Pub Date : 2026-01-08Print Date: 2026-01-01DOI: 10.1183/13993003.02309-2025
Stephanie Thee, Marcus A Mall
{"title":"Pulmonary exacerbations in cystic fibrosis during the era of CFTR modulator therapy.","authors":"Stephanie Thee, Marcus A Mall","doi":"10.1183/13993003.02309-2025","DOIUrl":"https://doi.org/10.1183/13993003.02309-2025","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"67 1","pages":""},"PeriodicalIF":21.0,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145932826","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}
Pub Date : 2026-01-08Print Date: 2026-01-01DOI: 10.1183/13993003.01947-2025
Robert J Homer
{"title":"Commentary on: Update of the international multidisciplinary classification of the interstitial pneumonias: an ERS/ATS statement.","authors":"Robert J Homer","doi":"10.1183/13993003.01947-2025","DOIUrl":"https://doi.org/10.1183/13993003.01947-2025","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"67 1","pages":""},"PeriodicalIF":21.0,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145932839","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}
Pub Date : 2025-12-18DOI: 10.1183/13993003.01830-2025
Ayadh Alayadhi,Arafa Aboelhassan,Nicola Foster,Julie A Barber,Patricia Alupo,Ram K Chandyo,Oscar Flores-Flores,Bruce Kirenga,Renata G Mendes,Shumonta A Quaderi,Arun K Sharma,Trishul Siddharthan,William Checkley,John R Hurst,
BACKGROUNDFEV1Q (Forced Expiratory Volume in 1 s Quotient) is a race-neutral expression of lung function. The validity and utility of FEV1Q across Global South populations has not been previously explored.METHODSWe conducted a post-hoc analysis of data from the Global Excellence in COPD Outcomes-1 (GECo1 and GECo2) studies in which a random age- and sex-stratified population of 10 709 people were recruited in Nepal, Peru and Uganda. The FEV1 first percentile (used to derive FEV1Q) was estimated in those with COPD by site and sex. We examined associations between FEV1Q, risk factors and respiratory morbidity. We estimated the rate of decline in FEV1Q. We evaluated the discriminative accuracy of FEV1Q in diagnosing COPD.FINDINGSThe first percentile FEV1 in those with COPD at 0·43 L in women and 0·52 L in men is similar to those previously used to calculate FEV1Q. Lower FEV1Q was associated with older age, lower socioeconomic status, shorter height, and greater smoking pack-years. We estimated that decline in FEV1Q with age was 0·65 (95%CI: 0·64; 0·67) units/10 years, more rapid in those continuing to smoke at 0·82 (95%CI: 0·77; 0·87) units/10 years. FEV1Q was lower in those with prior respiratory hospitalizations and impairment in daily activities due to respiratory disease, and associated with future hospitalization risk in the GECo2 study. Pre-bronchodilator FEV1Q had reasonable diagnostic accuracy for COPD (AUC 0·87(95%CI:0·85-0·88)), similar to pre-bronchodilator FEV1% predicted (AUC 0·88(95%CI:0·87-0·90)).INTERPRETATIONOur data support the validity and utility of FEV1Q as a race-neutral approach to lung function assessment in diverse settings, including the Global South where the burden of lung disease is greatest.FUNDINGThis study was funded by the Medical Research Council (grant MR/P008984/1) under a Global Alliance for Chronic Diseases call. JRH is funded by the NIHR (project reference 303125) using UK international development funding from the UK Government to support global health research. The views expressed in this publication are those of the authors and not necessarily those of the NIHR or the UK government.
