ERJ Open Research最新文献

The carbon footprint of inhalers used by 1314 people with unconfirmed asthma waiting for a GP-requested methacholine test in one centre was estimated to be 22 tons CO₂e. Solutions include ↓BPT wait-time (↓72% CO₂e) and switching MDI to DPI (↓81% CO₂e) https://bit.ly/4dxP7Pd.

Background: Thyroid transcriptional factor-1 (TTF-1) is associated with the development of interstitial lung disease (ILD) and is a mutational target in lung adenocarcinoma with ILD. TTF-1 expression is also associated with the efficacy of pemetrexed-based chemotherapy for nonsquamous nonsmall cell lung cancer (NS-NSCLC). However, the relationship between TTF-1 expression and the efficacy of immunotherapy using programmed cell death 1 inhibitor (PD-1i), especially in lung cancer patients with ILD, remains unclear.

Methods: Medical data of NS-NSCLC patients treated with PD-1i at multiple centres were analysed retrospectively. Patients were divided into those with or without concomitant ILD, with the two cohorts further stratified by TTF-1 expression.

Results: The study population included 62 NS-NSCLC patients, 34 with and 28 without ILD. Median progression-free survival (PFS) during PD-1i treatment was significantly shorter in TTF-1-negative than -positive patients (2.0 versus 12.1 months, p=0.004) in the ILD cohort but did not differ significantly in the non-ILD cohort (1.8 versus 2.6 months, p=0.63). Median overall survival (OS) was also significantly shorter in TTF-1-negative than -positive patients in the ILD cohort (14.5 versus 42.5 months, p=0.018) but not in the non-ILD cohort (33.7 versus 37.1 months, p=0.53). Cox regression analyses showed that absence of TTF-1 expression was an independent risk factor for PFS (hazard ratio (HR) 2.75, p=0.024) and OS (HR 2.81, p=0.012) in the ILD cohort.

Conclusion: TTF-1 expression in NS-NSCLC patients with ILD may predict prognosis when treated with PD-1i.

Background: Endothelial dysfunction was shown to contribute significantly to the elevated cardiovascular risk observed in the general population. However, the relationship between endothelial dysfunction and subclinical myocardial injury in obstructive sleep apnoea (OSA) patients remains unclear.

Methods: This cross-sectional study recruited 165 consecutive male patients diagnosed with OSA. All participants underwent overnight polysomnography to confirm the diagnosis and assess the severity of OSA. Subclinical myocardial injury was evaluated using high-sensitivity cardiac troponin I (hs-cTnI) measurements, while endothelial dysfunction was assessed through the peripheral arterial tonometry.

Results: Endothelial dysfunction was present in 80 (48.5%) of the subjects and hs-cTnI was detectable in 147 (89.1%) of the participants. When compared with OSA patients without endothelial dysfunction, those with endothelial dysfunction exhibited significantly lower percentages of hypertension (23.8% versus 43.5%, p=0.007) and abdominal obesity (76.3% versus 88.2%, p=0.043). Patients with endothelial dysfunction frequently manifest a lower apnoea-hypopnoea index and oxygen desaturation index. Despite comparable median hs-cTnI levels, a higher proportion of subjects with detectable hs-cTnI levels was observed among those with endothelial dysfunction (95% versus 83.5%, p=0.018). Logistic regression analysis indicated that endothelial dysfunction was significantly associated with a detectable level of hs-cTnI after adjustment for multiple confounders.

Conclusions: In male OSA patients, endothelial dysfunction appears to be potentially correlated with an increased risk of subclinical myocardial injury, as evidenced by the higher prevalence of detectable hs-cTnI levels. Further investigations are warranted to elucidate the role of endothelial dysfunction in predicting future cardiovascular mortality in this population.

Introduction: The definition of pulmonary hypertension (PH) was recently changed and led to a new subset of PH patients with mildly impaired pulmonary haemodynamics, characterised by a mean pulmonary artery pressure (mPAP) of 21-24 mmHg and with a pulmonary vascular resistance (PVR) >2 WU. We evaluated the association of PH-targeted therapy and outcome in mild precapillary PH using the PVRI GoDeep meta-registry.

Methods: All patients with mild precapillary PH (mPAP 21-24 mmHg, pulmonary arterial wedge pressure ≤15 mmHg and PVR >2 WU) diagnosed with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH) were enrolled. Patients were considered as "treated" if PH-targeted therapy was initiated within 6 months of diagnostic right heart catheterisation. Various statistical models, including in-depth sensitivity analyses, were used to examine the association between PH-targeted therapy and transplant-free survival.

Results: 132 patients with group 1 or group 4 mild PH were identified, of whom 34 patients received PH-targeted therapy. There were no differences in baseline haemodynamics between untreated and treated groups, whereas treated patients suffered more frequently from renal comorbidities and required long-term oxygen treatment more often. Most prescribed were phosphodiesterase-5-inhibitors. PH-targeted therapy was associated with significantly higher survival rates. Cox-regression analyses revealed significantly reduced hazard ratios among treated patients adjusted for various confounders. Subgroup analyses in PAH (n=78) similarly indicated higher survival rates and reduced hazard ratios in treated patients.

Conclusion: PH-targeted therapy may be associated with improved survival in PAH and CTEPH patients with mild PH. To mitigate potential bias of the results due to the retrospective study design, randomised controlled trials are warranted.

