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频道帖子
[Correspondence] Precision-guided immunomodulatory therapy in sepsis
https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(26)00153-0/fulltext?rss=yes
Erik H A Michels and colleagues developed a parsimonious three-biomarker framework (procalcitonin, soluble TREM-1, and IL-6) that quantifies the Dysregulated Immune Profile (DIP) as a continuous score (cDIP) beyond organ-failure-based clinical surrogates and identifies patients with differential responses to hydrocortisone.1
| 2 | [Correspondence] Precision-guided immunomodulatory therapy in sepsis
https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(26)00154-2/fulltext?rss=yes
We commend Erik H A Michels and colleagues1 for quantifying immune dysregulation in pneumonia and sepsis. Through dimensionality reduction and clustering with 35 biomarkers, they defined three Dysregulated Immune Profiles (DIPs) and a corresponding continuous score (cDIP). By training parsimonious models with three biomarkers, they facilitated the application of these clusters and score to datasets without extensive data, such as a subset (n=425) of the CAPE-COD trial2 (hydrocortisone vs placebo in community-acquired-pneumonia). | 51 |
| 3 | [Correspondence] Precision-guided immunomodulatory therapy in sepsis – Authors’ reply
https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(26)00155-4/fulltext?rss=yes
We agree with Yingying Yang and colleagues that similar continuous Dysregulated Immune Profile (cDIP) values could arise from different host–pathogen configurations. Robustly decomposing immune dysregulation into discrete pathogen-driven versus host-driven components is challenging, as these processes are intrinsically coupled. Pathogen burden, identity, and infection source undoubtedly shape the host response, yet substantial heterogeneity in immune dysregulation persists within each of these factors (see appendix 2 p 39 of the original Article1). | 48 |
| 4 | [Editorial] Dying with Dignity—time to cut the red tape
https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(26)00198-0/fulltext?rss=yes
While death is a certainty for us all, how and when we die is not. For people with a terminal illness, the reality of death must be confronted alongside common fears of prolonged pain and suffering as well as a loss of autonomy. Although good end-of-life care can manage most symptoms, there are some circumstances that cannot be palliated and a person might feel their quality of life is so poor they would prefer to die. The practice of medical aid in dying (MAiD; also called physician assisted death) allows someone with a terminal diagnosis to obtain medication from a physician to end their life. | 109 |
| 5 | Correlates of 5-year decline in 6-min walk distance in the COPDGene cohort
http://thorax.bmj.com/cgi/content/short/81/7/664?rss=1
Background
Change in 6-min walk distance (6MWD) over time serves as a measure of change in functional exercise performance. We analysed a large cohort of current or former tobacco smokers over a 5-year period to identify correlates of 6MWD decline.
Methods
A total of 4734 participants with normal spirometry or spirometric evidence of chronic obstructive pulmonary disease (COPD) who completed a 5-year follow-up in the COPDGene study were included. Baseline and 5-year assessments included 6MWD, spirometry, St. George’s Respiratory Questionnaire (SGRQ), gender, race and CT measures of emphysema, gas trapping and airway wall thickness. 6MWD decline correlates relative to baseline and 5-year changes were examined using univariate and multivariate linear regression.
Results
At baseline, 2573 had normal spirometry; 487 were classified as GOLD1, 1044 as GOLD2, 514 as GOLD3 and 116 as GOLD4. Average 5-year decline in 6MWD was 35.6±101.7 (SD) metres (p2=12.1% and 9.1%, respectively). 5 year change in variables assessed (including FEV1 and SGRQ) explained only small fractions of 6MWD decline variance (each R2≤5%).
Conclusion
6MWD declined significantly, but with high variability; spirometry, CT, health status, demographic and anthropometric measures accounted for only small portions of this variance. Our findings suggest that a meaningful decline in 6MWD observed over 5 years in COPD patients is in large part related to factors other than decline in pulmonary structure or function. | 178 |
| 6 | Has the time come for workplace screening for obstructive sleep apnoea (OSA)?
