighted estimates and relative standard errors were extracted and analysed. Prevalence was calculated using population data from the Australian 2021 Census.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The prevalence of self-reported current allergic rhinitis in Australia was 23.9% (95% CI: 23.1%–24.8%), food allergy was 7.0% (95% CI: 6.5%–7.5%), drug allergy was 5.2% (95% CI: 4.7%–5.6%), eczema was 1.6% (95% CI: 1.3%–1.9%), and diagnosed asthma was 10.8% (95% CI: 10.2%–11.5%). Food allergy and asthma prevalence were similar across childhood and adulthood, whereas the prevalence of allergic rhinitis increased sharply during early adulthood. Eczema was more common in childhood, while drug allergy was more common in later adulthood. Higher rates of allergic rhinitis, food allergy, and eczema were reported among individuals with more advantaged socio-economic status. In general, allergic diseases were less commonly reported by Indigenous Australians compared to non-Indigenous Australians, and by individuals born overseas compared to those born in Australia; however, prevalence varied markedly by region of birth, with some regions exhibiting higher reported rates.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>We identified a high overall prevalence of allergic diseases in Australia, with variations across populations. The differences across populations may reflect actual prevalence or disparities in disease recognition, reporting, or access to diagnostic services.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"56 10","pages":"1191-1204"},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.70288","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147621970","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}

{"title":"Mapping the Molecular Connectivity of Pollen Sensitization: A Multiplex Microarray Analysis of the Turkish Paediatric Cohort.","authors":"Alp Kazancioglu, Sevda Tuten Dal, Ilteber Konuralp, Ozge Soyer, Bulent Enis Sekerel","doi":"10.1111/cea.70380","DOIUrl":"10.1111/cea.70380","url":null,"abstract":"","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":" ","pages":"1276-1278"},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148301079","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional Genetic Variation in Ubiquitin D Promoter Influences Susceptibility to Atopic Dermatitis","authors":"Yi Ying Eliza Lim,&nbsp;Yang Yie Sio,&nbsp;Terence Yin Weng Lam,&nbsp;Yee-How Say,&nbsp;Kavita Reginald,&nbsp;Fook Tim Chew","doi":"10.1111/cea.70372","DOIUrl":"10.1111/cea.70372","url":null,"abstract":"&lt;p&gt;Atopic dermatitis (AD) is a chronic inflammatory skin disorder driven by complex interactions between genetic susceptibility, immune dysregulation and epithelial barrier dysfunction. Central to AD pathogenesis is sustained activation of the nuclear factor kappa B (NF-κB) pathway, which orchestrates the transcription of pro-inflammatory cytokines and chemokines in both immune and epithelial compartments [&lt;span&gt;1, 2&lt;/span&gt;]. While genome-wide association studies (GWAS) have identified numerous AD risk loci, the majority reside in non-coding regions and the functional mechanisms linking regulatory variation to disease remain poorly defined. Ubiquitin D (UBD, also known as FAT10) is a ubiquitin-like modifier that promotes proteasomal degradation of phosphorylated IκBα, thereby facilitating NF-κB nuclear translocation and transcriptional activity [&lt;span&gt;3&lt;/span&gt;]. Elevated UBD expression has been reported in multiple inflammatory and immune-mediated contexts, yet its genetic regulation and contribution to AD have not been previously elucidated.