The supply of pMDIs for our patients is about to be switched off. IRIS calls for greener next generation propellants (HFA-152a and HFO-1234ze) used in pMDIs to be excluded from the EU F-gas regulation and the proposed PFAS restriction. https://bit.ly/3OxQ2ry Globally, more than 650 million children and adults live with COPD or asthma, 48% of whom depend upon pressurised metered-dose inhalers (pMDIs) to deliver their inhaled medication [1, 2]. Inhaler choice is key to the effective management of these chronic respiratory diseases. Patient capability, engagement and satisfaction are important determinants when considering device selection and adherence [3]. It is, therefore, important to prescribe the “right” device to the appropriate patient. pMDIs deliver essential medications, as defined by the World Health Organization, and often are the only choice for some of the most vulnerable populations, including children <10 years old, those with more severe lung disease or suffering from acute attacks of breathlessness, and people who live in low- and middle-income countries (LMICs) [4].
The use of ultrasound (US) to guide percutaneous thoracic interventions improves safety and effectiveness of procedures and leads to reduced healthcare costs. A taskforce was convened to produce a statement on various clinical aspects of these procedures. The taskforce included respiratory physicians and nurses, thoracic surgeons, radiologists, and patient representatives. The statement covers the following procedures: thoracentesis, chest tube/indwelling catheter, medical thoracoscopy, and percutaneous biopsies of lung, pleura, mediastinum and cervical lymph nodes. Systematic searches were carried out for 18 PICO questions under five major topics to inform the writing of the statement. Narrative synthesis of the evidence from relevant literature is presented for each topic. Surveys and interviews with patients who underwent US-guided interventions were conducted to explore patient perspectives. Review of evidence is presented on: the use of US-guided interventions in diagnostic and treatment pathways for pleural and thoracic diseases (Section 1), comparative data on type/size of biopsy, chest tube size and disease outcome, optimal settings for procedures and portable ultrasound (Section 2), US specific methodology and association with outcomes, real-time US guidance for different interventions and contrast-enhanced US in procedure guidance (Section 3), diagnostic yield/treatment success and complications (Section 4) and training requirements (Section 5). Major themes emerging from patient surveys and interviews are presented in Section 6. Recommendations for future research conclude the statement. The use of US to guide percutaneous thoracic procedures is reported to show higher success and lower complication rates in the reviewed evidence. Further research is needed to better inform the procedural settings, techniques, and training.
Fibrosing interstitial lung diseases (ILDs) encompasses a large number of diverse conditions, the prototype being idiopathic pulmonary fibrosis (IPF), characterized by irreversible progression, accounting for loss of lung function, exercise intolerance, and complications especially acute exacerbation and respiratory failure leading to early mortality. A significant proportion of patients with fibrosing ILDs other than IPF will develop a progressive phenotype comparable to IPF. Progression occurs despite conventional treatment which, depending on the underlying condition, may include close monitoring, antigen eviction, glucocorticoids, immunosuppressive therapy, and pulmonary rehabilitation. Progressive pulmonary fibrosis (PPF) has a disease course similar to IPF, with worsening respiratory symptoms, decline in lung function, impairment of quality of life, and premature death. In 2019, a phase III trial demonstrated that treatment with the tyrosine kinase inhibitor nintedanib halves disease progression as measured by a decline in forced vital capacity over one year, and contributed to the validation of the PPF concept. In the 2022 international clinical practice guideline, nintedanib received a conditional recommendation to treat patients with PPF. In 2025, it was demonstrated that the phosphodiesterase 4B inhibitor nerandomilast further reduces disease progression in patients with PPF. Other smaller trials have suggested that pirfenidone may also benefit patients with PPF. Several newer compounds are currently being developed for both IPF and PPF. As a diagnosis of PPF identifies patients with fibrotic disease progression, early identification is warranted for the timely initiation of antifibrotic therapy, consideration of lung transplantation if eligible, and holistic care.
