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Background: Giant bullous emphysema is characterized by large bullae occupying at least one-third of the hemithorax and leading to compression of the surrounding lung parenchyma. Overdiagnosis can occur because of the atypical appearance of hyperplastic type II pneumocytes, which may be mistaken for malignant cells. Case presentation: A 48-year-old male with a history of smoking and occupational exposure presented with dyspnea and drowsiness. Initial chest X-ray revealed a tension pneumothorax, and subsequent chest CT revealed extensive bullous emphysema and lung cancer in the right middle lobe (RML). Pathologic examination initially indicated resected bullae to metastatic adenocarcinoma, but upon review, it was determined that the reactive alveolar cells were misdiagnosed as malignant. Conclusions: This case emphasizes the need for thorough histopathological assessment and prudent interpretation of atypical cellular morphology. [ABSTRACT FROM AUTHOR]

• Patients with comorbid cardiovascular and chronic obstructive pulmonary disease (COPD) and a recent hospitalised exacerbation, although common, are typically excluded from studies. • However, these patients are at increased risk of rehospitalisation and death. • This pragmatic study examined the effect of the addition of inhaled corticosteroid (ICS) to long-acting bronchodilators in these patients; unfortunately the planned number of patients was not recruited, limiting the strength of the conclusions. • The results suggest that ICS use does not reduce rehospitalisation/death (primary outcome), although all-cause and cardiovascular mortality rates were reduced. • Results also suggest that ICS use did not increase the risk of adverse events and/or pneumonia. Patients with chronic obstructive pulmonary disease (COPD) frequently have cardiovascular comorbidities, increasing the risk of hospitalised COPD exacerbations (H-ECOPDs) or death. This pragmatic study examined the effects of adding an inhaled corticosteroid (ICS) to long-acting bronchodilator(s) (LABDs) in patients with COPD and cardiac comorbidities who had a recent H-ECOPD. Patients >60 years of age with COPD and ≥1 cardiac comorbidity, within 6 months after discharge following an H-ECOPD, were randomised to receive LABD(s) with or without ICS, and were followed for 1 year. The primary outcome was the time to first rehospitalisation and/or all-cause death. The planned number of patients was not recruited (803/1032), limiting the strength of the conclusions. In the intention-to-treat population, 89/403 patients (22.1 %) were rehospitalised or died in the LABD group (probability 0.257 [95 % confidence interval 0.206, 0.318]), vs 85/400 (21.3 %) in the LABD+ICS group (0.249 [0.198, 0.310]), with no difference between groups in time-to-event (hazard ratio 1.116 [0.827, 1.504]; p = 0.473). All-cause and cardiovascular mortality were lower in patients receiving LABD(s)+ICS, with relative reductions of 19.7 % and 27.4 %, respectively (9.8 % vs 12.2 % and 4.5 % vs 6.2 %), although the groups were not formally statistically compared for these endpoints. Fewer patients had adverse events in the LABD+ICS group (43.0 % vs 50.4 %; p = 0.013), with 4.9 % vs 5.4 % reporting pneumonia adverse events. Results suggest addition of ICS to LABDs did not reduce the time-to-combined rehospitalisation/death, although it decreased all-cause and cardiovascular mortality. ICS use was not associated with an increased risk of adverse events, particularly pneumonia. [ABSTRACT FROM AUTHOR]

