Thorax最新文献

{"title":"Correction: Serum cytokine biosignatures for identification of tuberculosis among HIV-positive inpatients","authors":"BMJ Publishing Group Ltd and British Thoracic Society","doi":"10.1136/thorax-2023-220782corr1","DOIUrl":"https://doi.org/10.1136/thorax-2023-220782corr1","url":null,"abstract":"Zhang H, Li L, Liu Y , et al . Serum cytokine biosignatures for identification of tuberculosis among HIV-positive inpatients. Thorax 2024;79:465–471. The …","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"218 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836707","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":"Journal club","authors":"Niki Veale","doi":"10.1136/thorax-2025-223300","DOIUrl":"https://doi.org/10.1136/thorax-2025-223300","url":null,"abstract":"Patients with idiopathic pulmonary fibrosis (IPF) are at increased risk of developing lung cancer, and the coexistence of these diseases is associated with significantly worse overall survival compared with either condition alone. This is partly due to the clinical conundrums posed by IPF, as impaired lung function may preclude curative surgical resection, and other treatments can precipitate acute exacerbations in IPF. Pirfenidone has a well-established role in slowing the progressive decline in forced vital capacity (FVC), with small studies highlighting that it may also reduce the risk of lung cancer. Yoon and colleagues (ERJ 2025;65(2):2401484) conducted a retrospective study mining South Korea’s national health insurance database, identifying a cohort of 10 084 patients with IPF. By applying inverse probability treatment weighting to balance covariates between the two retrospective groups, they demonstrated that the incidence rate of lung cancer was 10.4 cases per 1000 person years in patients receiving pirfenidone compared with 27.9 cases per 1000 person years in patients not taking pirfenidone. These findings were validated in a clinical cohort where detailed case note review ensured accurate phenotyping of IPF. In this cohort, pirfenidone use was associated with a reduced risk of lung cancer development, with a weighted adjusted HR of …","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"22 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836706","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":"Variability in sensitivity to inflammation in muscle and lung of patients with COPD may underlie susceptibility to lung function decline","authors":"Paul R Kemp, Mark Griffiths, Michael I Polkey, Amanda Sathyapala","doi":"10.1136/thorax-2024-221901","DOIUrl":"https://doi.org/10.1136/thorax-2024-221901","url":null,"abstract":"Background Muscle wasting and weakness (sarcopenia) are commonly associated with COPD causing frailty and reduced quality of life. The contribution of inflammation to muscle loss and the susceptibility to rapid lung function decline is debated. We hypothesised that comparing the muscle transcriptome to circulating inflammatory cytokine profiles in patients would identify any contribution of systemic inflammation to muscle atrophy. Methods Quadriceps differential gene expression was determined between mild-COPD (n=28) and severe-COPD (n=51) using GSE100281. These microarray data were compared by biweight mid-correlation with lung function and plasma cytokine levels from the same patients. Results Patients with severe COPD had reduced fat-free mass index (a measurement of muscle mass) compared with patients with mild COPD despite similar physical activity and inflammatory cytokine levels. Gene sets associated with inflammation and epithelial mesenchymal transition (EMT) were elevated in severe COPD, suggesting that inflammation may contribute to the loss of muscle mass. In patients with severe COPD, EMT and inflammation gene sets were strongly associated with circulating proinflammatory and anti-inflammatory cytokines. However, in patients with mild COPD, anti-inflammatory cytokines showed negative associations with these gene sets and associations with proinflammatory cytokines were weak. In data from lung and blood samples, patients with severe COPD had elevated inflammatory and EMT gene expression compared with patients with mild COPD suggesting that this phenomenon is not muscle-specific. Conclusions In patients at the severe end of the COPD spectrum, the proinflammatory response in muscle predominates, whereas in patients at the mild end of the spectrum, the anti-inflammatory response predominates. This suggestion needs confirming in a longitudinal cohort. Data are available on reasonable request. The array data sets containing the expression data are freely available on the NCBI gene expression omnibus (<https://www.ncbi.nlm.nih.gov/geo/>). Data relating to physiology and circulating cytokine levels are available on reasonable request.","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"3 