{"title":"FEV1Q as a race-neutral assessment of lung function in Nepal, Peru and Uganda.","authors":"Ayadh Alayadhi,Arafa Aboelhassan,Nicola Foster,Julie A Barber,Patricia Alupo,Ram K Chandyo,Oscar Flores-Flores,Bruce Kirenga,Renata G Mendes,Shumonta A Quaderi,Arun K Sharma,Trishul Siddharthan,William Checkley,John R Hurst, ","doi":"10.1183/13993003.01830-2025","DOIUrl":"https://doi.org/10.1183/13993003.01830-2025","url":null,"abstract":"BACKGROUNDFEV1Q (Forced Expiratory Volume in 1 s Quotient) is a race-neutral expression of lung function. The validity and utility of FEV1Q across Global South populations has not been previously explored.METHODSWe conducted a post-hoc analysis of data from the Global Excellence in COPD Outcomes-1 (GECo1 and GECo2) studies in which a random age- and sex-stratified population of 10 709 people were recruited in Nepal, Peru and Uganda. The FEV1 first percentile (used to derive FEV1Q) was estimated in those with COPD by site and sex. We examined associations between FEV1Q, risk factors and respiratory morbidity. We estimated the rate of decline in FEV1Q. We evaluated the discriminative accuracy of FEV1Q in diagnosing COPD.FINDINGSThe first percentile FEV1 in those with COPD at 0·43 L in women and 0·52 L in men is similar to those previously used to calculate FEV1Q. Lower FEV1Q was associated with older age, lower socioeconomic status, shorter height, and greater smoking pack-years. We estimated that decline in FEV1Q with age was 0·65 (95%CI: 0·64; 0·67) units/10 years, more rapid in those continuing to smoke at 0·82 (95%CI: 0·77; 0·87) units/10 years. FEV1Q was lower in those with prior respiratory hospitalizations and impairment in daily activities due to respiratory disease, and associated with future hospitalization risk in the GECo2 study. Pre-bronchodilator FEV1Q had reasonable diagnostic accuracy for COPD (AUC 0·87(95%CI:0·85-0·88)), similar to pre-bronchodilator FEV1% predicted (AUC 0·88(95%CI:0·87-0·90)).INTERPRETATIONOur data support the validity and utility of FEV1Q as a race-neutral approach to lung function assessment in diverse settings, including the Global South where the burden of lung disease is greatest.FUNDINGThis study was funded by the Medical Research Council (grant MR/P008984/1) under a Global Alliance for Chronic Diseases call. JRH is funded by the NIHR (project reference 303125) using UK international development funding from the UK Government to support global health research. The views expressed in this publication are those of the authors and not necessarily those of the NIHR or the UK government.","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"19 1","pages":""},"PeriodicalIF":24.3,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145777456","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}
QUESTIONChronic lung allograft dysfunction (CLAD) is the leading cause of late graft failure after lung transplantation. Fibroblast activation protein (FAP) is selectively upregulated in activated fibroblasts under fibrotic conditions. We asked whether FAP expression is increased in chronic lung allograft dysfunction and whether it can serve as an early diagnostic marker.MATERIALS AND METHODSWe performed single-cell RNA sequencing on two murine orthotopic lung transplant models (C57BL/6→C57BL/10 and BALB/c→C57BL/6) and human lung tissue from five controls and five patients with CLAD. We quantified FAP expression by immunohistochemistry in transbronchial biopsies from 240 lung transplant recipients (62 with CLAD and 178 without CLAD). Receiver-operating characteristic curves determined an optimal FAP-positive area threshold. Kaplan-Meier analysis and Cox proportional hazards models assessed the association between FAP positivity and CLAD.RESULTSIn both murine and human single-cell data, FAP expression was confined to pathogenic fibroblast subsets and was significantly elevated in CLAD. In the clinical cohort, a threshold of 10.8 percent FAP-positive area discriminated chronic dysfunction with an area under the curve of 0.78 (95% CI, 0.72-0.85), sensitivity of 65%, and specificity of 84%. FAP positivity predicted shorter CLAD-free survival (p<0.0001) and overall survival (p=0.03). The hazard ratio for CLAD was 5.23 (95% CI, 3.11-8.82; p<0.001), remaining significant after multivariable adjustment (hazard ratio 5.43; 95% CI, 3.22-9.16; p<0.001).ANSWERFAP expression is elevated in CLAD and is associated with subsequent CLAD and survival. Tissue FAP may enable early risk stratification and inform clinical surveillance; however, given its moderate discrimination, prospective validation in multicenter cohorts is warranted.