Lymphangioleiomyomatosis (LAM) is a rare, destructive lung disease caused by mutations in TSC1 or TSC2, leading to mTORC1 hyperactivation. While mTOR inhibitor sirolimus, the only FDA approved drug for this disease, stabilizes lung function in most LAM patients, the drug does not eliminate LAM cells, underscoring a critical gap in our understanding of the tumor microenvironment and cellular heterogeneity that drive disease progression. This study provides the first comprehensive multiomics atlas of the human LAM niche, integrating single-cell/nucleus RNA-seq, single-nucleus ATAC-seq, and spatial transcriptomics to deconvolute its complex architecture. We elucidate LAM cellular heterogeneity by identifying three distinct subtypes: the canonical, uterine smooth muscle-like, mTORC1-hyperactive LAMCORE1; a novel, fibroblast-like LAMCORE2 subtype with potent extracellular matrix (ECM) remodeling activity; and LAMCORE3, a substate of LAMCORE1 that shares LAM and myogenic signatures but is characterized by a lower transcriptional activity and specific functional enrichment in protein translation.Our analysis reveals the transcriptomic heterogeneity of the LAM subtypes, orchestrated by distinct transcriptional drivers and networks. Furthermore, we uncover spatially resolved LAM-associated fibroblast (LAF) states, LAF-seed and LAF-niche, that orchestrate TGF-β signaling, ECM deposition and remodeling, and niche expansion. Spatial mapping uncovers a structured ecosystem where LAMCORE1 cells form a central core enmeshed with the lymphatic endothelium, which is surrounded by LAFs, LAMCORE2 cells, and reprogrammed immune and epithelial cells. Findings were validated through multimodal imaging technologies. Present work advances the field by providing the first high-resolution blueprint of the LAM niche microenvironment, revealing novel cell states and crosstalk that identify promising therapeutic targets.
Bronchiectasis and diabetes commonly coexist and are associated with immune dysfunction and increased susceptibility to infection. Although diabetes is associated with worse prognosis in cystic fibrosis-related bronchiectasis, data are scarce for its impact on non-cystic fibrosis bronchiectasis. This study aimed to characterise the impact of diabetes on clinical outcomes and microbial and inflammatory profiles in patients with bronchiectasis. This analysis comprised data from the European Bronchiectasis Registry (EMBARC), Respiratory Research Network of India (EMBARC-India), Chinese Bronchiectasis Registry (BE-China), and Australian Bronchiectasis Registry (ABR); 30 263 patients with CT-confirmed bronchiectasis in 33 countries were included in the analysis: 16 963 from EMBARC (Jan 12, 2015, to April 12, 2022), 2361 from EMBARC-India plus additional Asian countries (June 1, 2015, to Sept 1, 2017), 10 324 from BE-China (Jan 10, 2020, to March 31, 2024), and 615 from the ABR (March 7, 2016, to Sept 11, 2018). Clinical data were compared between patients with and without diabetes. Long-term outcome data were available in EMBARC and EMBARC-India. Microbiome and inflammatory profiles were characterised in a sub-cohort of EMBARC patients by sputum 16S rRNA sequencing (n=433) and serum Olink (n=479). 2487 (8·2%) of 30 263 patients with bronchiectasis had diabetes. Patients with diabetes had a higher prevalence of comorbidities than those without diabetes, including cardiovascular disorders (53·5% vs 21·8%, p<0·0001), asthma (27·5% vs 21·0%, p<0·0001), and chronic obstructive pulmonary disease (34·3% vs 19·0%, p<0·0001). Patients with diabetes had more severe disease than those without diabetes, with higher Bronchiectasis Severity Index scores (8 [IQR 5-12] vs 7 [4-10], p<0·0001) and UK Medical Research Council (MRC) dyspnoea scores (p<0·0001) and more hospital admissions in the