Background: Carbon monoxide (CO) poisoning affects several vital organs; however, the long-term damage to lungs has not been well investigated. Objective: This study investigated the morphological changes and the associated molecules 6 weeks after CO poisoning in rat models. Rats in the CO poisoning group were exposed to 1500 ppm CO in a gas chamber for 3 h. After 6 weeks, the rats in the control and CO poisoning groups were sacrificed. Pathological changes were assessed using hematoxylin and eosin staining. Western blotting and antibody arrays for inflammatory signaling molecules were performed using lung homogenates. Complete blood counts and Krebs Von Den Lungen (KL)-6 levels were compared among rats in the control group and those immediately and 6 weeks after CO poisoning using blood sampling from an indwelling catheter. Results: CO-poisoned lungs showed emphysematous changes with increased mean linear intercept (p = 0.0007). SERPINA1, IL-13, CD44, and GDF7 levels were significantly decreased, whereas TGFβ, ɑ-SMA, MMP9, and NF-κB levels were significantly increased in the CO-poisoned lungs. KL-6 serum levels were significantly higher in the CO-poisoned rats (p < 0.0001). Conclusion: This is the first study to demonstrate the long-term effects and emphysematous changes in CO-poisoned lung models. We recommend long-term monitoring following CO poisoning. [ABSTRACT FROM AUTHOR]

Rationale: Chronic obstructive pulmonary disease (COPD) results from gene–environment interactions over the lifetime. These interactions are captured by epigenetic changes, such as DNA methylation. Objectives: To systematically review the evidence form epigenome-wide association studies related to COPD and lung function. Methods: A systematic literature search performed on PubMed, Embase, and Cumulative Index to Nursing and Allied Health Literature (CINAHL) databases identified 1,947 articles that investigated epigenetic changes associated with COPD and/or lung function; 17 of them met our eligibility criteria, from which data were manually extracted. Differentially methylated positions (DMPs) and/or annotated genes were considered replicated if identified by two or more studies with a P < 1 × 10−4. Measurements and Main Results: Ten studies profiled DNA methylation changes in blood and seven in respiratory samples, including surgically resected lung tissue (n = 3), small airway epithelial brushings (n = 2), BAL (n = 1), and sputum (n = 1). Main results showed: 1) high variability in study design, covariates, and effect sizes, which prevented a formal meta-analysis; 2) in blood samples, 51 DMPs were replicated in relation to lung function and 12 related to COPD; 3) in respiratory samples, 42 DMPs were replicated in relation to COPD but none in relation to lung function; and 4) in COPD versus control studies, 123 genes (2.6% of total) were shared between one or more blood and one or more respiratory samples and associated with chronic inflammation, ion transport, and coagulation. Conclusions: There is high heterogeneity across published COPD and/or lung function epigenome-wide association studies. A few genes (n = 123; 2.6%) were replicated in blood and respiratory samples, suggesting that blood can recapitulate some changes in respiratory tissues. These findings have implications for future research. Systematic Review [protocol] registered with Open Science Framework (OSF). [ABSTRACT FROM AUTHOR]

Neck emphysema after tonsillectomy surgery is very rare. We present a case documenting the conservative management of a post-tonsillectomy neck swelling, accompanied by crepitus. Computed tomography revealed a large air density at the region of the right masticator space and the masseter muscle, proximal to other deep neck spaces and muscles. Further investigations of her associated symptoms resulted in an additional diagnosis of systemic lupus erythematosus. We have also explored the signs and symptoms associated with such cases, along with a discussion of the literature published on surgical emphysema post-tonsillectomy. [ABSTRACT FROM AUTHOR]

An 18‐year‐old healthy male complained of a 7‐day history of fever, cough, and sore throat, along with a three‐day history of left facial swelling. The x‐rays revealed subcutaneous emphysema in the chest, neck, face, and mediastinum region (Pneumomediastinum). Furthermore, an area of infiltration was visible, indicating pneumonia. Therefore, we immediately started him on intravenous antibiotics. We then moved the patient to an isolation room, considering pulmonary tuberculosis as one of the differential diagnoses. However, the Acid Fast Bacilli (AFB), Mycobacterium Tuberculosis Bacteria‐Polymerase Chain Reaction (MTB PCR), and sputum for gram stain and culture were all negative. On the other hand, the test for parainfluenza virus 3 was positive. The patient was observed with a daily chest x‐ray to monitor the progress of pneumonia and subcutaneous emphysema. Fortunately, the subcutaneous emphysema was significantly reduced on a daily basis until it was completely resolved before discharge home. [ABSTRACT FROM AUTHOR]

