Thorax最新文献

{"title":"Association of pulmonary artery radiation with pulmonary hypertension after lung cancer radiotherapy.","authors":"Katelyn M Atkins, Samuel C Zhang, Christopher E Kehayias, Christian Guthier, Katrina D Silos, Olivia Peony, Andrew Warrington, Mina Bakhtiar, Maria Oorloff, Cosmin Ciausu, Asneh Singh, John He, David E Kozono, David C Christiani, Cody Ramin, Anju Nohria, Andriana P Nikolova, Aaron B Waxman, Raymond H Mak","doi":"10.1136/thorax-2025-224178","DOIUrl":"10.1136/thorax-2025-224178","url":null,"abstract":"<p><strong>Background: </strong>Thoracic radiotherapy (RT) results in pulmonary fibrosis that has been hypothesised to increase the risk of pulmonary hypertension (PH); however, dose effects to cardiopulmonary structures predicting PH have not been systematically studied.</p><p><strong>Methods: </strong>Multi-institutional retrospective cohort analysis of patients with non-small cell lung cancer treated with thoracic RT. The pulmonary arteries (PA), distal pulmonary vasculature, lungs and heart were segmented. Radiotherapy dose parameters (mean, maximum and volume (V) receiving X Gy in 5 Gy increments) were extracted. Area under the receiver operating curve (AUROC) analyses estimating PH and Fine-Gray regressions were performed.</p><p><strong>Results: </strong>Of 848 patients included (n=746 discovery; n=102 validation), 49.9% were women and the median age was 65 years (IQR, 58-73 years). The 2-year cumulative incidence of PH was 11.6%. PA V10 Gy demonstrated the highest AUROC for predicting PH (0.58) and was significantly associated with the risk of PH on multivariable regression adjusting for cardiopulmonary risk factors in the discovery (subdistribution HR (sHR) 1.01; 95% CI 1.00 to 1.02; p=0.013) and validation (sHR 1.03, 95% CI 1.00 to 1.05; p=0.019) cohorts. In those who developed PH after RT (vs PH-negative), moderate or greater tricuspid disease and right ventricular systolic dysfunction (RVSD) were more common (18.7% vs 0.2% (p<0.001) and 3.3% vs 0.2% (p=0.003), respectively).</p><p><strong>Conclusions: </strong>PH was common following thoracic RT and associated with PA radiation dose. Patients with PH were more likely to harbour tricuspid disease and RVSD. These hypothesis-generating findings are suggestive that PH following thoracic RT may occur through a pathophysiological process distinct from RT-induced pulmonary fibrosis.</p>","PeriodicalId":23284,"journal":{"name":"Thorax","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13672040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148798234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of sex, socioeconomic deprivation, ethnicity and region on exacerbation rates and mortality of chronic respiratory diseases in England: population-based cohorts.","authors":"Hannah Whittaker, Thomas Bolton, Ian Sinha, Liam G Heaney, John Busby, Gwyneth A Davies, Aziz Sheikh, Jennifer K Quint","doi":"10.1136/thorax-2026-224765","DOIUrl":"https://doi.org/10.1136/thorax-2026-224765","url":null,"abstract":"<p><strong>Background: </strong>Inequalities in chronic respiratory diseases persist, yet up-to-date evidence on outcomes remains limited. We described national mortality and exacerbation rates in people with asthma and chronic obstructive pulmonary disease (COPD) since the beginning of the COVID-19 pandemic and assessed variation by inequalities.</p><p><strong>Methods: </strong>England primary care records from the General Practice Extraction Service data for Pandemic Planning and Research were linked to Hospital Episode Statistics and Office for National Statistics mortality data. Cohorts of primary care diagnosed asthma and COPD were defined prior to 1 November 2019. Monthly age-sex-standardised exacerbation rates (Systematized Nomenclature of Medicine Clinical Terms (SNOMED-CT) and Internationl Classification of Diseases (ICD) 10 codes) and mortality rates (ICD-10 codes) were calculated from 1 November 2019 to 31 March 2025, stratified by sex, Index of Multiple Deprivation (IMD), ethnicity and region.</p><p><strong>Results: </strong>The study included 7644 510 people with asthma and 1 211 975 with COPD. Mean monthly exacerbation rates were higher in females than males (33% and 30% higher for asthma and COPD, respectively), while mean monthly all-cause mortality rates were 13% and 15% higher in males than females. Mean monthly exacerbation and all-cause mortality rates were higher in IMD-1 compared with IMD-10 across all conditions (asthma: 123% and 100% higher, COPD: 68% and 41% higher, respectively). Mean monthly all-cause mortality and exacerbation rates were higher in the northeast than the southwest (asthma: 22% and 69% COPD: 15% and 42% higher, respectively). Outcome rates varied by ethnicity across conditions.</p><p><strong>Conclusions: </strong>Inequalities in chronic respiratory disease outcomes persist across England despite sustained policy focus on reducing health inequalities.