previous year (p<0·0001). After adjustment for confounders, outcomes were significantly worse in patients with diabetes than in those without diabetes, including more frequent exacerbations (incidence rate ratio [IRR] 1·18 [95% CI 1·09-1·28], p<0·0001), hospital admissions (IRR 1·57 [1·40-1·76], p<0·0001), and higher 5-year mortality (hazard ratio 1·80 [1·53-2·12], p<0·0001). The sputum microbiome was significantly altered in patients with diabetes compared to those without diabetes, with increased isolation of Enterobacteriaceae (p<0·0001), Moraxella catarrhalis (p=0·0035), and Haemophilus influenzae (p=0·046). In serum, Gal-4 and GDF-15, established biomarkers of disease severity and cardiovascular risk in diabetes, were significantly increased in patients with diabetes (Gal-4, p<0·0001; GDF-15, p=0·0019). Patients with diabetes and bronchiectasis are a high-risk population with more severe disease, worse outcomes, increased comorbidities, and increased risk of infections compared with patients without diabetes. These findings support inclusion of diabetes as a risk factor in individualised risk assessments for bronchiectasis. European Respiratory Society, Armata, AstraZeneca, Boehringer Ingelheim, Chiesi, CSL Behring, GSK, Grifols, Insmed, Janssen, Lifearc, Roche, Verona Pharma, Zambon, National Natural Science Foundation of China, Innovation Program of the Shanghai Municipal Education Commission, Program of the Shanghai Municipal Science and Technology Commission, Program of the Shanghai Shenkang Development Center, EU/European Federation of Pharmaceutical Industries and Associations, Innovative Medicines Initiative, and Inhaled Antibiotics in Bronchiectasis and Cystic Fibrosis Consortium.
Bronchiectasis is a heterogeneous chronic airway disease primarily driven by persistent infection, microbial dysbiosis and dysregulated host immunity. While culture-based microbiology has historically informed clinical management, advances in high-throughput sequencing and multi-omic technologies have transformed our understanding of the airway ecosystem, revealing that disease activity is shaped, not only by individual pathogens, but by complex and dynamic host-microbe interactions. Despite the breadth of descriptive microbiome data, translation into clinically actionable diagnostics or therapies has been limited. Importantly, cross-sectional correlations between microbiota and inflammation do not establish cause and effect, underscoring the need to embed host-microbiome profiling within both longitudinal and interventional therapeutic trials. In this review, we critically appraise current microbial and host multi-omics research in bronchiectasis, integrating microbiome studies with host inflammatory, proteomic and immunophenotyping data. We highlight themes emerging across cohorts, including low microbial diversity, pathogen dominance, loss of commensal networks and neutrophil-driven inflammation and discuss how these features align with biological endotypes associated with exacerbations and treatment response. Drawing on lessons from host-directed therapeutic successes, we examine translational roadblocks limiting microbiome-guided care. We further review emerging microbiome-modulating strategies such as pathogen-specific biologics, bacteriophage therapy, live biotherapeutic products, biofilm-targeting adjuncts and precision antibiotic stewardship. Finally, we propose a roadmap toward microbiome-informed precision medicine through harmonized methodologies, integration of host and microbial biomarkers into clinical trials and embedding multi-omics pipelines within large international registries. Collectively, these advances have the potential to shift bronchiectasis research and clinical management towards rationally designed, precision medicine-driven therapeutic strategies.
