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Journal of the Belgian Society of... 2024The air crescent (AC) is a common radiological sign. Even if its commonest aetiology remains pulmonary aspergillosis, various other causes have been described. In this...
The air crescent (AC) is a common radiological sign. Even if its commonest aetiology remains pulmonary aspergillosis, various other causes have been described. In this study, we report four rare causes of ACs seen on chest radiographs that haven't been described in the literature. The differential diagnosis of an air crescent sign on chest radiographs includes oesophageal bezoar, interstitial lung emphysema, central bronchial stenosis and perforated emphysematous cholecystitis.
PubMed: 38911284
DOI: 10.5334/jbsr.3583 -
BMC Pulmonary Medicine Jun 2024Interstitial pneumonia and emphysema may complicate patients with lung cancer. However, clinical significance of trivial and mild pulmonary abnormalities remains...
Deleterious impact of trivial to severe interstitial pneumonia and emphysema on mortality and acute exacerbation of interstitial pneumonia in patients with lung cancer: a retrospective cohort study.
BACKGROUND
Interstitial pneumonia and emphysema may complicate patients with lung cancer. However, clinical significance of trivial and mild pulmonary abnormalities remains unclear. In this study, we aimed to investigate whether trivial and mild interstitial pneumonia and emphysema, in addition to their advanced forms, impact the prognosis and lead to acute exacerbation of interstitial pneumonia (AEIP) in patients with lung cancer.
METHODS
This retrospective cohort study was conducted at a tertiary hospital and included patients with lung cancer. Computed tomography images were evaluated using the interstitial lung abnormality (ILA) score for interstitial pneumonia, which included no ILA, equivocal ILA, ILA, interstitial lung disease (ILD), and the Goddard score for emphysema. Cox analyses were performed using the ILA and Goddard scores as the main explanatory variables, adjusting for multiple covariates.
RESULTS
Among 1,507 patients with lung cancer, 1,033 had no ILA, 160 had equivocal ILA, 174 had ILA, and 140 had ILD. In total, 474 patients (31.5%) exhibited interstitial pneumonia and 638 (42.3%) showed emphysema. The log-rank trend test showed that survival probability was significantly better in patients with no ILA, followed by those with equivocal ILA, ILA, and ILD (P < 0.001). After adjustment, the ILA and Goddard scores remained significant variables for increased hazard ratios (HR) for mortality: no ILA (HR, 1.00: reference), equivocal ILA (HR, 1.31; 95% confidence interval [CI], 1.18-1.46; P < 0.001), ILA (HR, 1.71; 95% CI, 1.39-2.12; P < 0.001), ILD (HR, 2.24; 95% CI, 1.63-3.09; P < 0.001), and Goddard score (HR, 1.03; 95% CI, 1.01-1.06; P < 0.010). Moreover, both scores were associated with increased cause-specific HRs for AEIP.
CONCLUSION
Our results revealed that approximately one-third of patients with lung cancer had interstitial pneumonia when incorporating trivial and mild cases. Because interstitial pneumonia and emphysema, ranging from trivial to severe, significantly impact mortality and AEIP in patients with lung cancer, we should identify even trivial and mild cases of these pulmonary abnormalities among patients with lung cancer in addition to the advanced ones.
Topics: Humans; Retrospective Studies; Lung Diseases, Interstitial; Male; Female; Lung Neoplasms; Aged; Middle Aged; Tomography, X-Ray Computed; Pulmonary Emphysema; Prognosis; Disease Progression; Severity of Illness Index; Proportional Hazards Models
PubMed: 38909185
DOI: 10.1186/s12890-024-03105-7 -
Frontiers in Medicine 2024Currently, Chronic Obstructive Pulmonary Disease (COPD) has a high impact on morbidity and mortality worldwide. The increase of CD4+, CD8+ cells expressing NF-κB,...