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841453","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":"Building hypotheses to understand the synergistic effects of heat and pollution exposure in a changing climate","authors":"Sarah Chambliss, Ifeanyichukwu C Nduka, Geeta G Persad","doi":"10.1136/thorax-2025-223233","DOIUrl":"https://doi.org/10.1136/thorax-2025-223233","url":null,"abstract":"The increasing intensity, frequency and duration of extreme weather events due to climate change pose a broad range of health risks,1 and the synergistic effects of extreme temperature co-occurring with other hazardous exposures such as air pollution may result in higher risks of all-cause mortality and cardiovascular and respiratory morbidity than exposure to either event alone.2 3 There are a number of hypothesised mechanisms for this interaction effect, including increased susceptibility to heat effects on chronic conditions affected by air pollution exposure, exacerbation of pollution effects due to temperature-induced stress, and shared pathophysiological pathways (eg, systemic inflammation), but specific physiological mechanisms are not well understood.2 In this editorial, we discuss this aspect of a recently published study by Cheng et al in Thorax, ‘Ambient Formaldehyde Combined with High Temperature Exposure and Respiratory Disease Admissions Among Children: A Time-Series Study across Multiple Cities’.4 The expansion of environmental …","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"108 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841452","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":"Chronotherapy in asthma: BD or not BD? That is the question","authors":"Nicola Smallcombe, Richard Edward Russell","doi":"10.1136/thorax-2025-223094","DOIUrl":"https://doi.org/10.1136/thorax-2025-223094","url":null,"abstract":"Globally, asthma remains one of the most common chronic conditions. The UK has one of the highest prevalence rates in Europe,1 with asthma accounting for 2–3% of general practitioner consultations.2 Asthma control is achieved, in most, by taking inhaled corticosteroid (ICS) containing medication regularly using an effective inhaler technique. Anything that can be done to improve the efficacy of asthma medication would be helpful, and enabling clear instructions to be given to patients may increase overall adherence and thus reduce the risk of asthma attack and lower the significant symptom burden. It is well established that asthma demonstrates a rhythmic pattern of diurnal variation with worsening nocturnal and early morning symptoms.3 Symptoms, such as cough, tight chest and wheeze, are often worse overnight or in the early hours of the morning, with approximately 90% of asthma attacks happening within this time frame.4 In addition, significant fluctuations in lung function throughout the day, along with a noticeable decline at night, are known to be indicators of disease severity, inadequate control and increased mortality risk.5 Potential mechanisms have been discovered, which explain this phenomenon. In those patients with asthma demonstrating nocturnal symptoms, the activity of the glucocorticoid receptor has been shown to demonstrate reduced steroid responsiveness overnight.6 The PER3 gene, which is linked to chronotype, had been demonstrated previously by Krakowiak et al to exhibit significantly greater rhythmicity in individuals with asthma compared to healthy controls.7 It therefore follows that aligning drug administration with the body’s circadian rhythm—known as chronotherapy—would likely enhance the efficacy of inhaled corticosteroid treatment in patients with asthma. This is the focus of the study by Wang et al published in …","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"11 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836697","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":"You can’t always get what you want: evidence for exacerbation reduction with domiciliary oxygen therapy","authors":"Peter M A Calverley","doi":"10.1136/thorax-2025-223299","DOIUrl":"https://doi.org/10.1136/thorax-2025-223299","url":null,"abstract":"On a rather cold summer afternoon 45 years ago, I found myself, a humble research fellow, in a committee room in the University of Birmingham UK surrounded by famous professors and investigators of hypoxaemic lung disease. My chief, the late Professor David Flenley, had been asked by the British Council to lecture in China and had sent me to deputise for him on the writing committee of the Medical Research Council (MRC) trial of domiciliary oxygen therapy in what we now call chronic obstructive pulmonary disease (COPD). The paper we wrote (in which the authors kindly acknowledged my role) has had significant consequences for hundreds of thousands of patients in the 44 years since its publication.1 Ours remains the only randomised placebo-controlled study of home oxygen therapy in COPD