http://thorax.bmj.com/cgi/content/short/81/7/638?rss=1
Introduction Obstructive sleep apnoea (OSA) is a common condition whose prevalence is related to the prevalence of obesity. Although efficacious therapy in the form of continuous positive airway pressure (CPAP) exists, the traditional process of OSA diagnosis and subsequent delivery of CPAP is labour intensive and thus far no generalised workplace screening programme exists. However, four developments have prompted us to ask whether this should now change. These are, first, screening algorithms to identify high risk occupations and industries; second, the use of low-cost screening technologies (which have recently been reviewed by the National Institute for Health and Care Excellence, NICE);1 third, understanding of the science of CPAP adherence and, finally, increasing alternative options for those who do not tolerate CPAP, which both offer the prospect of more successful therapy than ever before. Therefore, we evaluated the case for workplace screening against the UK National Screening... | 140 |
| 7 | Multimodality curative-intent treatment in NSCLC: an unprecedented era of change 2017-2025
http://thorax.bmj.com/cgi/content/short/81/7/707?rss=1
Curative-intent multimodality treatment—combining local treatments such as surgery or radiotherapy with systemic therapy—is the cornerstone of care in stage II–III non-small cell lung cancer (NSCLC). Since 2017, the systemic therapy backbones with multimodality treatment have undergone a dramatic transformation, driven by a series of pivotal, practice-changing clinical trials. Immunotherapy and targeted therapies, previously confined to the advanced/metastatic setting, are now firmly embedded in curative-intent regimens. Maintenance immunotherapy following chemoradiation in unresectable stage III disease, adjuvant tyrosine kinase inhibitors in resected epidermal growth factor receptor/anaplastic lymphoma kinase-positive tumours, neoadjuvant and perioperative chemoimmunotherapy in resectable stage II/III NSCLC and adjuvant chemoimmunotherapy following resection have all become new standards of care.
This state-of-the-art review synthesises the key evidence underpinning these developments, highlights their clinical implications and identifies challenges to implementation—particularly the need for redefined clinical pathways, accurate pretreatment staging, timely biomarker testing and coordinated multidisciplinary decision-making. A novel treatment algorithm is proposed to support clinicians in navigating these complex treatment choices.
We conclude that immunotherapy and targeted agents have irrevocably altered curative-intent NSCLC care, establishing multiple new standards that sometimes overlap and compete. In the surgical multimodality treatment pathway, neoadjuvant and perioperative chemoimmunotherapy offers the opportunity to increase the uptake of systemic therapy in comparison to adjuvant therapy and is considered by these authors to represent the optimal treatment path for most patients.
In this unprecedented era of therapeutic expansion, the greatest challenge is no longer the absence of effective treatments, but the complexity of selecting, sequencing and delivering them, as well as patient optimisation. Lung cancer services must evolve through proactive pathway redesign, integrated diagnostics and new models of multidisciplinary care. High-quality, biomarker-driven and patient-centred care is now achievable for many patients with stage II–III NSCLC—but it will require system-level adaptation to deliver it. | 102 |
| 8 | Towards a better understanding of residual sleep apnoea: the role of quantitatively assessed ventilatory control instability
http://thorax.bmj.com/cgi/content/short/81/7/633?rss=1
Untreated obstructive sleep apnoea (OSA) is associated with a wide range of adverse health outcomes, including but not limited to cardiocerebrovascular disease, hypertension and cognitive impairment.1 Positive airway pressure (PAP) therapy remains the first-line treatment for moderate to severe OSA.1 2 However, approximately 10–25% of patients continue to exhibit residual sleep apnoea despite PAP therapy.3 Although several factors contribute to residual sleep apnoea, such as male sex, OSA severity, older age with more comorbidities and central apnoeas,3 4 the physiological mechanisms underlying residual sleep apnoea and the ability to predict it reliably prior to treatment initiation are not well established. Eschbach and colleagues leveraged data from two large randomised controlled trials, the Apnea Positive Pressure Long-term Efficacy Study5 and the Randomized Intervention with Continuous Positive Airway Pressure in Coronary Artery Disease and OSA cohorts, | 80 |
| 9 | The 2026 Tobacco and Vapes Act: on to the tobacco endgame
http://thorax.bmj.com/cgi/content/short/81/7/635?rss=1