Even with recent advances in pathobiology and treatment options, chronic obstructive pulmonary disease (COPD) remains a major contributor to morbidity and mortality. To develop new ways of combating this disease, breakthroughs in our understanding of its mechanisms are sorely needed. Investigating the involvement of underanalyzed lung cell types, such as endothelial cells (ECs), is one way to further our understanding of COPD. JCAD is a junctional protein in endothelial cells (ECs) arising from the KIAA1462 gene, and a mutation in this gene has been implicated in the risk of developing COPD. In our study, we induced inflammation and emphysema in mice via the global knockout of KIAA1462/JCAD (JCAD-KO) and confirmed it in HPMECs and A549 to examine how the loss of JCAD could affect COPD development. We found that KIAA1462/JCAD loss reduced acute lung inflammation after elastase treatment. Even after 3 weeks of elastase, JCAD-KO mice demonstrated a preserved lung parenchymal structure and vasculature. In vitro, after KIAA1462 expression is silenced, both endothelial and epithelial cells showed alterations in pro-inflammatory gene expression after TNF-α treatment. We concluded that JCAD loss could ameliorate COPD through its anti-inflammatory and anti-angiogenic effects, and that KIAA1462/JCAD could be a novel target for COPD therapy. [ABSTRACT FROM AUTHOR]

You must change your perspective in order to have a deeper comprehension of the connection between metabolic syndrome (MetS) and chronic obstructive pulmonary disease (COPD). This means using a patient management approach that is more system- and holistic-focused. This change recognizes the reality that the human body is a complex network of interrelated organs and systems and that illness in one area of the body may spread to seemingly unrelated areas of the body. Aim: The purpose of this study is to determine the lipid profile, mean blood glucose while fasting, impaired fasting glucose, and COPD patients with and without MetS. Materials & methods: After receiving permission from the Institutional Ethics Committee, the researchers started to work on their project. Patients diagnosed with MetS/COPD numbered a total of one hundred. We obtained information on the patient's whole medical history, including details about their occupation, income, smoking habits, diabetes, hypertension, and acute episodes. When determining body composition, height and mass were also taken into consideration. Every patient had a chest x-ray as well as an electrocardiogram. Result: The study indicated that fifty-five percent of patients had abdominal obesity, fifty-two percent had hypertension, fifty-two percent had impaired fasting glucose, forty-two percent had elevated triglycerides, and forty-eight percent had inadequate HDL cholesterol. We found hypertension, diabetes, and dyslipidemia to be the most frequent factors, contrary to global research that found abdominal obesity to be the most common. Our department must enhance non-communicable disease screening to detect COPD patients with undiagnosed diabetes, dyslipidemia, or hypertension. Conclusion: Abdominal obesity, high blood pressure, high triglycerides, and low HDL cholesterol were more common in metabolic syndrome patients. Many differences existed between the groups. Patients with COPD who also have diabetes, impaired fasting glucose, dyslipidemia, or high blood pressure should begin adequate antihypertensive medicine, oral hypoglycemic drugs or insulin, and lipid-lowering therapy. Patients with COPD who only have one of these conditions should begin all four therapies. Patients diagnosed with MetS had significantly higher levels of body mass index (BMI), weight, waist-hip ratio, hip circumference, and VLDL cholesterol. [ABSTRACT FROM AUTHOR]