&lt;/p&gt;&lt;p&gt;We conducted a GWAS of 5323 Singaporean and Malaysian Chinese individuals, comprising 1261 &lt;span&gt;ad&lt;/span&gt; cases and 4062 controls, using five genotyping arrays with imputation against the 1000 Genomes Phase III Beijing Han Chinese reference panel [&lt;span&gt;4, 5&lt;/span&gt;]. A genome-wide significant association was detected at chromosome 6p22.1 within the promoter region of &lt;i&gt;UBD&lt;/i&gt;, led by rs995185 (&lt;i&gt;p&lt;/i&gt; = 1.7 × 10&lt;sup&gt;−15&lt;/sup&gt;; OR = 1.46, 95% confidence interval, CI = 1.33–1.61). This association was further validated in an independent Precision Health Research, Singapore (PRECISE-SG100K) cohort comprising 741 &lt;span&gt;ad&lt;/span&gt; cases and 14,123 controls of Singaporean Chinese individuals. Fixed-effect meta-analysis of both cohorts demonstrated that the minor allele ‘T’ of rs995185 was significantly associated with AD, with a pooled OR of 1.295 (95% CI = 1.206–1.390, &lt;i&gt;p&lt;/i&gt; &lt; 0.0001). Although a second promoter SNP of &lt;i&gt;UBD&lt;/i&gt;, rs362513, did not independently reach genome-wide significance and exhibited low linkage disequilibrium with rs995185 (&lt;i&gt;r&lt;/i&gt;&lt;sup&gt;2&lt;/sup&gt; = 0.13), its regulatory position prompted further haplotype-level interrogation. In the GWAS cohort (&lt;i&gt;n&lt;/i&gt; = 5323), haplotype analysis of these two variants revealed three common promoter haplotypes, among which the rs362513-G/rs995185-A haplotype (Haplotype 2) was significantly enriched in controls and conferred protection against AD (Figure 1A).&lt;/p&gt;&lt;p&gt;To characterize these promoter haplotypes, we cloned approximately 2 kb of the &lt;i&gt;UBD&lt;/i&gt; promoter encompassing each haplotype into luciferase reporter constructs. In HEK293T cells, Haplotype 2 consistently exhibited markedly reduced promoter activity compared with the other haplotypes at both 24- and 48-h time points (Figure 1B). Notably, this suppression occurred despite the presence of the rs995185-A allele. These findings suggest a regulatory cascade in which rs362513-G attenuat","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"56 10","pages":"1237-1239"},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.70372","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148249233","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}

{"title":"The Gap Between Prescription and Practice: Adrenaline Autoinjector Carriage in an Australian Cohort","authors":"Jason Chun Lao,&nbsp;Yi Tong Vincent Aw,&nbsp;Reina Zaragoza,&nbsp;Jamma Li,&nbsp;Therese Boyle,&nbsp;Suran L Fernando,&nbsp;Shruti Swamy","doi":"10.1111/cea.70316","DOIUrl":"10.1111/cea.70316","url":null,"abstract":"&lt;p&gt;Rapid administration of intramuscular adrenaline is the gold standard, life-saving treatment for anaphylaxis [&lt;span&gt;1-3&lt;/span&gt;]. Guidelines strongly recommend prescription of adrenaline autoinjectors (AAI) for at-risk patients [&lt;span&gt;1, 2&lt;/span&gt;]. Despite an increase in AAI prescriptions in line with these recommendations, fatalities from anaphylaxis continue to occur in the community, often attributable to adrenaline administration delays from patients not carrying their AAI [&lt;span&gt;3&lt;/span&gt;]. There remains limited data on the efficacy of AAI during anaphylaxis [&lt;span&gt;3&lt;/span&gt;]. For this paper, anaphylaxis is defined as per the World Allergy Organization (WAO) definition [&lt;span&gt;1&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;Previous studies identified suboptimal rates of AAI carriage (44%–67%) in various countries, including USA [&lt;span&gt;4&lt;/span&gt;], Netherlands [&lt;span&gt;5&lt;/span&gt;] and Australia [&lt;span&gt;6&lt;/span&gt;]. Reasons for not carrying an AAI included patients forgetting to carry their AAI, belief that they are unlikely to be exposed to the allergen [&lt;span&gt;7&lt;/span&gt;], limited availability of AAI [&lt;span&gt;8&lt;/span&gt;], and parental anxiety in injecting their children [&lt;span&gt;9&lt;/span&gt;].&lt;/p&gt;&lt;p&gt;The latest Australian data from 2017 explored rates of AAI carriage in young adolescents (10–14 years) [&lt;span&gt;6&lt;/span&gt;], with wider paediatric and adult data lacking. Our audit sought to obtain local data on AAI carriage rates and related barriers in a mixed paediatric and adult setting.