as the US Nocturnal Oxygen Therapy Trial (NOTT) compared 12 with 24 hours (in practice 17 hours) of therapy.2 The MRC study was arduous for both patients and investigators with regular arterial gas monitoring, cardiac catheterisation and exercise testing. Only 89 patients were recruited compared with 203 in the USA. However, even with this modest number of patients, there was a clear reduction in mortality with oxygen therapy and a stabilisation of the pulmonary artery pressure, the presumed mechanism …","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"54 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836705","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":"The impact of dosage timing for inhaled corticosteroids in asthma: a randomised three-way crossover trial","authors":"Ran Wang, Robert Maidstone, Dave Singh, David Ray, Andrew S Loudon, Angela Simpson, Hannah Jane Durrington","doi":"10.1136/thorax-2024-222073","DOIUrl":"https://doi.org/10.1136/thorax-2024-222073","url":null,"abstract":"Background Asthma demonstrates a robust daily rhythm, with airflow obstruction and airway inflammation peaking overnight. Aligning the timing of drug administration with rhythms in disease (chronotherapy) may improve therapeutic efficacy. We aimed to evaluate the impact of dosage timing for inhaled corticosteroids in asthma. Methods This is a randomised three-way crossover trial. Participants with mild to moderate atopic asthma were randomised to beclometasone dipropionate: (1) 400 µg once daily between 08:00 and 09:00 (ODAM); (2) 400 µg once daily between 15:00 and 16:00 (ODPM); and (3) 200 µg twice daily between 08:00 and 09:00 and between 20:00 and 21:00 (BD) for 28 days, with a 2 week washout period in between treatment periods. Six-hourly spirometry and biomarkers were measured over 24 hours following the run-in period and at the end of each treatment period. Results Of 25 participants, 21 completed all regimens. ODPM was superior in improving 22:00 FEV1 (median (IQR): +160 (+70, +270) ml) compared with ODAM (−20 (−80, +230) ml) and BD (+80 (−20, +200) ml). ODPM resulted in better overnight (22:00 and 04:00) suppression in blood eosinophil counts compared with BD and ODAM. All regimens improved asthma control and reduced fractional exhaled nitric oxide and serum cortisol levels with no difference among dosing regimens. Conclusion ODPM better suppresses the nocturnal dip in lung function and peak of blood eosinophil counts compared with BD and ODAM; this was without an increase in adverse events. Future trials are warranted to validate these findings in real-life settings and to determine which population may best benefit from chronotherapy. Data are available upon reasonable request. The study protocol is available on trial registration website. Individual participant data that underlie the results reported in this article after deidentification will be shared 3 years following article publication with investigators whose proposed use of data has been approved by the study sponsor. Proposal will be directed to pmoore@crosolutions.co.uk. To gain access, data requestors will need to sign a data access agreement.","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"1 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143836699","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":"Impact of quantitative radiological features of interstitial lung disease on immunomodulatory treatment response in three autoimmune interstitial lung disease cohorts","authors":"Scott M Matson, Grace Hyun J Kim, Stephen M Humphries, Michael D Roth, Jonathan Goldin, Donald P Tashkin, Mei Leng, Bryant R England, Joyce S Lee, Elizabeth R Volkmann","doi":"10.1136/thorax-2024-222367","DOIUrl":"https://doi.org/10.1136/thorax-2024-222367","url":null,"abstract":"Background The defining radiological features of autoimmune interstitial lung disease (ILD) are ground glass opacification (GGO) and fibrosis. The associations between these features and physiological response to immunomodulation remain unclear. Methods This study leveraged three autoimmune ILD cohorts: two with systemic sclerosis (SSc) and one with rheumatoid arthritis (RA) which were selected for inherent differences in fibrotic extents/patterns. Linear regression models examined associations between baseline quantitative GGO, fibrosis, their ratio and forced vital capacity (FVC)%-predicted changes after 12 months of immunomodulatory therapy. Results Patients with SSc-ILD (N=262) exhibited a higher GGO-to-fibrosis ratio compared with patients with RA-ILD (N=130) (mean ratio 3.0 vs 0.25). Increased GGO-to-fibrosis was not associated with improved FVC%-predicted in any cohort. Conversely, in patients with SSc-ILD treated with cyclophosphamide (CYC), increased fibrosis (estimate 0.17 (95% CI 0.003, 0.33); p=0.04) and increased GGO (estimate 0.15 (95% CI 0.004, 0.30); p=0.044) were both significantly