The goal of the tobacco endgame is that no one starts to smoke, that everyone who smokes is supported to quit and that reductions in consumption and profitability mean that the tobacco industry, which continues to be the main barrier to progress, ceases to be commercially viable.1 2 Passage of the 2026 Tobacco and Vapes Act3 into UK law (box 1) is a milestone on this journey and exemplifies the ‘forward-looking tobacco control measures’ called for by Article 2.1 of the WHO Framework Convention on Tobacco Control (FCTC).4 5 Box 1The UK Tobacco and Vapes Act 2026 Summary and Timeline October 2026 Minimum age of sale of 18 for all consumer nicotine-products (currently only in place for e-cigarettes and tobacco, but not novel products like pouches) as well as non-nicotine vapes. Ban on the free... | 75 |
| 10 | Functional decline in COPD: looking beyond FEV1
http://thorax.bmj.com/cgi/content/short/81/7/631?rss=1
Chronic obstructive pulmonary disease (COPD) is increasingly recognised as a systemic disease in which extrapulmonary comorbidities, including sarcopenia, osteoporosis and cardiovascular disease, contribute to symptoms, decreased functional capacity and mortality.1 As such, predicting functional decline in COPD using traditional lung function parameters alone can be difficult. 6-minute walk distance (6MWD) has emerged as a simple, validated measure of physical performance and an important prognostic tool in COPD.2 Notably, declines in 6MWD are more strongly associated with mortality than declines in forced expiratory volume in one second (FEV1),3 and 6MWD remains an independent predictor of survival after accounting for airflow limitation in COPD.4 Given the prognostic value of 6MWD, identifying patients with COPD at greatest risk for functional decline is crucial. In this issue of the journal, Boriek et al sought to address this gap by examining 4734 tobacco-exposed COPDGene participants with... | 82 |
| 11 | Beyond bronchopulmonary dysplasia: early-life determinants and divergent lung function trajectories of prematurity-associated lung disease
http://thorax.bmj.com/cgi/content/short/81/7/629?rss=1
Respiratory follow-up of children and adults born prematurely thus far has largely focused on those with the diagnostic label of bronchopulmonary dysplasia (BPD) which is assigned early in life.1 While BPD remains clinically important, especially during early infancy in those born extremely preterm (2 3 while a significant proportion who had BPD in infancy have relatively preserved respiratory outcomes. This disconnect has catalysed the development of the concept of prematurity-associated lung disease (PLD)4—a framework that encompasses the many risk factors beyond BPD and recognises the... | 79 |
| 12 | Elastic parametric response mapping: localising reversible small airway disease in COPD
http://thorax.bmj.com/cgi/content/short/81/7/626?rss=1
Chronic obstructive pulmonary disease (COPD) is responsible for 3.7 million deaths annually, with an increasing global prevalence projected to reach 592 million by 2050.1 2 Contemporary understanding recognises COPD as a heterogeneous syndrome requiring multilevel characterisation across phenotypes (emphysema-dominant, asthma-COPD overlap, early disease states such as pre-COPD, frequent exacerbator), molecular endotypes and measurable biomarkers that together identify treatable traits.3 4 The neutrophil-centric (T2-low) endotype, driven by IL-1β/IL-8/IL-17 pathways, represents the majority and is typically corticosteroid-resistant.5 The eosinophil-predominant (T2-high) endotype, present in 20%–40% of patients and mediated by IL-4/IL-5/IL-13, demonstrates responsiveness to corticosteroids and biologics, with blood eosinophil counts guiding therapy as a continuous biomarker.6 7 This framework has been operationalised through the treatable traits approach8 9 and is embraced in the 2025 GOLD guidelines, which formally integrate biologics such as dupilumab... | 72 |
| 13 | Trends in asthma-related paediatric mortality
http://thorax.bmj.com/cgi/content/short/81/7/702?rss=1
Asthma is a leading cause of paediatric mortality. This study aims to elucidate trends in paediatric mortality over time. Using US Centers for Disease Control (CDC) WONDER data, we conducted a cross-sectional analysis of paediatric asthma-related mortality between 1999 and 2023, overall and stratified by year, age, sex, race and region. Negative binomial regression was used to test the linear temporal trend and conduct group comparisons in asthma-related mortality rates. Over the study period, there were 5357 asthma deaths. The mortality rate was 3 per 1 000 000 children and rates remained stable over this period. Asthma mortality was higher in males, children 10–19 years (compared to children 5–9 years) and black (relative to white) children. Advances in the treatment of paediatric asthma should be aimed at reducing mortality and addressing differential health outcomes among black children. | 68 |
| 14 | Clinical, molecular and microbial characterisation of the eosinophilic endotype of bronchiectasis: data from the EMBARC-BRIDGE study
http://thorax.bmj.com/cgi/content/short/81/7/642?rss=1
Objectives
Eosinophilic bronchiectasis is defined by a blood eosinophil count (BEC) ≥300 cells/µL, but blood eosinophils imperfectly reflect airway eosinophilic inflammation. Here, we investigated the relationship between eosinophilic airway inflammation, blood eosinophils and clinical severity in bronchiectasis and explored the phenotype associated with eosinophilic bronchiectasis.
