Lung最新文献

Background: Hemoptysis, the expectoration of blood from the lower respiratory tract, varies in severity and necessitates effective management to mitigate morbidity. Traditional treatments include bronchial artery embolization and pharmacological approaches. Tranexamic acid (TXA), an antifibrinolytic agent known for its efficacy in reducing bleeding during surgery and trauma, is being explored for its efficacy in treating Hemoptysis via both intravenous and inhalational routes. Inhalational administration has garnered interest because of its targeted action and minimal systemic effects. This study aimed to assess the effectiveness of inhalational TXA in nonmassive hemoptysis.

Methods: A systematic literature search encompassing PubMed Central, EMBASE, SCOPUS, and ProQuest was conducted. Randomized controlled trials (RCTs) and observational studies assessing the effectiveness of inhalational tranexamic acid for nonmassive hemoptysis were included. Comparative intervention effect estimates from meta-analyses are reported as pooled odds ratios and pooled mean differences with 95% confidence interval (CI).

Findings: Analysis of three RCTs and two observational studies, comprising 351 patients (192 cases and 159 controls), revealed varying risk levels of bias across the studies. Nebulized tranexamic acid was 3.85 times more likely to achieve hemoptysis cessation than alternative treatments across all RCTs. Moreover, patients receiving nebulized tranexamic acid required fewer (43%) pulmonary interventional procedures than those receiving other treatments. Despite showing a trend towards reducing posttherapy bleeding (20 ml less), conclusive results were hindered by wide CI, necessitating further investigation.

Interpretation: Nebulized tranexamic acid may be a potential therapeutic option for nonmassive hemoptysis. While our analysis suggests its potential benefits in halting bleeding and reducing the need for invasive procedures, the quality of the available evidence is limited due to the risk of bias and study limitations. This underscores the necessity for additional randomized controlled trials with larger sample sizes and rigorous study designs to strengthen evidence and optimize clinical utility.

Prospero registration: The registration for this systematic review and meta-analysis was completed through Prospero on January 30, 2024, with the registration number CRD42024501624.

Purpose: Electronic noses (eNose) and gas chromatography mass spectrometry (GC-MS) are two important breath analysis approaches for differentiating between respiratory diseases. We evaluated the performance of a novel electronic nose for different respiratory diseases, and exhaled breath samples from patients were analyzed by GC-MS.

Materials and methods: Patients with lung cancer, pneumonia, structural lung diseases, and healthy controls were recruited (May 2019-July 2022). Exhaled breath samples were collected for eNose and GC-MS analysis. Breathprint features from eNose were analyzed using support vector machine model and leave-one-out cross-validation was performed.

Results: A total of 263 participants (including 95 lung cancer, 59 pneumonia, 71 structural lung disease, and 38 healthy participants) were included. Three-dimensional linear discriminant analysis (LDA) showed a clear distribution of breathprints. The overall accuracy of eNose for four groups was 0.738 (194/263). The accuracy was 0.86 (61/71), 0.81 (77/95), 0.53 (31/59), and 0.66 (25/38) for structural lung disease, lung cancer, pneumonia, and control groups respectively. Pair-wise diagnostic performance comparison revealed excellent discriminant power (AUC: 1-0.813) among four groups. The best performance was between structural lung disease and healthy controls (AUC: 1), followed by lung cancer and structural lung disease (AUC: 0.958). Volatile organic compounds revealed a high individual occurrence rate of cyclohexanone and N,N-dimethylacetamide in pneumonic patients, ethyl acetate in structural lung disease, and 2,3,4-trimethylhexane in lung cancer patients.

Conclusions: Our study showed that the novel eNose effectively distinguishes respiratory diseases and holds potential as a point-of-care diagnostic tool, with GC-MS identifying candidate VOC biomarkers.

Purpose: This study examined the concavity (angle β, central and peripheral concavity) of the descending limb of the maximal expiratory flow-volume (MEFV) curves to reflect various ventilatory defects, including obstructive, restrictive, or mixed patterns.

Methods: We conducted a cross-sectional study collecting spirometry data from a healthcare center and a tertiary hospital between 2017 and 2022, with additional raw flow-volume curve data from primary healthcare institutions in 2023. We analyzed differences in concavity between spirometric patterns. Receiver operating characteristic curves were used to assess the predictive power of concavity for spirometric patterns. The relationship among concavity indices was examined.

Results: This study included 18,938 cases, with 22% exhibiting an obstructive pattern. The dataset comprised 14,868 cases for training, 3716 cases for validation, and 354 cases for testing. In the training set, the mean angle β were 180.3 ± 12.4 and 148.5 ± 12.7 degrees in normal and obstruction patterns. The angle β had an AUC of 0.970 (95% CI 0.966-0.973) for identifying normal and obstructive patterns, with a cut-off value of 163.0 degrees. In the validation set, out of 2311 cases with a normal forced vital capacity (FVC), 3.1% cases exhibited a Z-score of forced expiratory volume in 1 s to FVC ratio (FEV₁/FVC) ≥  - 1.645 but an angle β < 163.0 degrees. In testing set, a correlation coefficient of - 0.96 and - 0.79 was found between the angle β and the central or peripheral concavity.