&lt;/p&gt;&lt;p&gt;All patients or carers of patients (carers), who had been prescribed an AAI consented to complete a survey during their routine outpatient allergy clinic visit at an Australian metropolitan tertiary hospital from May 2024 to August 2025. A full list of questions is available online (see data availability statement). Besides demographics, patients were surveyed for AAI carriage habits and reasons for non-carriage if individuals did not always carry their AAI. This audit was approved as a quality improvement initiative with formal ethics approval waived. Statistical comparison was performed using Fisher's Exact test (MedCalc, version 23.3.7).&lt;/p&gt;&lt;p&gt;A total of 152 patients/carers responded, comprising 31 adults (≥ 18 years) and 121 children, with a mean age of 13 years (Table 1). An average of 2 devices were carried (Range: 0–6). Fifty-one percent (&lt;i&gt;n&lt;/i&gt; = 78) of respondents reported a history of anaphylaxis, with 27% (&lt;i&gt;n&lt;/i&gt; = 21) having been within the last year. 98% of respondents were prescribed an AAI for food allergies, with two respondents for insect allergies and one for drug allergy.&lt;/p&gt;&lt;p&gt;Regarding AAI carriage frequency, only 55% (&lt;i&gt;n&lt;/i&gt; = 84) reported that they always carry their AAI (Table 1). Adults (68%) and carers of preschool children (62%) were more likely to always carry an AAI, compared to carers of primary school (48%) and high school (46%) children &lt;i&gt;(p = 0.035)&lt;/i&gt;. Respondents who did not always carry their AAI were asked to select all circumstances where they would carry their AA","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"56 10","pages":"1250-1252"},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.70316","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811729","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}

{"title":"Asthma Incidence and Risk Factors in Tuberculosis Survivors: A Longitudinal Analysis of National Health Data","authors":"Jong Geol Jang,&nbsp;Kyu Na Lee,&nbsp;Kyungdo Han,&nbsp;Ho Joo Yoon,&nbsp;Sang-Heon Kim,&nbsp;Dong Wook Shin,&nbsp;Hyun Lee","doi":"10.1111/cea.70366","DOIUrl":"10.1111/cea.70366","url":null,"abstract":"&lt;p&gt;Tuberculosis remains a leading cause of morbidity and mortality worldwide, with approximately 10.8 million incident cases reported in 2023 [&lt;span&gt;1&lt;/span&gt;]. Even after completing treatment, a substantial proportion of TB survivors experience chronic respiratory sequelae, including bronchiectasis and chronic obstructive pulmonary disease (COPD) [&lt;span&gt;2&lt;/span&gt;]. However, the potential risk of asthma following TB has been less investigated and remains inconclusive.&lt;/p&gt;&lt;p&gt;The effect of TB on asthma development can be hypothesized in two opposing ways. Immunologically, TB infection induces a predominantly Th1-driven response, which may theoretically have an inverse relationship with asthma, typically characterized by allergen-triggered Th2-driven inflammation [&lt;span&gt;3&lt;/span&gt;]. Conversely, another plausible hypothesis is that structural lung damage, airway remodelling, and airflow obstruction resulting from TB infection could predispose individuals to asthma development [&lt;span&gt;2, 4&lt;/span&gt;]. In line with these opposing mechanisms, previous studies have reported inconsistent results, mostly derived from cross-sectional designs that limit the ability to establish a temporal relationship [&lt;span&gt;4, 5&lt;/span&gt;]. Therefore, we conducted a nationwide longitudinal cohort study to clarify whether TB survivors are at increased risk of incident asthma and to identify associated risk factors.&lt;/p&gt;&lt;p&gt;We used linked data from the Korea Disease Control and Prevention Agency TB registry and the National Health Insurance Service (NHIS). Among newly registered TB cases aged ≥ 20 years between 2013 and 2017, TB survivors were 1:1 matched by age and sex with controls and followed until asthma diagnosis, death, or December 31, 2021. Pulmonary TB was identified using ICD-10 codes A15–A16 (excluding A17–A19) and TB-specific NHIS codes (V206, V246, V000). Asthma was defined as ≥ 3 outpatient visits or ≥ 1 hospitalization with codes J45 or J46. Hazard ratios (HRs) for asthma incidence were estimated using the Cox proportional hazards regression model, adjusting for age, sex, body mass index (BMI), smoking status, alcohol consumption, income level, residential area and Charlson Comorbidity Index (CCI). Stratified analyses were conducted for all variables. All analyses were performed using SAS version 9.4 (SAS Institute Inc., Cary, NC, USA). Detailed methodology is available in the Open Science Framework repository (https://doi.org/10.17605/OSF.IO/285RA).