Methods
Sputum from 180 patients with stable CT-confirmed bronchiectasis was utilised to investigate airway levels of eosinophil proteins (eosinophil peroxidase (EPX), eosinophil derived-neurotoxin (EDN), eosinophil cationic protein (ECP), major basic protein (MBP) and Galectin-10 (Gal-10)) using a novel stable isotope dilution liquid chromatography-tandem mass spectrometry (LC-MS/MS) assay. To profile eosinophilic bronchiectasis, a nested analysis of patients with BEC
Results
Sputum concentrations of Gal-10, ECP and EDN were weakly but significantly associated with radiological severity, FEV1 and sputum culture positivity for Pseudomonas aeruginosa. Airway eosinophil protein concentrations did not associate with exacerbation frequency. Total eosinophil protein concentration moderately correlated with BECs (r=0.33 95% CI 0.14 to 0.49, p=0.0007). Nested analysis revealed increased sputum PCR-positivity for P. aeruginosa (26.7% vs 7.7%, p=0.033) and an increased frequency of patients showing signs of Aspergillus sensitisation (defined as Aspergillus-specific IgE titres >0.35 kUA/L, 24.5% vs 3.8%) in eosinophilic bronchiectasis. Sputum inflammatory biomarkers and clinical parameters did not differ between groups.
Conclusions
LC-MS/MS can detect eosinophilic inflammation within bronchiectasis sputum. Weak associations between elevated airway eosinophil proteins, bronchiectasis severity and P. aeruginosa infection were observed. Direct measurement of eosinophilic airway inflammation provides additional information in addition to BECs. Eosinophilic bronchiectasis associated with P. aeruginosa infection and Aspergillus sensitisation. | 72 |
| 15 | Primary adenoid cystic carcinoma of the trachea
http://thorax.bmj.com/cgi/content/short/81/7/705?rss=1
Case summary A 72-year-old woman presented with a 6-month history of productive cough, hoarseness and exertional dyspnoea. She is a never-smoker with a history of treated bowel cancer, basal cell carcinoma and hiatus hernia. Physical examination, chest X-ray and blood tests were unremarkable. Spirometry and transfer factor were normal, but her flow volume loop showed fixed large-airway obstruction. CT thorax revealed subglottic stenosis and diffuse tracheal thickening sparing the posterior membrane (figure 1a, b), initially suggestive of relapsing polychondritis. Despite high-dose steroids and immunosuppressive therapy, there was no clinical response and her symptoms progressed. Bronchoscopy was therefore performed. This revealed multilevel, multinodular lesions in the upper trachea (figure 2). Biopsy demonstrated lamina propria infiltration by tumour composed of anastomosing strands, solid nests, tubules and cribriform arrangements (figure 1). These histological features are diagnostic of primary adenoid cystic carcinoma1... | 81 |
| 16 | Elastic parametric response mapping: quantitative CT scoring for local COPD severity
http://thorax.bmj.com/cgi/content/short/81/7/654?rss=1
Background
Current quantitative chest CT techniques improve chronic obstructive pulmonary disease (COPD) phenotyping but do not capture spatial variability and potentially reversible disease in local lung parenchyma.
Methods
Applying elastic principal graphing to CT scans from Genetic Epidemiology of COPD study participants (age 45–80 years; ≥10 pack-years), we developed elastic parametric response mapping (ePRM), a tiered scoring system (tiers 0–3 and tier Op, ie, lung opacities) that classifies lung subvolumes based on their relative composition of normal lung, emphysema, small airways disease and parenchymal disease. For 3631 participants with longitudinal data, we evaluated how relative tier assignment and mean tier position of subvolumes changed over 5 years and how they associated with forced expiratory volume in 1 s (FEV1) change. We stratified analyses by baseline spirometry: no airflow obstruction, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 1–2 and GOLD 3–4.