{"title":"Exploring fibroblast activation protein as an early biomarker in chronic lung allograft dysfunction.","authors":"Yudai Miyashita,Taisuke Kaiho,Hideki Nagata,Takashi Hiroshima,Yusuke Sugiura,Kaijie Zhang,Megan E Kelly,Yuanqing Yan,Takahide Toyoda,Alicia Steffens,Haiying Sun,Hiam Abdala-Valencia,Toru Kimura,Bowen Wang,Carl Atkinson,Ankit Bharat,Takashi Kanou,Yasushi Shintani,Chitaru Kurihara","doi":"10.1183/13993003.01738-2025","DOIUrl":"https://doi.org/10.1183/13993003.01738-2025","url":null,"abstract":"QUESTIONChronic lung allograft dysfunction (CLAD) is the leading cause of late graft failure after lung transplantation. Fibroblast activation protein (FAP) is selectively upregulated in activated fibroblasts under fibrotic conditions. We asked whether FAP expression is increased in chronic lung allograft dysfunction and whether it can serve as an early diagnostic marker.MATERIALS AND METHODSWe performed single-cell RNA sequencing on two murine orthotopic lung transplant models (C57BL/6→C57BL/10 and BALB/c→C57BL/6) and human lung tissue from five controls and five patients with CLAD. We quantified FAP expression by immunohistochemistry in transbronchial biopsies from 240 lung transplant recipients (62 with CLAD and 178 without CLAD). Receiver-operating characteristic curves determined an optimal FAP-positive area threshold. Kaplan-Meier analysis and Cox proportional hazards models assessed the association between FAP positivity and CLAD.RESULTSIn both murine and human single-cell data, FAP expression was confined to pathogenic fibroblast subsets and was significantly elevated in CLAD. In the clinical cohort, a threshold of 10.8 percent FAP-positive area discriminated chronic dysfunction with an area under the curve of 0.78 (95% CI, 0.72-0.85), sensitivity of 65%, and specificity of 84%. FAP positivity predicted shorter CLAD-free survival (p<0.0001) and overall survival (p=0.03). The hazard ratio for CLAD was 5.23 (95% CI, 3.11-8.82; p<0.001), remaining significant after multivariable adjustment (hazard ratio 5.43; 95% CI, 3.22-9.16; p<0.001).ANSWERFAP expression is elevated in CLAD and is associated with subsequent CLAD and survival. Tissue FAP may enable early risk stratification and inform clinical surveillance; however, given its moderate discrimination, prospective validation in multicenter cohorts is warranted.","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"47 1","pages":""},"PeriodicalIF":24.3,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145777460","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}
Pub Date : 2025-12-18DOI: 10.1183/13993003.01979-2025
Vanessa E Murphy
{"title":"Decreasing inhaled corticosteroids in pregnancy increases the risk for asthma exacerbations: time for new approaches to solve a decades-old problem.","authors":"Vanessa E Murphy","doi":"10.1183/13993003.01979-2025","DOIUrl":"https://doi.org/10.1183/13993003.01979-2025","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"6 1","pages":""},"PeriodicalIF":24.3,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145777464","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}
Pub Date : 2025-12-18DOI: 10.1183/13993003.02003-2025
Dave Singh,Marc Miravitlles
{"title":"Alvelestat for alpha-1 antitrypsin deficiency-associated emphysema: the hope for an oral treatment.","authors":"Dave Singh,Marc Miravitlles","doi":"10.1183/13993003.02003-2025","DOIUrl":"https://doi.org/10.1183/13993003.02003-2025","url":null,"abstract":"","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":"248 1","pages":""},"PeriodicalIF":24.3,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145777463","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}
Background: Asthma exacerbations during pregnancy are associated with adverse maternal and perinatal outcomes. Identifying modifiable risk factors is essential for improving health outcomes. We aimed to describe exacerbation patterns during pregnancy and identify exacerbation risk factors, particularly modifiable risk factors such as inhaled corticosteroid use.