Background: Low-grade systemic inflammation is linked to abnormal spirometry. Impulse oscillometry (IOS) is sensitive in detecting peripheral airway dysfunction, but inflammation in relation to IOS is poorly studied. The objectives of the present study were to analyse associations between C-reactive protein (CRP), blood eosinophils (B-Eos), blood neutrophils (B-Neu), blood lymphocytes (B-Lym), blood leukocytes (B-Leu), blood monocytes (B-Mono) and IOS.

Methods: Blood biomarkers and IOS were assessed in 10 602 adults (aged 50-65 years) within the Swedish CardioPulmonary bioImage Study (SCAPIS). Upper tertiles for CRP (>1.80 mg·L^-1), B-Eos (>0.20 10⁹·L^-1), B-Neu (>3.40 10⁹·L^-1), B-Lym (>2.00 10⁹·L^-1), B-Leu (>6.10 10⁹·L^-1) and B-Mono (>0.50 10⁹·L^-1) were analysed in relation to the following abnormal IOS indices: resistance at 5 Hz, resistance at 20 Hz, area of reactance, resonant frequency (>95th percentile) and reactance at 5 Hz (<5th percentile), based on healthy, never-smoking SCAPIS participants.

Results: Abnormal IOS was observed in 1715 (16.2%), of which 580 (33.8%) also had abnormal spirometry. Having several blood biomarkers in the upper tertile (1, 2-3 or 4-6 versus 0) was overall associated with abnormal IOS; adjusted odds ratios (OR) and 95% confidence intervals (CI) ranging from 1.19 (1.02-1.38) to 2.27 (1.79-2.89). Furthermore, having 2-3 or more blood biomarkers versus 0 in the upper tertile was overall linked to abnormal IOS in participants with normal spirometry; adjusted OR (95% CI) ranging from 1.43 (1.17-1.75) to 1.75 (1.29-2.38).

Conclusions: Low-grade systemic inflammation was related to abnormal IOS and appeared consistent even when participants had normal spirometry.

In people with chronic respiratory disease undertaking pulmonary rehabilitation, approximately 1/3 developed an exacerbation; however, there was no difference between telerehabilitation and centre-based group settings, and no effect on programme completion https://bit.ly/4bXe2dy.

Background: Lung function outcomes in pulmonary Langerhans cell histiocytosis (PLCH) patients are variable and difficult to predict. Our goal was to identify different forced expiratory volume in 1 s (FEV₁) trajectories in these patients during long-term follow-up.

Methods: All newly diagnosed adult PLCH patients seen between January 2004 and April 2018 were eligible for inclusion in our prospective cohort. The primary end-point was the identification of FEV₁ trajectories using a joint latent class model for longitudinal and time-to-event data. Internal validation was performed via bootstrapping.

Results: Among the 191 patients included (mean age of 39±12 years, 59% females, 96% current smokers), who were followed for a median of 5.1 years (interquartile range 3.2-6.0), two FEV₁ trajectories were identified. Patients with trajectory 1 (n=157, 82.2%) were characterised by a normal FEV₁ at diagnosis (mean predicted value (pred) of 95±3%) that remained stable over time (annual variation of 0.2% pred, 95% CI -0.8-0.4). Patients with trajectory 2 (n=34, 17.8%) had a decreased initial FEV₁ (63±7% pred) and an annual decrease of -1.8% pred (-3.4--0.2). Trajectory 2 was associated with increased mortality (hazard ratio 9.46, 95% CI 1.24-72.2; p=0.03).

Conclusions: FEV₁ remained stable in most PLCH patients, but the subgroup of patients that experienced a significant decrease in FEV₁ over time had a poorer prognosis. These patients should be closely monitored for early therapeutic intervention. These results need to be confirmed in an external validation cohort.

ERJ Open Research has reached an important milestone: its 10th anniversary. The journal remains dedicated to fostering innovation, collaboration and mentorship in the decade ahead. https://bit.ly/3PS6UXk.

Background: The ECLIPSE study was a large, international, prospective, controlled, observational study that included COPD patients (Global Initiative for Chronic Obstructive Lung Disease (GOLD) grades 2-4), as well as smoking and non-smoking participants with normal spirometry, aged 40-75 years, who were followed-up regularly for 3 years. Here we sought to contrast the clinical and biological characteristics of young COPD versus controls of similar age and older COPD patients included in ECLIPSE.

Methods: We compared 106 young (<50 years) and 488 old (>70 years) COPD patients, as well as 119 young smokers and 92 nonsmoker controls (<50 years) with normal spirometry.

Results: Young COPD patients: 1) were more symptomatic than young controls, often reported a family history of chronic bronchitis, emphysema and asthma, as well as a personal history of asthma and bronchitis, and suffered from a similar disease burden to older patients; 2) were at higher risk of substantial forced expiratory volume in 1 s decline over time; and 3) had reduced serum levels of CC16 (a lung-derived anti-inflammatory protein that relates to lung damage) and, at the same time, reduced pro-inflammatory markers compared to older COPD patients.

Conclusions: Young COPD patients suffer from significant disease burden, display an altered biomarker and disease progression profile reflected by an accelerated risk of lung function decline highlighting the need for early life diagnosis, prevention approaches and treatment.