</p>","PeriodicalId":23284,"journal":{"name":"Thorax","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148798285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Persistence of static lung hyperinflation in adults with cystic fibrosis treated with elexacaftor-tezacaftor-ivacaftor.","authors":"Théo Dhote, Clémence Martin, Isabelle Fajac, Frédérique Aubourg, Reem Kanaan, Nicolas Carlier, Isabelle Honoré, Johanna Fesenbeckh, Jennifer Da Silva, Thierry Perez, Pierre-Régis Burgel","doi":"10.1136/thorax-2026-225174","DOIUrl":"https://doi.org/10.1136/thorax-2026-225174","url":null,"abstract":"<p><strong>Background: </strong>This study sought to describe the prevalence of lung hyperinflation in adults (≥18 years) with cystic fibrosis (awCF) and the effects of elexacaftor-tezacaftor-ivacaftor (ETI) on hyperinflation.</p><p><strong>Methods: </strong>Consecutive awCF who initiated ETI at Cochin Hospital (Paris, France) and had performed body plethysmography within 12 months prior to ETI initiation were included. Abnormal lung volumes (including total lung capacity (TLC) and residual volume (RV)) were defined as > upper limit of normal (ULN) using the Global Lung Initiative reference values. Lung hyperinflation was defined as RV/TLC>ULN. Variables associated with hyperinflation prior to ETI initiation were identified using multivariate logistic regression analysis. Evolution of hyperinflation was examined by comparing data prior to and after 12 months on ETI.</p><p><strong>Findings: </strong>Body plethysmography was available prior to ETI initiation in 297 awCF, of which 286 had also body plethysmography at 12 months after ETI initiation. Prior to ETI initiation, TLC, RV and RV/TLC ratio values greater than ULN were found in 14%, 69% and 76% of awCF, respectively. RV/TLC ratio inversely correlated with percent predicted forced expiratory volume in 1 s (ppFEV₁; r=-0.86). Increasing age and the number of days on intravenous antibiotics in the previous year were independently associated with RV/TLC>ULN. RV/TLC decreased after 12 months of ETI (median (IQR) absolute decrease; -5.4 (-10.3 to -0.3) %, p<0.0001; n=286) but remained above ULN in 65% of awCF, including in some with normal ppFEV₁.</p><p><strong>Interpretation: </strong>Lung hyperinflation usually persists in awCF treated with ETI despite improvement in ppFEV₁ and lung volumes.</p>","PeriodicalId":23284,"journal":{"name":"Thorax","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148798310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular scissors for inflamed lungs: targeting ubiquitin-specific peptidases in acute lung injury.","authors":"Hannah Rose McLeod, Suguru Yamamoto, Koichi Yuki","doi":"10.1136/thorax-2026-225655","DOIUrl":"10.1136/thorax-2026-225655","url":null,"abstract":"","PeriodicalId":23284,"journal":{"name":"Thorax","volume":" ","pages":""},"PeriodicalIF":9.1,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13592672/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148758911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Never say die: making a death from asthma a never event.","authors":"Dominick Shaw, Katie Pink, P Jane McDowell, Tom Fardon","doi":"10.1136/thorax-2025-224234","DOIUrl":"10.1136/thorax-2025-224234","url":null,"abstract":"","PeriodicalId":23284,"journal":{"name":"Thorax","volume":" ","pages":"836-837"},"PeriodicalIF":9.1,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147857406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"'Mind the gap'.","authors":"Johan Meurling, Joerg Steier","doi":"10.1136/thorax-2026-224806","DOIUrl":"10.1136/thorax-2026-224806","url":null,"abstract":"","PeriodicalId":23284,"journal":{"name":"Thorax","volume":" ","pages":"828-829"},"PeriodicalIF":9.1,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147435991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of ambient air pollution exposure on lung function in cystic fibrosis: old stories or breaking news?","authors":"Anja Maria Schaffer, Christine Rass, Sarah Schlagenhaufen, Florian Singer","doi":"10.1136/thorax-2025-224631","DOIUrl":"10.1136/thorax-2025-224631","url":null,"abstract":"","PeriodicalId":23284,"journal":{"name":"Thorax","volume":" ","pages":"821-822"},"PeriodicalIF":9.1,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147843368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptomic signatures of IPF in ALI-cultured airway cells and their therapeutic implications.","authors":"Robert Lorenz Chua, Carmen Veith, Marc A Schneider, Katharina Jechow, Gelsomina Kaufhold, Said Alkildani, Michelle Wild, Alexander Sudy, Elizabeth Chang Xu, Michael Kreuter, Agnes Boots, Roland Eils, Nicolas C Kahn, Christian Conrad","doi":"10.1136/thorax-2025-223325","DOIUrl":"10.1136/thorax-2025-223325","url":null,"abstract":"<p><strong>Introduction: </strong>Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with limited treatment options. Most single-cell studies rely on end-stage explant lungs, leaving early disease mechanisms poorly understood. Profiling earlier stages may reveal distinct cellular phenotypes that could be pharmacologically targeted. Recent evidence also implicates airway epithelial cells in IPF disease development and progression.