Methods: This was a cohort study using UK primary care and hospital data (2004-2020) to identify pregnant women with asthma. Exacerbations were defined as a short course of oral corticosteroids, emergency department visit or unscheduled hospital admission. Multivariable logistic regression was used to assess associations between maternal characteristics and exacerbations (primary outcome) and inhaled corticosteroid use (secondary outcome).
Results: Among 40 196 pregnant women with asthma, total exacerbations declined by ∼30% during pregnancy. However, exacerbations associated with hospital admission increased by 30-45% during the second and third trimesters, declining abruptly after delivery. Inhaled corticosteroid prescriptions were reduced in 31% of women during pregnancy. Decreased inhaled corticosteroid use was associated with suboptimal asthma control pre-pregnancy, age, ethnicity and smoking. The strongest exacerbation risk factors were a history of exacerbations (adjusted OR 4.09, 95% CI 3.81-4.39), reduced inhaled corticosteroid use during pregnancy (adjusted OR 2.29, 95% CI 2.12-2.47) and ≥4 prescriptions per year for inhaled corticosteroids plus another preventer before pregnancy (adjusted odds ratio 2.11, 95% CI 1.87-2.37). Additional risk factors included blood eosinophilia, smoking and obesity.
Conclusions: Despite fewer total exacerbations, exacerbations associated with a hospital admission increased during pregnancy. One third of women reduced inhaled corticosteroid use during pregnancy, yet this was the second largest exacerbation risk factor and is completely modifiable. Other major risk factors were type 2 inflammation and another modifiable risk factor, suboptimal asthma control pre-pregnancy.
{"title":"Pregnancy, asthma and exacerbations: a population-based cohort.","authors":"Bohee Lee, Ernie Wong, Tricia Tan, Hitasha Rupani, Chloe I Bloom","doi":"10.1183/13993003.01327-2025","DOIUrl":"10.1183/13993003.01327-2025","url":null,"abstract":"<p><strong>Background: </strong>Asthma exacerbations during pregnancy are associated with adverse maternal and perinatal outcomes. Identifying modifiable risk factors is essential for improving health outcomes. We aimed to describe exacerbation patterns during pregnancy and identify exacerbation risk factors, particularly modifiable risk factors such as inhaled corticosteroid use.</p><p><strong>Methods: </strong>This was a cohort study using UK primary care and hospital data (2004-2020) to identify pregnant women with asthma. Exacerbations were defined as a short course of oral corticosteroids, emergency department visit or unscheduled hospital admission. Multivariable logistic regression was used to assess associations between maternal characteristics and exacerbations (primary outcome) and inhaled corticosteroid use (secondary outcome).</p><p><strong>Results: </strong>Among 40 196 pregnant women with asthma, total exacerbations declined by ∼30% during pregnancy. However, exacerbations associated with hospital admission increased by 30-45% during the second and third trimesters, declining abruptly after delivery. Inhaled corticosteroid prescriptions were reduced in 31% of women during pregnancy. Decreased inhaled corticosteroid use was associated with suboptimal asthma control pre-pregnancy, age, ethnicity and smoking. The strongest exacerbation risk factors were a history of exacerbations (adjusted OR 4.09, 95% CI 3.81-4.39), reduced inhaled corticosteroid use during pregnancy (adjusted OR 2.29, 95% CI 2.12-2.47) and ≥4 prescriptions per year for inhaled corticosteroids plus another preventer before pregnancy (adjusted odds ratio 2.11, 95% CI 1.87-2.37). Additional risk factors included blood eosinophilia, smoking and obesity.</p><p><strong>Conclusions: </strong>Despite fewer total exacerbations, exacerbations associated with a hospital admission increased during pregnancy. One third of women reduced inhaled corticosteroid use during pregnancy, yet this was the second largest exacerbation risk factor and is completely modifiable. Other major risk factors were type 2 inflammation and another modifiable risk factor, suboptimal asthma control pre-pregnancy.</p>","PeriodicalId":12265,"journal":{"name":"European Respiratory Journal","volume":" ","pages":""},"PeriodicalIF":21.0,"publicationDate":"2025-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12713386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144948358","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}
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