Alpha-1-antitrypsin deficiency is a genetic disorder caused by mutations in the SERPINA1 gene encoding alpha-1-antitrypsin (AAT), the major serine protease inhibitor in plasma. Reduced AAT levels are associated with elevated risk of developing emphysema mainly due to uncontrolled activity of neutrophil elastase in the lungs. The prevalent Z-AAT mutant and many rare pathogenic AAT variants also predispose to liver disease due to their accumulation as polymeric chains in hepatocytes. Part of these polymers are secreted into the bloodstream and could represent biomarkers of intra-hepatic accumulation. Moreover, being inactive, they further lower lung protection against proteases. Aim of our study is to accurately quantify the percentage of circulating polymers (CP) in a cohort of subjects with different SERPINA1 genotypes. CP concentration was measured in plasma or Dried Blood Spot (DBS) by a sensitive sandwich ELISA based on capture by the polymer-specific 2C1 monoclonal antibody. CP were significantly elevated in patients with the prevalent PI*SZ and PI*ZZ genotypes, with considerable intra-genotype variability. Notably, higher percentage of polymers was observed in association with elevated C-reactive protein. CP levels were also increased in carriers of the Mmalton variant, and of Mprocida, I, Plowell and Mherleen in heterozygosity with Z-AAT. These findings highlight the importance of implementing CP quantification in a clinical laboratory. Indeed, the variable amount of CP in patients with the same genotype may correlate with the variable severity of the associated lung and liver diseases. Moreover, CP can reveal the polymerogenic potential of newly discovered ultrarare AAT variants. [ABSTRACT FROM AUTHOR]

Background: This is a retrospective cohort study from a single center of Chest Medical District of Nanjing Brain Hospital Affiliated to Nanjing Medical University, Jiangsu Province, China. It was aim to evaluate the diagnostic value of radial endobronchial ultrasound (R-EBUS) combination with rapid on-site evaluation (ROSE) guided transbronchial lung biopsy (TBLB) for peripheral pulmonary lesions in patients with emphysema. Methods: All 170 patients who underwent PPLs with emphysema received an R-EBUS examination with or without the ROSE procedure, and the diagnostic yield, safety, and possible factors influencing diagnosis were analyzed between the two groups by the SPSS 25.0 software. Results: The pooled and benign diagnostic yields were not different in the two groups (P = 0.224, 0.924), but the diagnostic yield of malignant PPLs was significantly higher in the group with ROSE than the group without ROSE (P = 0.042). The sensitivity of ROSE was 79.10%, the specificity, 91.67%, the positive predictive value, 98.15%, and the negative predictive value, 84.62%. The diagnostic accuracy, was 95.52%. In the group of R-EBUS + ROSE, the procedural time and the number of times of biopsy or brushing were both significantly reduced (all P<0.05). The incidence of pneumothorax (1.20%) and bleeding (10.84%) in the group of R-EBUS + ROSE were also less than those in the group of R-EBUS (P<0.05). The lesion's diameter ≥ 2 cm, the distance between the pleura and the lesion ≥ 2 cm, the positive air bronchograms sign, the location of the ultrasound probe within the lesion, and the even echo with clear margin feature of lesion ultrasonic image, these factors are possibly relevant to a higher diagnostic yield. The diagnostic yield of PPLs those were adjacent to emphysema were lower than those PPLs which were away from emphysema (P = 0.048) in the group without ROSE, however, in the group of R-EBUS + ROSE, there was no such difference whether the lesion is adjacent to emphysema or not (P = 0.236). Conclusion: Our study found that the combination of R-EBUS and ROSE during bronchoscopy procedure was a safe and effective modality to improve diagnostic yield of PPLs with emphysema, especially for malignant PPLs. The distance between the pleura and the lesion ≥ 2 cm, the positive air bronchograms sign, the location of the ultrasound probe within the lesion, and the even echo with clear margin feature of lesion ultrasonic image, these factors possibly indicated a higher diagnostic yield. Those lesions' position is adjacent to emphysema may reduce diagnostic yield but ROSE may make up for this deficiency. [ABSTRACT FROM AUTHOR]

Summary of Key Points: Eligibility criteria for lung cancer screening increasingly need to consider family history of lung cancer, as well as age and smoking status.Lung cancer screening will reveal a multitude of incidental findings, of variable clinical significance, and with a need for clear pathways of management.Pulmonary nodule sampling is enhanced by intra‐procedural imaging and cutting‐edge robotic technology.Systematic thoracic lymph node sampling has implications for treatment efficacy.Bronchoscopic ablative techniques are feasible for peripheral lung cancers.Bronchoscopic sampling continues to have a high yield for lung cancer molecular characterization.Immunotherapy indications have expanded to include early stage and resectable lung cancer. [ABSTRACT FROM AUTHOR]