In lung cancer, adequate treatment selection relies on accurate diagnosis and staging. Tissue sampling is generally indicated. This guideline explores the role of endosonography via the major airways (EBUS-TBNA) and oesophagus (EUS-FNA). EUS-FNA can also be performed using an EBUS-scope (EUS-B-FNA). Task force members were selected from ERS (European Respiratory Society), ESGE (European Society of Gastrointestinal Endoscopy), and ESTS (European Society of Thoracic Surgeons). Twelve guideline questions were formulated. Systematic literature searches were performed in MEDLINE and Embase (final searches: Apr-2025). GRADE methodology was applied for assessing the certainty of evidence and developing recommendations. In (suspected) non-small cell lung cancer (NSCLC), endosonography is recommended over mediastinoscopy for mediastinal nodal tissue staging. Systematic staging is suggested over targeted staging as the minimal standard. Ideally, combined EBUS-TBNA+EUS(-B)-FNA is performed instead of EBUS-TBNA alone. Add-on mediastinoscopy after a negative endosonography is not recommended. Endosonography is suggested over mediastinoscopy for re-staging after induction therapy. EBUS-TBNA and EUS(-B)-FNA are recommended for centrally located tumours adjacent to the major airways/oesophagus. Both EUS-B-FNA and EUS-FNA are suggested for left adrenal gland analysis. It is suggested that competence is acquired in a simulation-based environment and ensured using valid assessment methods. 21G/22G TBNA needles are considered the standard; there is insufficient evidence to support the structural use of alternative needle sizes/types or cryobiopsy. EBUS-TBNA has high suitability rate for PD-L1 assessment. Endobronchial and oesophageal endosonography provide accurate and minimally invasive tests for the diagnosis and staging of lung cancer.
Viral respiratory infections are the leading trigger of asthma exacerbations and impaired epithelial type I and III interferon responses may contribute to more severe exacerbations. Azithromycin reduces exacerbations clinically, but its effects on epithelial antiviral immunity remain unclear. This study investigated whether azithromycin treatment enhances airway epithelial antiviral responses and modulates alarmin concentration in patients with uncontrolled asthma. In the investigator-initiated, double-blind, placebo-controlled AZIMUNE trial, 40 adults with uncontrolled asthma were randomized (1:1) to azithromycin (500 mg, three times/week) or placebo (500 mg/week) for 12 weeks. Bronchial epithelial cells were obtained via bronchoscopy at baseline and after week 12, and cultured and infected ex vivo with rhinovirus. Protein levels of IFN-β, IFN-λ, alarmins (IL-33 and thymic stromal lymphopoietin (TSLP)), and proinflammatory cytokines were quantified. Azithromycin significantly increased rhinovirus-induced concentration of IFN-β (p=0.047) and IFN-λ (p=0.013) in azithromycin group (n=16) compared with baseline, whereas no change was seen in the placebo group (n=16). Azithromycin treatment also reduced IL-33 concentration (p=0.001), while TSLP levels were unaffected. Clinical outcomes improved numerically in the azithromycin group, but differences versus placebo were not statistically significant. Azithromycin enhances epithelial antiviral immunity and attenuates IL-33 concentration in response to rhinoviral infection in asthma. The dual immunomodulatory effect of azithromycin supports its role as adjunctive therapy to prevent virus-induced exacerbations.
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While high-intensity interval training (HIIT) has shown effectiveness in improving cardiorespiratory fitness (CRF) across various chronic respiratory diseases, its impacts on individuals with post-infectious bronchiolitis obliterans (PIBO) remain unexplored. To assess the effects of a home-based remotely-supervised HIIT programme on CRF, clinical and functional variables in patients with PIBO. Participants of this assessor-blinded, multicentre, randomized controlled trial were individuals with PIBO aged 6 to 20 years. An exercise group (EXE) underwent two 40-min sessions of HIIT remotely supervised in real time per week. Sessions were continued for 16 weeks. The control group (CON) adhered to general physical activity recommendations. The primary outcome was peak oxygen consumption (VO2peak), time to ventilatory threshold (VT1), percentage of VO2 at VT1, and ventilatory equivalent for carbon dioxide, determined via cardiopulmonary exercise testing on a treadmill. Secondary outcomes were lung function (spirometry), muscle strength (dynamometry), functional capacity (30-second Sit-To-Stand test), body mass index, and Saint George Respiratory Questionnaire. Fifty-one PIBO patients were enrolled (EXE=25; CON=26) (mean age 13.3±4.2 years; females 49%; FEV1 -3.56±1.28 (z-score); VO2peak 36.8±8.6 mL.kg-1.min-1). The HIIT intervention resulted in improvements in VO2peak (Δ=3.39; p=0.04), time (min) to VT1 (Δ=1.05; p=0.04), and in the number of repetitions in the 30s-STS (Δ=2.21; p=0.04). No differences were found in the other variables. Our real-time, remotely-supervised HIIT intervention was effective at significantly increasing CRF and functional capacity in children and adolescents with PIBO.