Conclusion: The concavity of the descending limb of MEFV curves may be crucial in identifying spirometric patterns.

Background: The antibiotic resistance of Pseudomonas aeruginosa (PA) is increasingly severe in bronchiectasis patients. However, there is currently a lack of research on the clinical outcomes of carbapenem-resistant PA (CRPA) isolation in hospitalized exacerbations of bronchiectasis (HEB) patients. We investigated the incidence, risk factors, and clinical outcomes of PA and CRPA isolation in HEB patients.

Methods: This was an observational, retrospective cohort study of PA and CRPA isolated from sputum or bronchoalveolar lavage fluid cultures of HEB patients from January 1, 2018 to December 31, 2022. The primary outcomes were respiratory failure, mechanical ventilation, and length of hospital stay. The incidence, risk factors, and clinical outcomes of PA and CRPA isolation were analyzed using multivariate logistic and Poisson regression.

Results: Among 1,286 patients, the prevalence of PA, CRPA, and multi-drug resistant PA isolation was 20.61% (n = 265), 3.81% (n = 49), and 5.83% (n = 75), respectively. CRPA isolation was associated with an increased risk for respiratory failure (adjusted odds ratio (aOR) 2.56; 95% confidence interval (CI) [1.29, 5.11]; p = 0.007), mechanical ventilation (aOR 3.65; 95% CI [1.50, 8.92]; p = 0.004), and length of hospital stay (Coefficient (Coef) 0.27; 95% CI [0.18,0.35]; p < 0.001) compared to non-CRPA. Antibiotic treatment decreased the risk of respiratory failure (aOR 0.37; 95% CI [0.17, 0.80]; p = 0.011), mechanical ventilation (aOR 0.36; 95% CI [0.13, 0.99]; p = 0.047), and length of hospital stay (Coef - 0.23; 95% CI [- 0.33, - 0.14]; p < 0.001).

Conclusions: CRPA isolation was identified in more severe bronchiectasis patients and significantly increased the risk of respiratory failure, mechanical ventilation and length of hospital stay, while antibiotic treatment reduced this risk.

Purpose: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrotic lung disorder characterized by dry cough, fatigue, and exacerbated dyspnea. The prognosis of IPF is notably unfavorable, becoming extremely poor when the disease advances acutely. Effective therapeutic intervention is essential to mitigate disease progression; hence, early diagnosis and treatment are paramount. When high-resolution computed tomography (HRCT) reveals usual interstitial pneumonia (UIP), a diagnosis of IPF can be established. However, when HRCT fails to conclusively confirm IPF, the diagnostic pathway becomes intricate and necessitates a multidisciplinary approach involving clinicians, radiologists, and pathologists. Consequently, the objective of this study was to investigate new diagnostic approaches through bronchoalveolar lavage (BAL) analysis.

Methods: BAL is a commonly utilized diagnostic tool for interstitial lung diseases. We review the application of bronchoalveolar lavage (BALF) in idiopathic pulmonary fibrotic disease, emphasizing that the cellular and solute composition of the lower respiratory tract offers valuable insights.

Results: This review delineates the advancements in diagnosing IPF cases that remain indeterminate via HRCT, leveraging BALF analysis. In contrast to surgical lung biopsy, BAL is minimally invasive and offers potential diagnostic utility through the identification of specific BALF biomarkers.

Conclusion: Augment the clinical diagnostic armamentarium for IPF, particularly in scenarios where HRCT findings are inconclusive.

Purpose: Patients with chronic lower respiratory diseases (CLRD) are at a higher risk of lung cancer. Less is known regarding how the risk of CLRD-associated lung cancer death might have changed on a national scale over the past 20 years across demographic and regional groups.

Methods: We calculated age-adjusted mortality rates (AAMR) for lung cancer death among people with CLRD using 1999-2020 data from the CDC WONDER multiple cause of death database. Rates were compared between demographic groups and time periods.

Results: Rates of lung cancer death among people with CLRD were highest among White Americans compared to other racial groups. Elevated rates of lung cancer death were seen among men (AAMR = 25.054, 95% CI: 24.960-25.148) and those aged 65 + (AAMR = 44.776, 95% CI: 44.638-44.913) compared to their counterparts. Rates were higher in the Midwest (AAMR ratio = 1.410, 95% CI: 1.401-1.418) and the South (AAMR ratio = 1.290, 95% CI: 1.282-1.298) compared to the Northeast. Rates were elevated in rural areas (AAMR ratio = 1.444, 95% CI: 1.438-1.451). Between 1999 and 2004 and 2016-2020, the AAMR of CLRD-associated lung cancer death decreased from 21.647 (95% CI: 21.528-21.765) to 17.221 (95% CI: 17.123 - 17.318). Rates decreased over time across demographic groups.