Impaired and limited alveolar regeneration upon injury advances pulmonary disorders and irreversibly affects millions of people worldwide. Adult mammals do not have a strong potential to regenerate functional lung tissues, while neonatal lungs robustly proliferate and regenerate the functional tissue within a week of birth upon injury. The differential composition of the extracellular matrix (ECM) of neonatal tissues favors cellular proliferation and migration, fostering lung regeneration. Regardless, conventional ECM therapies employ adult-derived tissues. Therefore, the potential differences in regenerative properties of adult and neonatal lung ECM were investigated using in vitro and in vivo lung emphysema model. Decellularization of the neonatal and adult lungs was performed using freeze-thaw cycle method. Decellularization process was structurally characterized using SEM and immunostaining. In vitro treatment of neonatal lung-derived ECM (NECM) significantly enhanced the cellular migration and proliferation compared to adult-lung derived ECM (AECM) treated cigarette smoke-extract (CSE)-stimulated A549 cells. Following the administration of AECM and NECM, we observed a significant decline in emphysematous features and an improvement in lung functions in NECM group. NECM treatment increased the ratio of HOPX+/SpC+ cells with an active proliferation in SpC+ cells shown by colocalization of SpC+/Ki67+ and SpC+/Brdu+ cells. Moreover, NECM treatment activated the Neureguline-1/Erbb2 signaling and fostered a regenerative environment by upregulating the expression of regenerative genes including FGF, WNTs and AXIN-2 as compared to AECM treatment. Our findings suggested the potential utilization of NECM as novel therapeutics in regenerative medicine, deviating from the conventional application of adult-derived ECM treatments in pre-clinical and clinical research. [Display omitted] • dECM derived from neonatal lungs ameliorates the emphysematous features and normalizes lung function. • dECM derived from neonatal lungs encourages AT2 cell proliferation and its transdifferentiation into AT1 cells encouraging regeneration. • dECM derived from neonatal lungs upregulates the mRNA expression of regeneration-associated genes. • Xylitol, significant metabolite in dECM of neonatal lungs, promotes cell proliferation and migration, supports lung regeneration. [ABSTRACT FROM AUTHOR]

There is limited literature regarding seasonal influenza vaccination (SIV) among those with a history of chronic obstructive pulmonary disease (HCOPD) prior to the COVID-19 pandemic, and no information on the topic assessing the years following the pandemic. This cross-sectional study used the Behavioral Risk Factor Surveillance Survey (BRFSS) data from the years 2017 to 2022 (n = 822,783 adults ages 50–79 years; 50.64% males). The exposure was a HCOPD, and the outcome was SIV within the past year. Weighted and adjusted logistic regression models were conducted overall and by the significant effect modifiers: smoking status, sex, and year. Having an HCOPD significantly increases the weighted adjusted odds (WAO) of SIV when compared to not having an HCOPD overall and by smoking status, sex, and year. For 2017 through 2022, among all current, former, and never smokers with an HCOPD, the WAO of SIV were: 1.36 (1.28, 1.45), 1.35 (1.27, 1.43), and 1.18 (1.09, 1.27), respectively. Among males with an HCOPD who were current, former, and never smokers, the WAO of SIV were: 1.35 (1.23, 1.48), 1.45 (1.33, 1.58), and 1.23 (1.05, 1.44), respectively. Among females with an HCOPD who were current, former, and never smokers, the WAO of SIV were: 1.31 (1.20, 1.43), 1.24 (1.15, 1.35), and 1.13 (1.04, 1.23), respectively. Study findings suggest males had significantly greater WAO ratios of receiving SIV than females in 2020 and 2022, during and after the COVID-19 pandemic. More specifically, males with an HCOPD who were former smokers had significantly greater WAOR of receiving SIV than females in 2020 and 2022. Understanding the potential barriers to SIV receipt by smoking status and sex, especially during a pandemic, and especially for individuals impacted by an HCOPD, is essential for better health interventions in times of a national crisis such as a pandemic. Additionally, SIV receipt is low among those with an HCOPD, and efforts should be made to improve this. [ABSTRACT FROM AUTHOR]