Granulomatous-Lymphocytic Interstitial Lung Disease (GLILD) is a lung disease first described in people affected by common variable immunodeficiency disorders (CVID). Despite growing recognition of GLILD, there is no accepted diagnostic and management guideline, and current practice varies significantly across centres and countries. This clinical practice guideline provides evidence- and consensus-based recommendations on the screening and diagnosis of GLILD in patients with CVID. A panel representing multiple interdisciplinary perspectives convened with methodologists to prioritize clinical questions, review and assess the evidence using GRADE (Grading of Recommendations Assessment, Development and Evaluation) methodology. Evidence-to-Decision frameworks were used to decide on the direction and strength of recommendations. Screening for GLILD is recommended in all adult CVID patients, preferably using high resolution computed tomography. Evaluation should be performed by a multidisciplinary team. Routine lung biopsies are not mandatory but necessary for atypical presentations. As part of the diagnostic process, pulmonary infections should be excluded and lymphocytic alveolitis sought after by means of bronchoalveolar lavage. The severity of lung function impairment should be evaluated using pulmonary function tests including gas transfer assessment. Most of the recommendations are graded as conditional because of low certainty in the evidence regarding health effects. This guideline allows for international homogeneity in the diagnosis of GLILD, thereby paving the way for improved comparability between centers, improving equity in health care for those affected by GLILD and facilitating multicenter research collaborations for future studies.
Ostensibly healthy individuals of different geographic ancestries have appreciably different spirometric volumes for any specific sex, age, and height. Traditionally, ancestry has been felt to be an integral component of prediction formulas for pulmonary function. A more recently stated alternate view is that socioeconomic status is the primary correlate of these differences, in other words that these differences are acquired, not inherent. Adopting this view, in 2023 the American Thoracic Society and European Respiratory Society recommended that all individuals, regardless of ancestry, should have spirometry assessed using a single set of "race-neutral" prediction values produced by weighted averaging of previously-defined ancestral groups. We re-review the literature and couple it with anthropological data to support the conclusion that ancestral differences are primarily inherent and thus should be included in volume prediction equations for healthy individuals. In support of this, we document not only physiological evidence, but also discuss the role of human thoracic morphology in the light of ecogeographic variation that has arisen due to our diverse evolutionary histories.
Paediatric tuberculosis (TB), particularly drug-resistant TB (DR-TB), is associated with significant mortality. However, the global burden of childhood TB remains poorly understood. We analysed incident cases, deaths, and age-standardised incidence and mortality rates among children (0-14 years) with multidrug-resistant/rifampicin-resistant tuberculosis (MDR/RR-TB) and extensively drug-resistant tuberculosis (XDR-TB) using the Global Burden of Disease (GBD) 2021 database. Data were stratified by age, sex, region, country, and HIV/AIDS status. Annual and average annual percentage changes were assessed using joinpoint regression analysis. Secondary analyses compared adult and paediatric TB trends in the End TB era and evaluated the potential impact of the COVID-19 pandemic on childhood TB. Sensitivity analyses were performed using the recently released GBD 2023 database. In 2021, an estimated 32 515 (95% UI: 20 968-51 288) paediatric MDR/RR-TB incident cases and 1193 (806-1814) XDR-TB cases occurred globally, with 5887 (2467-11 332) and 253 (109-508) corresponding deaths, respectively; all estimates were lower than counterfactual projections for 2021 in the absence of COVID-19. Since 2005, age-standardised incidence and mortality rates for MDR/RR-TB and mortality rate for XDR-TB have slowly trended downwards, while their proportional contributions to total incident cases and deaths have increased. Children who are female, younger, from low sociodemographic regions, and HIV-coinfected are disproportionately affected. No significant impact of the End TB Strategy on paediatric TB trends was observed after 2015. Cross-dataset comparisons showed concordant principal findings. The global burden of paediatric DR-TB is substantial, with marked disparities across vulnerable populations and regions. Targeted intervention should be tailored to strategically address regional development status, HIV prevalence, and local health policies.