INTRODUCTION
Currently, Chronic Obstructive Pulmonary Disease (COPD) has a high impact on morbidity and mortality worldwide. The increase of CD4+, CD8+ cells expressing NF-κB, STAT4, IFN-γ and perforin are related to smoking habit, smoking history, airflow rate, obstruction and pulmonary emphysema. Furthermore, a deficiency in CD4CD25Foxp3 regulatory T cells (Tregs) may impair the normal function of the immune system and lead to respiratory immune disease. On the other hand, the anti-inflammatory cytokine IL-10, produced by Treg cells and macrophages, inhibits the synthesis of several pro-inflammatory cytokines that are expressed in COPD. Therefore, immunotherapeutic strategies, such as Photobiomodulation (PBM), aim to regulate the levels of cytokines, chemokines and transcription factors in COPD. Consequently, the objective of this study was to evaluate CD4STAT4 and CD4CD25Foxp3 cells as well as the production of CD4IFN- γ and CD4CD25IL-10 in the lung after PBM therapy in a COPD mice model.
METHODS
We induced COPD in C57BL/6 mice through an orotracheal application of cigarette smoke extract. PMB treatment was applied for the entire 7 weeks and Bronchoalveolar lavage (BAL) and lungs were collected to study production of IFN- γ and IL-10 in the lung. After the last administration with cigarette smoke extract (end of 7 weeks), 24 h later, the animals were euthanized. One-way ANOVA followed by NewmanKeuls test were used for statistical analysis with significance levels adjusted to 5% ( < 0.05).
RESULTS
This result showed that PBM improves COPD symptomatology, reducing the number of inflammatory cells (macrophages, neutrophils and lymphocytes), the levels of IFN-γ among others, and increased IL-10. We also observed a decrease of collagen, mucus, bronchoconstriction index, alveolar enlargement, CD4+, CD8+, CD4+STAT4+, and CD4+IFN-γ+ cells. In addition, in the treated group, we found an increase in CD4+CD25+Foxp3+ and CD4+IL-10+ T cells.
CONCLUSION
This study suggests that PBM treatment could be applied as an immunotherapeutic strategy for COPD.
PubMed: 38903812
DOI: 10.3389/fmed.2024.1347517 -
Inflammation and Regeneration Jun 2024Tobacco smoking causes pulmonary inflammation, resulting in emphysema, an independent risk factor for lung cancer. Induction of insulin-like growth factor 2 (IGF2) in...
BACKGROUND
Tobacco smoking causes pulmonary inflammation, resulting in emphysema, an independent risk factor for lung cancer. Induction of insulin-like growth factor 2 (IGF2) in response to lung injury by tobacco carcinogens, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol and polycyclic aromatic hydrocarbon benzo[a]pyrene in combination (NB), is critical for the proliferation of alveolar type 2 cells (AT2s) for lung repair. However, persistent IGF2 overexpression during NB-induced severe injury results in hyperproliferation of AT2s without coordinated AT2-to-AT1 differentiation, disrupting alveolar repair, which leads to the concurrent development of emphysema and lung cancer. The current study aims to verify the role of IGF2 signaling in the associated development of emphysema and cancer and develop effective pharmaceuticals for the diseases using animal models that recapitulate the characteristics of these chronic diseases.
METHODS
The pathogenesis of pulmonary emphysema and cancer was analyzed by lung function testing, histological evaluation, in situ zymography, dihydroethidium staining, and immunofluorescence and immunohistochemistry analyses utilizing mouse models of emphysema and cancer established by moderate exposure to NB for up to seven months.
RESULTS
Moderate NB exposure induced IGF2 expression in AT2s during the development of pulmonary emphysema and lung cancer in mice. Using AT2-specific insulin receptor knockout mice, we verified the causative role of sustained IGF2 signaling activation in AT2s in emphysema development. IGF2-targeting strategies, including voltage-dependent calcium channel blocker (CCB) and a neutralizing antibody, significantly suppressed the NB-induced development of emphysema and lung cancer. A publicly available database revealed an inverse correlation between the use of calcium channel blockers and a COPD diagnosis.
CONCLUSIONS
Our work confirms sustained IGF2 signaling activation in AT2s couples impaired lung repair to the concurrent development of emphysema and cancer in mice. Additionally, CCB and IGF2-specific neutralizing antibodies are effective pharmaceuticals for the two diseases.