</p><p><strong>Methods: </strong>To investigate early-stage IPF mechanisms, we profiled the airway mucosa of newly diagnosed, treatment-naïve patients using single-cell RNA-sequencing of air-liquid interface cultures. We further assessed the transcriptional and functional responses of these cells to antifibrotic drugs (nintedanib and pirfenidone) and a Src kinase inhibitor (saracatinib).</p><p><strong>Results: </strong>Profiling of 129 986 transcriptomes identified primed fibroblasts (<i>PDGFRA</i> ⁺, <i>SPP1</i> ⁺), dysregulated basal cells (<i>TP63⁺</i> , <i>KRT5⁺</i> , <i>FN1⁺</i> ), and proinflammatory airway epithelial cells (SAA, CXCL, CCL). Integrative analyses with explant-derived IPF atlases revealed different basal and fibroblast phenotypes spanning tissue regions and disease stages. In vitro, bronchial epithelial cells stimulated fibroblast proliferation and activation, and fibroblasts remained sensitive to TGF-β. While all three drugs attenuated many IPF signatures, saracatinib most effectively suppressed fibroblast activation and epithelial proliferation.</p><p><strong>Conclusions: </strong>This study defines epithelial-mesenchymal programmes of the airway mucosa at an early, diagnostic stage of IPF and demonstrates distinct drug responses at single-cell resolution. By linking airway-derived phenotypes to antifibrotic efficacy, our findings highlight the therapeutic potential of saracatinib and may inform future treatment strategies.</p>","PeriodicalId":23284,"journal":{"name":"Thorax","volume":" ","pages":"859-870"},"PeriodicalIF":9.1,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13479674/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146228915","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Airway microbiota in young people across four continents differ by country, asthma status and inflammatory phenotype.","authors":"Steven L Taylor, Collin R Brooks, Lucy Pembrey, Sarah K Manning, Levi Elms, Harriet Mpairwe, Camila A Figueiredo, Aida Y Oviedo, Martha Chico, Jeroen Burmanje, Hajar Ali, Irene Nambuya, Pius Tumwesige, Steven Robertson, Charlotte E Rutter, Karin van Veldhoven, Susan M Ring, Mauricio L Barreto, Philip J Cooper, Álvaro A Cruz, Neil Pearce, Geraint B Rogers, Jeroen Douwes","doi":"10.1136/thorax-2025-222965","DOIUrl":"10.1136/thorax-2025-222965","url":null,"abstract":"<p><strong>Background: </strong>Asthma is an umbrella diagnosis encompassing distinct pathophysiological mechanisms. While a global problem, our understanding of the interplay between respiratory microbiology and airway inflammation is largely from populations in high-income settings. As a result, treatment approaches align poorly with asthma characteristics in less studied populations.</p><p><strong>Objective: </strong>To identify conserved and geographically distinct relationships between airway inflammation and microbiota characteristics in young people with and without asthma.</p><p><strong>Methods: </strong>We conducted a cross-sectional study performing inflammatory phenotyping, microbiota analysis and enumeration of total bacteria, <i>Haemophilus influenzae</i> and <i>Moraxella catarrhalis</i> on 488 induced sputum samples from participants from Brazil (asthma: 68; non-asthma: 8), Ecuador (asthma: 89; non-asthma: 30), Uganda (asthma: 61; non-asthma: 8), New Zealand (asthma: 129; non-asthma: 58) and the UK (asthma: 25; non-asthma: 20). Microbiota characteristics were compared by country, asthma status and inflammatory characteristics, adjusting for age and sex.</p><p><strong>Results: </strong>Asthma inflammatory phenotypes and microbiology differed between countries, with Uganda characterised by higher neutrophils, microbial diversity and bacterial abundance. Comparison of airway inflammation with microbiota characteristics showed conserved relationships across centres, with airway neutrophil proportion explaining variance in microbiota Bray-Curtis dissimilarity (p<0.001) and being positively associated with bacterial abundance, including <i>H. influenzae</i> and <i>M. catarrhalis</i> load (all p<0.05). In contrast, eosinophil proportion was less strongly associated with microbiota dissimilarity (p=0.033) and only associated with <i>Streptococcus</i> abundance. Country-specific associations between airway inflammation and microbiology were evident.</p><p><strong>Conclusion: </strong>Both airway inflammation and microbiology varied geographically in young people with asthma. Associations between microbiota characteristics and neutrophilic phenotype were conserved.</p>","PeriodicalId":23284,"journal":{"name":"Thorax","volume":" ","pages":"903-912"},"PeriodicalIF":9.1,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13479613/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146093899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Making sense of azithromycin resistance patterns: what have we learnt and what should we do?","authors":"Will Carroll, James Chapman, Francis J Gilchrist","doi":"10.1136/thorax-2026-225025","DOIUrl":"10.1136/thorax-2026-225025","url":null,"abstract":"","PeriodicalId":23284,"journal":{"name":"Thorax","volume":" ","pages":"819-820"},"PeriodicalIF":9.1,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147983153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}