associated with FVC% improvement. Given the negative direction of the estimate for GGO-to-fibrosis ratio (estimate −0.33 (95% CI −0.61, –0.06); p=0.016), CYC was associated with greater FVC% improvement in patients with a higher degree of fibrosis relative to GGO. No significant correlation was seen in patients with SSc-ILD treated with mycophenolate (N=56) or in patients with RA-ILD treated with immunomodulation (N=130). Discussion Increased quantitative GGO relative to fibrosis was not significantly associated with improved response to immunomodulation in patients with RA-ILD and SSc-ILD. However, increased quantitative fibrosis and GGO extent were associated with improved response to CYC in SSc-ILD. More research is needed to understand how to use radiological features to guide treatment selection in ILD. Data are available upon reasonable request.","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"22 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819007","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":"64-year-old man with a raised hemidiaphragm","authors":"Lucy O’Malley, Abdisamad Ali, Ajit Thomas, Shiva Bikmalla, Naveed Mustfa","doi":"10.1136/thorax-2024-222273","DOIUrl":"https://doi.org/10.1136/thorax-2024-222273","url":null,"abstract":"A 64-year-old male retired firefighter and never-smoker presented to the ventilation team with a 6-month history of breathlessness on minimal exertion, orthopnoea, nocturia and preference to sleep on his left-hand side. His only medical history was atrial fibrillation (AF) that was treated with cardioversions and ablations a few months ago. The clinical examination was unremarkable except for reduced air entry at the right base. Oxygen saturation was 96% on room air. A chest radiograph (CXR) confirmed right base atelectasis and new elevated right hemidiaphragm (figure 1a,b) compared with a CXR 7 months earlier (figure 1a). CT confirmed a raised right hemidiaphragm and excluded pleural effusion, mediastinal lymphadenopathy or pathology to explain raised hemidiaphragm (figure 2). Figure 1 (a) Baseline normal chest radiograph (CXR), taken 7 months prior to symptom onset, (b) CXR 3 months after symptom onset, demonstrating elevated hemidiaphragm, (c) CXR after 18 months confirming …","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"25 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819006","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":"Inherited predisposition to pneumothorax: estimating the frequency of Birt-Hogg-Dubé syndrome from genomics and population cohorts","authors":"Bryndis Yngvadottir, Lucy Richman, Avgi Andreou, Jessica Woodley, Anita Luharia, Derek Lim, Genes & Health Research Team, Eamonn R Maher, Stefan J Marciniak","doi":"10.1136/thorax-2024-221738","DOIUrl":"https://doi.org/10.1136/thorax-2024-221738","url":null,"abstract":"Birt-Hogg-Dubé syndrome (BHDS) is the most common monogenic cause of pneumothorax. Most affected families have pathogenic variants in the FLCN gene. Using large genomic registries (UK Biobank (UKB), 100,000 Genomes Project and East London Genes & Health) including >550 000 individuals, we demonstrate that the frequency of clinically validated loss-of-function FLCN variants is 1 in 2710 to 4190. While the lifetime risk of pneumothorax in FLCN mutation carriers in the UKB and a BHDS clinical cohort was substantial (28.4% and 37.3%, respectively, to age 65 years), the lifetime risk of renal cancer was significantly lower in UKB than in BHDS patients (1% vs 32.1%). These findings highlight the importance of clinical context in managing individuals with FLCN mutations. 100kGP: Research on the de-identified patient data used in this publication can be carried out in the Genomics England Research Environment subject to a collaborative agreement that adheres to patient led governance. All interested readers will be able to access the data in the same manner that the authors accessed the data. For more information about accessing the data, interested readers may contact research-network@genomicsengland.co.uk or access the relevant information on the Genomics England website: <https://www.genomicsengland.co.uk/research>. UKB: Data from UK Biobank is available on application from <https://www.ukbiobank.ac.uk/> All researchers who wish to access the research resource must register with UK Biobank by completing the registration form in the Access Management System (AMS). <https://www.ukbiobank.ac.uk/> enable-your-research/register ELGH: The VCF data (accession number EGAD00001005469) is available from the EBI-EGA genotype phenotype archive (www.ebi.ac.uk/ega). Users need to complete the standard Wellcome Sanger Institute Data Access Agreement.","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"59 1","pages":""},"PeriodicalIF":10.0,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143813596","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}