PubMed: 38902841
DOI: 10.1186/s41232-024-00344-3 -
International Journal of Chronic... 2024Cigarette smoking is the most recognized risk factor of chronic obstructive pulmonary disease (COPD) in China. However, there are no studies analyzing the impact of... (Comparative Study)
Comparative Study
PURPOSE
Cigarette smoking is the most recognized risk factor of chronic obstructive pulmonary disease (COPD) in China. However, there are no studies analyzing the impact of different smoking behaviors on pulmonary function and pulmonary hypertension (PH) among Chinese male patients with COPD.
PATIENTS AND METHODS
Chinese male smokers with COPD performed pulmonary function tests. Clinical characteristics, smoking behavior features, spirometry and echocardiographic results were compared between the two groups stratified by initial smoking age (18 years old) or complicated PH.
RESULTS
The early-smoking group had more respiratory symptoms, more severe smoking behavior, worse pulmonary function with lower FEV1%pre (38.5% vs 70.2%) and FEV1/FVC% (47.5% vs 63.8%), and higher systolic pulmonary artery pressure (sPAP: 38.6 vs 33.9 mmHg) than the late-smoking group. Initiating smoking before adulthood was an independently contributing factor of ventilatory dysfunction and Global Initiative for Obstructive Lung Disease (GOLD) stage escalation. It also had a significant interaction with long smoking duration (≥30 years), characterized by markedly decreased lung volumes (VC%pre: 64.0% vs 84.5%), impaired diffusing capacity (DLCO%pre: 58.0% vs 76.8%) and severe emphysema (RV/TLC%pre: 145.2% vs 130.2%). COPD patients complicated with PH exhibited worse ventilatory function (FEV1%pre: 43.2% vs 56.2%), impaired diffusion capacity (DLCO%pre: 56.7% vs 77.1%) and decreased lung volume (VC%pre: 67.67% vs 75.38%). Both severe smoking behaviors and impaired pulmonary function had close correlations with sPAP.
CONCLUSION
The early-smoking group exhibited predominantly ventilation dysfunction and had complex interactions with long smoking duration to further affect lung volume and diffusion capacity. Different smoking behaviors influenced variations of pulmonary dysfunction and comorbid PH in patients with COPD.
Topics: Humans; Male; Pulmonary Disease, Chronic Obstructive; Middle Aged; Lung; China; Hypertension, Pulmonary; Risk Factors; Aged; Forced Expiratory Volume; Smoking; Vital Capacity; Spirometry; Pulmonary Diffusing Capacity; Time Factors; Severity of Illness Index; Smokers; Arterial Pressure; Pulmonary Artery; Cross-Sectional Studies; East Asian People
PubMed: 38895046
DOI: 10.2147/COPD.S455323 -
International Journal of Molecular... May 2024Chronic obstructive pulmonary disease (COPD), the major leading cause of mortality worldwide, is a progressive and irreversible respiratory condition characterized by... (Review)
Review
Chronic obstructive pulmonary disease (COPD), the major leading cause of mortality worldwide, is a progressive and irreversible respiratory condition characterized by peripheral airway and lung parenchymal inflammation, accompanied by fibrosis, emphysema, and airflow limitation, and has multiple etiologies, including genetic variance, air pollution, and repetitive exposure to harmful substances. However, the precise mechanisms underlying the pathogenesis of COPD have not been identified. Recent multiomics-based evidence suggests that the plasticity of alveolar macrophages contributes to the onset and progression of COPD through the coordinated modulation of numerous transcription factors. Therefore, this review focuses on understanding the mechanisms and functions of macrophage polarization that regulate lung homeostasis in COPD. These findings may provide a better insight into the distinct role of macrophages in COPD pathogenesis and perspective for developing novel therapeutic strategies targeting macrophage polarization.
Topics: Pulmonary Disease, Chronic Obstructive; Humans; Macrophages, Alveolar; Animals; Macrophage Activation; Macrophages; Lung
PubMed: 38891820
DOI: 10.3390/ijms25115631 -
Cureus Jun 2024Lung cancer, a leading cause of global cancer-related deaths, necessitates the development of innovative diagnostic techniques. Traditional bronchoscopy, while useful,...