Clinical trials assessing the management of pneumonia use heterogeneous outcomes, often lacking patient relevance or standardisation. We developed two core outcome sets (COSs) for future clinical trials evaluating interventions in community-acquired pneumonia (CAP) and nosocomial pneumonia (hospital-acquired pneumonia and ventilator-associated pneumonia) to improve the consistency and comparability of evidence. A multistage, multistakeholder process was undertaken, comprising 1) a systematic review of previously used outcomes conducted by our team, 2) qualitative interviews with patients and 3) a two-round online Delphi survey involving 289 participants (patients, relatives and healthcare professionals) from 58 countries. This diverse sample ensured a broad representation of clinical and patient perspectives. Final outcomes were agreed upon through structured voting in two virtual consensus meetings in April 2025. The final COS for CAP includes: treatment success/failure, all-cause mortality, serious adverse events, readmissions (admission for community-based trials), duration of symptoms and time to clinical stability (for hospitalised patients). The nosocomial pneumonia COS includes: treatment success/failure, all-cause mortality, serious adverse events, readmission and need for ventilatory support. The panel suggested measuring mortality at 30 days from study enrolment and readmission at 30 days post-discharge. These COSs, developed by a European Respiratory Society Task Force, provide a standardised framework for outcome selection in pneumonia trials and were informed by broad stakeholder input, including patients. Their use is expected to improve the relevance, quality and comparability of future research in pneumonia.
Obesity is associated with poorer asthma outcomes and an increased risk of exacerbations, but the underlying mechanisms remain incompletely understood. Small airway dysfunction (SAD) may represent a key mechanistic link between excess body weight and adverse asthma outcomes. In this multicenter observational study, adult patients with asthma underwent clinical characterization, spirometry and impulse oscillometry (IOS). SAD was defined using a composite criterion based on peripheral airway resistance (R5-20), reactance area (AX) and the ratio of peripheral to total airway resistance (R5-20)/R5. Associations between body mass index (BMI), SAD and severe asthma exacerbations were assessed using multivariable regression models. Non-linear relationships were explored using generalized additive models and mediation analyses quantified the contribution of SAD to the obesity-exacerbation association. Among 1169 patients, IOS-defined SAD was significantly more prevalent in individuals with BMI≥30 kg·m-2. Increasing BMI was associated with worse oscillometric parameters (p<0.0001), following a non-linear pattern with steeper deterioration beyond BMI values of approximately 28-30 kg·m-2. SAD was independently associated with obesity (adjusted OR 2.11, 95% CI 1.56-2.86) and with severe asthma exacerbations in the previous year (adjusted OR 2.01, 95% CI 1.53-2.65, both p<0.0001). Mediation analyses showed that SAD accounted for 26%-41% of the association between obesity and exacerbation risk (p=0.004 and 0.03). Spirometric indices provided limited additional information. Oscillometry-defined small airways dysfunction (SAD) represents a non-linear functional trait underlying the association between obesity and severe asthma exacerbations, supporting its clinical relevance in obese patients with asthma and identifying SAD as a potential treatable trait.
Mepolizumab reduced blood and sputum eosinophils, but not eosinophil-derived neurotoxin https://bit.ly/4r8x9tb Reply to W. Zhan and co-workers: The recently published MUCOSA trial in the European Respiratory Journal, which evaluated the effects of mepolizumab on objective cough frequency in patients with refractory chronic cough (RCC), has prompted a re-evaluation of the role of eosinophils in cough pathophysiology [1].