Background: Emphysema is generally considered a poor prognostic factor for patients with nonsmall cell lung cancer; however, whether the poor prognosis is due to highly malignant tumors or emphysema itself remains unclear. This study was designed to determine the prognostic value of emphysema in patients with early-stage nonsmall cell lung cancer. Methods: A total of 721 patients with clinical stage IA nonsmall cell lung cancer who underwent complete resection between April 2007 and December 2018 were retrospectively analyzed regarding clinicopathological findings and prognosis related to emphysema. Results: The emphysematous and normal lung groups comprised 197 and 524 patients, respectively. Compared with the normal lung group, lymphatic invasion (23.9% vs. 14.1%, P = 0.003), vascular invasion (37.6% vs. 17.2%, P < 0.001), and pleural invasion (18.8% vs. 10.9%, P = 0.006) were observed more frequently in the emphysema group. Additionally, the 5-year overall survival rate was lower (77.1% vs. 91.4%, P < 0.001), and the cumulative incidence of other causes of death was higher in the emphysema group (14.0% vs. 3.50%, P < 0.001). Multivariable Cox regression analysis of overall survival revealed that emphysema (vs. normal lung, hazard ratio 2.02, P = 0.0052), age > 70 years (vs. < 70 years, hazard ratio 4.03, P < 0.001), and SUVmax > 1.8 (vs. ≤ 1.8, hazard ratio 2.20, P = 0.0043) were independent prognostic factors. Conclusions: Early-stage nonsmall cell lung cancer with emphysema has a tendency for the development of highly malignant tumors. Additionally, emphysema itself may have an impact on poor prognosis. [ABSTRACT FROM AUTHOR]

Abstract Background The first 24 h of infection represent a critical time window in interactions between pathogens and host tissue. However, it is not possible to study such early events in human lung during natural infection due to lack of clinical access to tissue this early in infection. We, therefore, applied RNA sequencing to ex vivo cultured human lung tissue explants (HLTE) from patients with emphysema to study global changes in small noncoding RNA, mRNA, and long noncoding RNA (lncRNA, lincRNA) populations during the first 24 h of infection with influenza A virus (IAV), Mycobacterium bovis Bacille Calmette-Guerin (BCG), and Pseudomonas aeruginosa. Results Pseudomonas aeruginosa caused the strongest expression changes and was the only pathogen that notably affected expression of microRNA and PIWI-associated RNA. The major classes of long RNAs (> 100 nt) were represented similarly among the RNAs that were differentially expressed upon infection with the three pathogens (mRNA 77–82%; lncRNA 15–17%; pseudogenes 4–5%), but lnc-DDX60-1, RP11-202G18.1, and lnc-THOC3-2 were part of an RNA signature (additionally containing SNX10 and SLC8A1) specifically associated with IAV infection. IAV infection induced brisk interferon responses, CCL8 being the most strongly upregulated mRNA. Single-cell RNA sequencing identified airway epithelial cells and macrophages as the predominant IAV host cells, but inflammatory responses were also detected in cell types expressing few or no IAV transcripts. Combined analysis of bulk and single-cell RNAseq data identified a set of 6 mRNAs (IFI6, IFI44L, IRF7, ISG15, MX1, MX2) as the core transcriptomic response to IAV infection. The two bacterial pathogens induced qualitatively very similar changes in mRNA expression and predicted signaling pathways, but the magnitude of change was greater in P. aeruginosa infection. Upregulation of GJB2, VNN1, DUSP4, SerpinB7, and IL10, and downregulation of PKMYT1, S100A4, GGTA1P, and SLC22A31 were most strongly associated with bacterial infection. Conclusions Human lung tissue mounted substantially different transcriptomic responses to infection by IAV than by BCG and P. aeruginosa, whereas responses to these two divergent bacterial pathogens were surprisingly similar. This HLTE model should prove useful for RNA-directed pathogenesis research and tissue biomarker discovery during the early phase of infections, both at the tissue and single-cell level.