Conclusion: CLRD-associated lung cancer deaths significantly decreased in the United States between 1999 and 2020. Despite this progress, White people, men, older adults (65 +), and people in rural areas continue to experience higher CLRD-associated lung cancer mortality rates than their counterparts.

Purpose: This study investigated the efficacy and underlying mechanism of the mitochondrial fusion promoter M1 in mitigating cigarette smoking (CS)-induced airway inflammation and oxidative stress both in vitro and in vivo models.

Methods: Cigarette smoke extract (CSE)-treated airway epithelial cells (BEAS-2B) and CS-exposed mice were pretreated with M1, followed by the measurement of proinflammatory cytokines, oxidative stress, mitochondrial fusion proteins (MFN2 and OPA1) and fission proteins (DRP1 and MFF). Molecular pathways were elucidated through transcriptomic analysis and Western blotting.

Results: M1 pretreatment in CSE-treated cells significantly reduced the release of inflammatory cytokines (interleukin (IL)-6, IL-8 and tumor necrosis factor (TNF)-α); reduced malondialdehyde (MDA) and reactive oxygen species (ROS) levels; increased superoxide dismutase (SOD) activity; protected mitochondrial function by increasing the expression of mitochondrial fusion proteins (MFN2 and OPA1) and decreasing the expression of mitochondrial fission proteins (DRP1 and MFF). M1 attenuated CS-induced lung histologic damage and mucus hypersecretion in mice, relieved high oxidative stress and reduced the release of IL-6 and IL-8 in BALF. Similarly, it also protected mitochondrial function by regulating the CS-induced imbalance of mitochondrial dynamic proteins. Transcriptome sequencing and Western blotting showed that M1 inhibited CSE- or CS-induced activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB/AKT) signaling pathway.

Conclusion: M1 plays a protective role in inflammation, oxidative stress and mitochondrial dynamics dysfunction caused by CS by inhibiting the PI3K-AKT signaling pathway; thus, it has therapeutic potential for the treatment of CS-induced airway disorders.

Introduction: Early detection of cardiac sarcoidosis (CS) is crucial due to its association with severe complications such as ventricular arrhythmias, heart failure, and sudden cardiac death. Advanced imaging techniques like cardiac magnetic resonance imaging (CMR) and 18F-Fluorodeoxyglucose Positron Emission Tomography/Computed Tomography (FDG-PET/CT) are effective in detecting CS but not easily accessible. The optimal method for selecting patients for advanced screening remains uncertain.

Methods: In this retrospective cohort study, all extracardiac sarcoidosis patients screened for CS were reviewed. CS was defined as a multidisciplinary team (MDT) consensus diagnosis. Univariate and multivariate binary logistic regressions were used to identify factors associated with CS, assessing their diagnostic performance, and integrating them into a diagnostic model.

Results: Out of 354 patients (average age 51.5 years, 52.5% male), 18.4% were diagnosed with CS. In our cohort, male gender, a QRS duration > 120 ms, and nsVT on Holter monitoring were identified as significant markers associated with CS. Combining age, gender, AV-block or QRS > 120ms on ECG, and nsVT on Holter monitoring provided the highest diagnostic accuracy (AUC of 0.82). Cardiac biomarkers NT-proBNP and troponin T did not improve the diagnostic performance.

Conclusion: In our cohort, male gender, a QRS duration > 120 ms, and nsVT on Holter monitoring were identified as significant markers associated with the presence of cardiac sarcoidosis. These clinical markers may aid in selecting sarcoidosis patients for screening with advanced cardiac imaging, potentially leading to earlier detection and management of the disease.

Introduction: An easy-to-implement and accurate lung function assessment tool for preterm infants is crucial to manage lifelong respiratory morbidities. We aimed to determine which pulmonary function parameters in preterm infants can predict the trajectory of airway obstruction and asthma development after 4 years of age.

Methods: We evaluated 52 preterm infants who had undergone both tidal breathing flow-volume loop (TBFVL) and multiple-breath washout (MBW) analyses in infancy and spirometry after the age of 4 years. We evaluated the association between pulmonary function parameters in infancy and childhood and the pulmonary function trajectory until 13 years of age and compared the changes in this trajectory according to pulmonary function parameters in infancy.

Results: Time to peak expiratory flow/expiratory time (T_PEF/T_E) in infancy was associated with FEV₁, FEF_25-75, and dysanapsis ratio in childhood and differed according to level of airway obstruction assessed by FEV₁, FEV₁/FVC, and FEF_25-75, an asthma development. T_PEF/T_E was a significant predictive factor for airway obstruction and asthma after 4 years of age, after adjusting for sex, extreme prematurity, duration of supplementary oxygen and mechanical ventilation, and recurrent wheezing during infancy. In premature infants with lower T_PEF/T_E, subsequent pulmonary function parameters remained low until 13 years of age.

Conclusion: In preterm infants, T_PEF/T_E could be useful to predict airway obstruction and asthma after 4 years of age and even a lower pulmonary function trajectory until 13 years of age. This information may help clinicians to provide lifelong care for pulmonary morbidity in children and adolescents born preterm.