Breaking New Ground in Interventional Pulmonology: Integrating Cone Beam CT and Robotic-Assisted Bronchoscopy for High-Risk Pneumothorax in Peripherally Located Solitary Pulmonary Nodules.
Lung cancer, a leading cause of global cancer-related deaths, necessitates the development of innovative diagnostic techniques. Traditional bronchoscopy, while useful, has limitations in diagnosing peripheral pulmonary lesions (PPLs) and carries a higher risk of complications such as pneumothorax. However, the field of interventional pulmonology has seen significant advancements, including the introduction of robotic-assisted bronchoscopy (RAB), cone-beam computed tomography (CBCT), radial endobronchial ultrasound (R-EBUS), and rapid on-site evaluation (ROSE). These advancements have greatly improved the precision of diagnosing high-risk PPLs. This report presents the case of a 60-year-old female smoker with chronic obstructive pulmonary disease and extensive centrilobular emphysema, who had a peripherally located high-risk pulmonary nodule. She was successfully diagnosed with metastatic adenocarcinoma using an integrated approach, despite the challenging location of the lesion and high risk of pneumothorax. The integration of RAB with CBCT and augmented fluoroscopy offers a groundbreaking approach for diagnosing and managing difficult-to-reach, high-risk pulmonary nodules, marking a significant stride in the field of interventional pulmonology.
PubMed: 38887749
DOI: 10.7759/cureus.62532 -
Cureus May 2024Chronic obstructive pulmonary disease (COPD), a heterogeneous respiratory disease driven by various genetic and environmental factors, presents significant challenges in... (Review)
Review
Chronic obstructive pulmonary disease (COPD), a heterogeneous respiratory disease driven by various genetic and environmental factors, presents significant challenges in diagnosis and management. Traditional approaches focused on phenotypic classification, but recent paradigms emphasize identifying and addressing treatable traits to personalize treatment strategies. Treatable traits facilitate personalized interventions, optimizing symptom control, and reducing exacerbation risk. Dyspnea and exacerbations, recognized as key traits, guide treatment decisions and follow-up management. Various interventions, including bronchodilators, corticosteroids, and lifestyle modifications, target specific traits like airway inflammation, mucus overproduction, and emphysema. Strategies for assessing and addressing treatable traits during initial encounters and follow-up visits enhance disease monitoring and treatment efficacy. Comprehensive trait assessment demands resources and specialized monitoring, posing barriers to widespread implementation. The lack of standardized protocols and evolving evidence further complicates decision-making and clinical practice. Despite these challenges, the shift toward treatable traits-based management signifies a pivotal advancement in COPD care, emphasizing holistic approaches tailored to individual patient needs. Recognizing and addressing treatable traits offers personalized interventions, enhancing symptom control and disease management. Embracing treatable traits-based approaches holds promise for improving clinical outcomes and enhancing the quality of life for individuals living with COPD.
PubMed: 38882972
DOI: 10.7759/cureus.60423 -
International Journal of Chronic... 2024In recent years, the incidence of chronic obstructive pulmonary disease (COPD) has been increasing year by year, but therapeutic drugs has no breakthrough. The total...
PURPOSE
In recent years, the incidence of chronic obstructive pulmonary disease (COPD) has been increasing year by year, but therapeutic drugs has no breakthrough. The total alkaloid extract from Bulbus (BFP-TA) is widely used in treating lung diseases. Therefore, this study aimed to investigate the protective effect and mechanism of BFP-TA in COPD mice.
METHODS
BFP-TA was prepared by macroporous adsorbent resin, and the material basis of BFP-TA was analyzed by HPLC-ELSD and UHPLC-MS/MS. Then, the COPD mouse model was induced by cigarette smoke (CS) for 12 weeks, administered at weeks 9-12. Subsequently, the body weight, lung-body ratio, pulmonary function, histopathology, and the levels of pro-inflammatory cytokines, matrix metalloproteinases (MMPs) and oxidative stress markers in the serum of mice were determined. The expressions of related protein of EMT and MAPK signaling pathways in the lung tissues of mice were detected by Western blot.