Abstract Background Giant bullous emphysema is characterized by large bullae occupying at least one-third of the hemithorax and leading to compression of the surrounding lung parenchyma. Overdiagnosis can occur because of the atypical appearance of hyperplastic type II pneumocytes, which may be mistaken for malignant cells. Case presentation A 48-year-old male with a history of smoking and occupational exposure presented with dyspnea and drowsiness. Initial chest X-ray revealed a tension pneumothorax, and subsequent chest CT revealed extensive bullous emphysema and lung cancer in the right middle lobe (RML). Pathologic examination initially indicated resected bullae to metastatic adenocarcinoma, but upon review, it was determined that the reactive alveolar cells were misdiagnosed as malignant. Conclusions This case emphasizes the need for thorough histopathological assessment and prudent interpretation of atypical cellular morphology.

Roberto W Dal Negro,1 Paola Turco,1 Massimiliano Povero2 1National Centre for Respiratory Pharmacoeconomics and Pharmacoepidemiology - CESFAR, Verona, Italy; 2AdRes Health Economics and Outcomes Research, Turin, ItalyCorrespondence: Massimiliano Povero, Email m.povero@adreshe.comBackground: Chronic Obstructive Pulmonary Disease (COPD) is a respiratory condition characterized by heterogeneous abnormalities of the airways and lung parenchyma that cause different clinical presentations. The assessment of the prevailing pathogenetic components underlying COPD is not usually pursued in daily practice, also due to technological limitations and cost.Aim: To assess non-invasively the lung emphysema component of COPD by the simultaneous measurement of DLNO and DLCO via a single-breath (sDLNO and sDLCO).Methods: COPD patients aged ≥ 40 years of both genders were recruited consecutively and labelled by computed tomography as “with significant” emphysema (> 10% of CT lung volume) or “with negligible” emphysema otherwise. Current lung function tests such as sDLNO, sDLCO and Vc (the lung capillary blood volume) were measured. All possible subsets of independent spirometric and diffusive parameters were tested as predictors of emphysema, and their predicted power compared to each parameter alone by ROC analysis and area under the curve (AUC).Results: Thirty-one patients with “significant emphysema” were compared to thirty-one with “negligible emphysema”. FEV1 and FEV1/FVC seemed to be the best spirometric predictors (AUC 0.80 and 0.81, respectively), while sDLCO and Vc had the highest predicted power among diffusive parameters (AUC 0.92 and 0.94, respectively). sDLCO and Vc values were the parameters most correlated to the extent of CT emphysema. Six subsets of independent predictors were identified and included at least one spirometric and one diffusive parameter. According to goodness-to-fit scores (AIC, BIC, log-likelihood and pseudo R2), RV coupled with sDLCO or Vc proved the best predictors of emphysema.Conclusion: When investigating the parenchymal destructive component due to emphysema occurring in COPD, sDLNO, sDLCO and Vc do enhance the predictive power of current spirometric measures substantially. sDLNO, sDLCO and Vc contribute to phenotype of the main pathogenetic components of COPD easily and with high sensitivity. Organizational problems, radiation exposure, time and costs could be reduced, while personalized and precision medicine could be noticeably implemented.Keywords: COPD, parenchymal destruction, emphysema, lung capillary blood volume, simultaneous single-breath NO and CO diffusing capacity, precision medicine