&lt;/p&gt;&lt;p&gt;A total of 28,384 individuals were included (14,192 in each group). Mean age was 51.1 ± 14.9 years, and 68.3% were male. Compared to matched controls, TB survivors had a higher prevalence of underweight (11.4% vs. 3.3%), smoking, heavy drinking and comorbidities including COPD, bronchiectasis, and a CCI score ≥ 3 (all &lt;i&gt;p&lt;/i&gt; &lt; 0.001). In contrast, hypertension and dyslipidemia were more frequent in the control group. During a median follow-up of 5.1 years (interquartile range, 3.8–6.5), 2768 participants (1632 TB sur","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"56 10","pages":"1253-1255"},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.70366","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148161981","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}

{"title":"Phase Ib/II Study of Preliminary Efficacy, Safety and Pharmacodynamics of MG-K10, a Humanised Monoclonal Antibody Targeting IL-4Rα, in Adult Chinese Patients With Asthma","authors":"Mo Xian,&nbsp;Xu Shi,&nbsp;Ruoran Li,&nbsp;Li Zhao,&nbsp;Bing Zhuan,&nbsp;Bi Chen,&nbsp;Hanbing Shi,&nbsp;Zaiyi Wang,&nbsp;Feng Wu,&nbsp;Jian Guo,&nbsp;Yousheng Chen,&nbsp;Wei Dang,&nbsp;Jinlin Guo,&nbsp;Di Qin,&nbsp;Chenghai Zhang,&nbsp;Jing Li,&nbsp;Nanshan Zhong","doi":"10.1111/cea.70345","DOIUrl":"10.1111/cea.70345","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>MG-K10 is a long-acting, humanised monoclonal antibody against interleukin-4 receptor alpha (IL-4Rα), which inhibits IL-4 and IL-13-mediated signalling to reduce type 2 inflammation in asthma.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This Phase Ib/II study aimed to evaluate the preliminary efficacy, safety and pharmacodynamic characteristics of MG-K10 in Chinese patients with asthma.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This study included an initial phase Ib to evaluate safety and tolerability, followed by a phase II study in which eligible patients with moderate-to-severe asthma were randomised 1:1:1 to receive MG-K10 300 mg every 2 weeks (Q2W), MG-K10 300 mg every 4 weeks (Q4W), or a matched placebo (2 mL) Q2W subcutaneously for 24 weeks. The primary endpoint was the absolute change from baseline in the prebronchodilator forced expiratory volume in 1 s (FEV₁) at week 12. Secondary efficacy endpoints, including asthma control, the rate of severe exacerbations and safety, were assessed. This trial is registered with ClinicalTrials.gov (NCT05382910).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 64, 60 and 63 patients were randomised to the MG-K10 Q2W, MG-K10 Q4W and placebo groups respectively. At week 12, the least squares mean improvements in prebronchodilator FEV₁ were significantly greater in both MG-K10 groups than in the placebo group [Q2W vs. placebo: 0.35 L (95% CI, 0.208–0.490), Q4W vs. placebo: 0.30 L (95% CI, 0.156 to 0.441), both <i>p</i> &lt; 0.0001]. Greater FEV₁ improvements were observed in patients with baseline blood eosinophils ≥ 0.3 × 10⁹/L. The incidence of adverse events was similar across groups [MG-K10 300 mg, Q2W (79.7%), MG-K10 300 mg Q4W (85.0%) and placebo groups (79.4%)]. MG-K10 was safe and well-tolerated, and consistent with the known safety signals.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>MG-K10 was superior to placebo in improving lung function, enhancing asthma control and reducing severe exacerbations in patients with asthma. The once-every-4-week regimen offers extended dosing intervals that may enhance medication adherence.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10207,"journal":{"name":"Clinical and Experimental Allergy","volume":"56 10","pages":"1177-1190"},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cea.70345","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148053070","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}