RESULTS
The alkaloid relative content of BFP-TA is 64.28%, and nine alkaloids in BFP-TA were identified and quantified by UHPLC-MS/MS. Subsequently, the animal experiment showed that BFP-TA could improve pulmonary function, and alleviate inflammatory cell infiltration, pulmonary emphysema, and collagen fiber deposition in the lung of COPD mice. Furthermore, BFP-TA could decrease the levels of pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β), MMPs (MMP-9 and MMP-12) and MDA, while increase the levels of TIMP-1 and SOD. Moreover, BFP-TA could decrease the protein expressions of collagen I, vimentin, α-SMA, MMP-9, MMP-9/TIMP-1, Bax, p-JNK/JNK, p-P38/P38, and p-ERK/ERK, while increase the level of E-cadherin.
CONCLUSION
This study is the first to demonstrate the protective effect of BFP-TA in CS-induced COPD mouse model. Furthermore, BFP-TA may improve airway remodeling by inhibiting the EMT process and potentially exert anti-inflammatory effect by inhibiting the MAPK signaling pathway.
Topics: Animals; Pulmonary Disease, Chronic Obstructive; Disease Models, Animal; Alkaloids; Lung; Oxidative Stress; Anti-Inflammatory Agents; Male; Fritillaria; Plant Extracts; Cytokines; Smoke; Inflammation Mediators; Mice, Inbred C57BL; Epithelial-Mesenchymal Transition; Airway Remodeling; Cigarette Smoking; MAP Kinase Signaling System; Mice; Antioxidants; Signal Transduction
PubMed: 38881716
DOI: 10.2147/COPD.S459166 -
BMC Pulmonary Medicine Jun 2024Lung cancer (LC) commonly occurs in patients with combined pulmonary fibrosis and emphysema (CPFE) and chronic obstructive pulmonary disease (COPD), but comparative...
BACKGROUND
Lung cancer (LC) commonly occurs in patients with combined pulmonary fibrosis and emphysema (CPFE) and chronic obstructive pulmonary disease (COPD), but comparative research is limited. This study examines clinical characteristics, treatments, and prognosis in LC patients with CPFE or COPD.
METHODS
The retrospective study involved 75 lung cancer patients with CPFE and 182 with COPD. It analyzed clinical features, tumor pathology, pulmonary function, laboratory parameters, and treatment responses.
RESULTS
Notable differences were found between the CPFE + LC and COPD + LC groups. Both groups were mostly elderly, male smokers. The CPFE + LC group had higher BMI and more adenocarcinoma and squamous cell carcinoma, while COPD + LC had predominantly squamous cell carcinoma. CPFE + LC tumors were mostly in the lower lobes; COPD + LC's were in the upper lobes. The CPFE + LC group showed higher tumor metastasis rates, more paraseptal emphysema, and elevated levels of TG, CEA, NSE, and Killer T Cells. In advanced stages (IIIB-IV), the CPFE + LC group receiving first-line treatment had shorter median progression-free survival (PFS) and a higher risk of progression or death than the COPD + LC group, regardless of whether it was non-small cell lung cancer (NSCLC) or small cell lung cancer (SCLC). No significant PFS difference was found within CPFE + LC between chemotherapy and immunotherapy, nor in immune-related adverse events between groups, with interstitial pneumonia being common.
CONCLUSION
This study emphasizes distinct lung cancer characteristics in CPFE or COPD patients, highlighting the need for tailored diagnostic and treatment approaches. It advocates for further research to improve care for this high-risk group.
Topics: Humans; Male; Retrospective Studies; Lung Neoplasms; Pulmonary Disease, Chronic Obstructive; Female; Aged; Middle Aged; Prognosis; Pulmonary Fibrosis; Pulmonary Emphysema; Carcinoma, Non-Small-Cell Lung; Aged, 80 and over; Progression-Free Survival; Carcinoma, Squamous Cell
PubMed: 38851701
DOI: 10.1186/s12890-024-03088-5