Results
The proportion of tier 0 subvolumes decreased with worsening airflow obstruction, while tier 2 and 3 proportions increased. Tier 1 proportions were similar in GOLD 1–2 (25.7%) and GOLD 3–4 (28.1%), with over half of subvolumes remaining in tier 1 or reverting to tier 0 at year 5. In contrast to tiers 0 and 2, baseline mean tier 1 position was strongly predictive of reassignment to more advanced tiers at year 5 in participants without airflow obstruction, GOLD 1–2 and GOLD 3–4 (area under the curves (95% CIs) 0.86 (0.85 to 0.87), 0.90 (0.89 to 0.91) and 0.92 (0.90 to 0.93), respectively). A higher per cent volume of lung retained in tier 1 was associated with less FEV1 decline in all groups.
Conclusion
CT ePRM categorises local lung tissue into distinct and potentially reversible tiers of disease severity. | 89 |
| 17 | Journal club
http://thorax.bmj.com/cgi/content/short/81/7/718?rss=1
Cell free DNA in pleural disease Plasma circulating tumour DNA (ctDNA) has a low detection rate for isolated malignant pleural effusion (MPE) in non-small cell lung cancer (NSCLC). Pleural fluid cell free DNA (cfDNA) detects all extracellular DNA fragments, not limited to DNA from tumour cells, and may improve detection rates. Wang et al (European Journal of Cancer, 2025; 217; https://doi.org/10.1016/j.ejca.2025.115224) conducted a prospective study of 50 patients with cytology positive newly diagnosed NSCLC with MPE, comparing pleural cfDNA next generation sequencing (NGS) with pleural cell pellet Sanger sequencing and routine tissue testing. Actionable driver mutations were identified in 90% of patients overall. Pleural cfDNA NGS achieved the highest diagnostic yield, detecting actionable alterations in 88% of cases compared with 78% using Sanger sequencing and 66% using routine testing (p=0.031). EGFR mutations predominated, particularly L858R and exon 19 deletions, alongside HER2 exon 20 insertions, ALK and... | 96 |
| 18 | Granules of truth: unpacking the eosinophilic endotype in bronchiectasis
http://thorax.bmj.com/cgi/content/short/81/7/621?rss=1
Bronchiectasis is a heterogeneous disease characterised by chronic inflammation leading to irreversible airway dilatation.1 Traditionally, bronchiectasis was thought to be solely caused by neutrophilic inflammation, but recent studies have shown that approximately 20% of individuals with bronchiectasis have evidence of eosinophilic inflammation, irrespective of known eosinophilic diseases such as asthma and allergic bronchopulmonary aspergillosis (ABPA).2 This finding has generated significant interest, as it may portend that bronchiectasis in some individuals is spurred on by type 2 (T2) inflammation. However, most studies to date defined eosinophilic bronchiectasis using an elevated blood eosinophil count (BEC)≥300 cells/µL. While BEC was modestly correlated with sputum eosinophils,2 there has been a paucity of data demonstrating T2 inflammation in individuals with eosinophilic bronchiectasis. In their Thorax paper, Pollock and colleagues leverage the EMBARC-BRIDGE cohort to move beyond BECs and interrogate eosinophilic inflammation directly within the airway using a novel proteomic... | 146 |
| 19 | [News] 2026 American Thoracic Society International Conference
https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(26)00193-1/fulltext?rss=yes
The pro-inflammatory cytokine IL-33 is thought to play a role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Results were presented from two phase 3 randomised double-blind trials, AERIFY-1 and AERIFY-2, which assessed the anti-IL-33 human IgG4P monoclonal antibody itepekimab versus placebo over 52 weeks in former smokers (cessation at least 6 months before screening) with moderate-to-severe COPD. 1127 participants with a mean age of 68 years, with a smoking history of 40·9 – 44·0 pack-years were enrolled in AERIFY-1; 377 participants received 300 mg itepekimab via subcutaneous injection every 4 weeks, 375 received itepekimab 300 mg every 2 weeks, and 375 received placebo. | 336 |
| 20 | [Comment] Sugammadex versus neostigmine and postoperative pulmonary complications: a word of caution
https://www.thelancet.com/journals/lanres/article/PIIS2213-2600(26)00185-2/fulltext?rss=yes
Neuromuscular blockade is often used to optimise muscle relaxation and surgical conditions in anaesthetised patients with endotracheal intubation. At the end of surgery, it is of paramount importance that patients have a complete recovery of this neuromuscular blockade so that respiratory and upper airway muscles ensure an adequate breathing pattern and intact oropharyngeal reflexes to prevent aspiration, respiratory insufficiency, and other postoperative pulmonary complications.1 Many patients receive medications for a timely neuromuscular blockade reversal, and the most efficient pharmacological strategy has been investigated for decades. | 437 |