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The trade-offs between regulatory preferences, trial success probability, and patient exclusion by eligibility criteria in randomised controlled trials (RCTs) of biologics for severe asthma remain poorly understood. We assessed biologic effectiveness and effect modification by nine RCT-derived criteria in a large real-world cohort of subspecialist-treated patients with severe asthma. CHRONICLE was a multicentre, prospective, noninterventional cohort of US adults (aged ≥18 years) with severe asthma (NCT03373045). We performed a meta-analysis of six RCTs to estimate pooled rate ratios (RRs) for FDA-approved biologics and compared with incidence rate ratios (IRRs) from a self-controlled case-series (SCCS) using CHRONICLE data, analysing severe asthma exacerbation rates during biologic-exposed and unexposed periods. Subgroup analyses examined between-group comparisons (inclusion versus exclusion) across nine RCT-based criteria. Biologics reduced exacerbation rates in both RCT meta-analysis (RR 0.53, 95% CI 0.47-0.60) and real-world SCCS of 480 patients from 85 sites (enrolled February 28, 2018-October 28, 2024) (IRR 0.43, 0.39-0.48). Significant effect modification (ratio of ratios, ratio of IRR, 95% CI), with exclusion as the reference) was observed for smoking history (0.50, 0.38-0.66), exacerbation history (0.49, 0.36-0.65), FeNO (0.63, 0.42-0.92), and BEC (0.65, 0.51-0.82). No significant differences were observed for COPD, bronchiectasis, or FEV1-based criteria, which excluded the most patients in the cohort. Criteria based on elevated type 2 biomarkers, minimal smoking, and exacerbation history enrich trial populations likely to benefit from biologics. Spirometry-based exclusions appear to have limited influence on treatment response, and there is a risk that they unduly restrict generalisability. AstraZeneca.
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Bendopnoea (breathlessness on bending forward) is reported often by patients with pleural effusion, but its prevalence and clinical relevance are unexplored. This study prospectively enrolled unselected patients with pleural effusion. Bendopnoea was assessed by time-to-breathlessness when bending patients forward for up to 60 s (60 s-BT). Post-hoc analyses using a 30-second cut-off were also conducted. Two hundred patients (median age=72 years; 61% male) were included; n=88 underwent therapeutic drainage (median=1.50 [Q1-Q3=1.11-2.47] litres). Effusions were commonly malignant and occupied >25% of hemithorax (74%). Most patients had bendopnoea on the 60 s-BT (56%) and reported it "impacted daily activities" (74%). The estimated median time-to-bendopnoea was 43 (95% CI 30-59) seconds. Bendopnoea was more common with larger pleural effusions on chest radiographs (p=0.0332 and p=0.0217 using 60-second and 30-second cut-offs respectively). Patients with bendopnoea on 60 s-BT were more breathless (median: 48 [22-67] versus 30 [5-54] millimetres (mm) on a 100 mm Visual Analog Scale (VAS), p=0.0002) and shorter 6-minute walk distance (6-MWD, median: 200 [128-333] versus 310 [223-371] metres (m), p=0.0013). Similar relevance was found using a 30-second cut-off.The proportion of patients with bendopnoea on 60 s-BT significantly decreased from 62% to 32% post-drainage, p<0.001. Those with bendopnoea (versus those without) had significantly greater improvement in 6-MWD post-drainage (median 66 [2-101] versus 16 [-40-65] m, p=0.0165). Larger effusion (OR=5.08, 95%CI=1.25-20.66), inverted/flattened hemidiaphragm on ultrasonography (OR=3.93, 95%CI=1.32-11.68 and higher BMI (OR=1.18, 95%CI=1.08-1.28) were associated with bendopnoea (60 s-BT) multivariably. Bendopnoea is a simple and worthwhile symptom to recognise in patients with pleural effusion.