Abstract Background This is a retrospective cohort study from a single center of Chest Medical District of Nanjing Brain Hospital Affiliated to Nanjing Medical University, Jiangsu Province, China. It was aim to evaluate the diagnostic value of radial endobronchial ultrasound (R-EBUS) combination with rapid on-site evaluation (ROSE) guided transbronchial lung biopsy (TBLB) for peripheral pulmonary lesions in patients with emphysema. Methods All 170 patients who underwent PPLs with emphysema received an R-EBUS examination with or without the ROSE procedure, and the diagnostic yield, safety, and possible factors influencing diagnosis were analyzed between the two groups by the SPSS 25.0 software. Results The pooled and benign diagnostic yields were not different in the two groups (P = 0.224, 0.924), but the diagnostic yield of malignant PPLs was significantly higher in the group with ROSE than the group without ROSE (P = 0.042). The sensitivity of ROSE was 79.10%, the specificity, 91.67%, the positive predictive value, 98.15%, and the negative predictive value, 84.62%. The diagnostic accuracy, was 95.52%. In the group of R-EBUS + ROSE, the procedural time and the number of times of biopsy or brushing were both significantly reduced (all P

Kristine Jensen,1 Thomas Egenod,2 Daniel P Franzen,3,4 Michael Perch1,5 1Department of Cardiology, Section for Lung Transplantation and Respiratory Medicine, Rigshospitalet Heart Center, Copenhagen, Denmark; 2Department of Interventional Pulmonology, Dupuytren University Hospital, Limoges, France; 3Department of Internal Medicine, Uster Hospital, Uster, Switzerland; 4Department of Pulmonology, University of Zurich, Zurich, Switzerland; 5Department of Clinical Medicine, University of Copenhagen, Copenhagen, DenmarkCorrespondence: Michael Perch, Department of Cardiology, Section for Lung Transplantation and Respiratory Medicine, Rigshospitalet, Heart Center, Inge Lehmanns Vej 7, Copenhagen, 2100, Denmark, Email Michael.perch@regionH.dkAbstract: Endoscopic lung volume reduction (ELVR) is an established treatment option for patients with severe emphysema. Not all patients are candidates for this type of intervention, and in the context of significant airway secretions, they may be excluded from treatment. Bronchial Rheoplasty (BR) was developed to treat mucus hypersecretion by delivering nonthermal pulsed electric fields to the airway epithelium and submucosa. The literature to date demonstrates that patients treated with BR in clinical studies have a reduction in airway goblet cell hyperplasia as well as substantive clinical improvement in the setting of chronic bronchitis (CB). In this case series, we present four patients treated at three different institutions who had previously undergone ELVR with beneficial outcome. However, over time, these patients subsequently developed worsening clinical issues, including complaints of increased and thickened mucus, along with exacerbations in the setting of a loss of some ELVR-associated benefits. These patients then underwent exploratory treatment with BR with the intent of reducing their secretion burden and potentially restoring the efficacy associated with the initial placement of the airway valves. All BR procedures were well tolerated, and three of the four patients showed substantial improvement in their symptom burden. Airway examinations during the second of the two BR procedures also revealed what appeared to be less airway mucosal inflammation and a decrease in the quantity of airway secretions. Therefore, treatment with BR may have the potential to improve and restore the initial benefits associated with ELVR, thus enhancing long-term outcomes. Further clinical studies with sufficient follow-up are warranted to assess this in a larger cohort of patients, and to determine whether treatment with BR prior to ELVR may make more patients eligible for this treatment through reduction in their secretions and/or symptoms.Keywords: bronchial rheoplasty, endobronchial valves, emphysema

Abstract There is limited evidence regarding the causal inference of emphysema and functional small airway disease in the subsequent progression of chronic obstructive pulmonary disease (COPD). Patients consisting of two independent cohorts diagnosed with COPD and underwent two serial chest CT scans were included. Total percent emphysema (PRMEmph) and fSAD (PRMfSAD) was quantified via PRM. To investigate the progression of emphysema, we divided COPD patients with PRMEmph