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Human adenovirus (HAdV) infection in newborns is a rare condition that typically affects multiple organ systems and has a high mortality rate. We report a case of neonatal HAdV-D37 infection that presented with fever and respiratory distress that was confirmed by metagenomic next-generation sequencing using blood and bronchoalveolar lavage fluid. We treated the patient with intravenous immunoglobulin, methylprednisolone, and anticoagulants, and the patient recovered. Our review of 41 cases of HAdV found that treatment with intravenous immunoglobin might have improved the outcome of HAdV-D infection. We further suggest that glucocorticoid therapy may have additional therapeutic validity in the setting of severe or disseminated disease and that monitoring coagulation function and timely anticoagulation treatment should be considered to prevent complications associated with disseminated intravascular coagulation. [ABSTRACT FROM AUTHOR]

The article presents a question and answer related to nursing care for patients after endobronchial valve therapy.

Background: Chronic obstructive pulmonary disease (COPD) has been linked to immune responses to lung-associated self-antigens. Exposure to cigarette smoke (CS), the main cause of COPD, causes chronic lung inflammation, resulting in pulmonary matrix (ECM) damage. This tissue breakdown exposes collagen V (Col V), an antigen typically hidden from the immune system, which could trigger an autoimmune response. Col V autoimmunity has been linked to several lung diseases, and the induction of immune tolerance can mitigate some of these diseases. Evidence suggests that autoimmunity to Col Vmight also occur in COPD; thus, immunotolerance to Col V could be a novel therapeutic approach. Objective: The role of autoimmunity against collagen V in COPD development was investigated by analyzing the effects of Col V-induced tolerance on the inflammatory response and lung remodeling in a murine model of CSinduced COPD. Methods: Male C57BL/6 mice were divided into three groups: one exposed to CS for four weeks, one previously tolerated for Col V and exposed to CS for four weeks, and one kept in clean air for the same period. Then, we proceeded with lung functional and structural evaluation, assessing inflammatory cells in bronchoalveolar lavage fluid (BALF) and inflammatory markers in the lung parenchyma, inflammatory cytokines in lung and spleen homogenates, and Tcell phenotyping in the spleen. Results: CS exposure altered the structure of elastic and collagen fibers and increased the pro-inflammatory immune response, indicating the presence of COPD. Col V tolerance inhibited the onset of emphysema and prevented structural changes in lung ECM fibers by promoting an immunosuppressive microenvironment in the lung and inducing Treg cell differentiation. Conclusion: Induction of nasal tolerance to Col V can prevent inflammatory responses and lung remodeling in experimental COPD, suggesting that autoimmunity to Col V plays a role in COPD development. [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]

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]

The system of nitric oxide synthases (NOSs) is comprised of three isoforms: nNOS, iNOS, and eNOS. The roles of NOSs in respiratory diseases in vivo have been studied by using inhibitors of NOSs and NOS-knockout mice. Their exact roles remain uncertain, however, because of the non-specificity of inhibitors of NOSs and compensatory up-regulation of other NOSs in NOS-KO mice. We addressed this point in our triple-n/i/eNOSs-KO mice. Triple-n/i/eNOSs-KO mice spontaneously developed pulmonary emphysema and displayed exacerbation of bleomycin-induced pulmonary fibrosis as compared with wild-type (WT) mice. Triple-n/i/eNOSs-KO mice exhibited worsening of hypoxic pulmonary hypertension (PH), which was reversed by treatment with sodium nitrate, and WT mice that underwent triple-n/i/eNOSs-KO bone marrow transplantation (BMT) also showed aggravation of hypoxic PH compared with those that underwent WT BMT. Conversely, ovalbumin-evoked asthma was milder in triple-n/i/eNOSs-KO than WT mice. These results suggest that the roles of NOSs are different in different pathologic states, even in the same respiratory diseases, indicating the diversity of the roles of NOSs. In this review, we describe these previous studies and discuss the roles of NOSs in respiratory health and disease. We also explain the current state of development of inorganic nitrate as a new drug for respiratory diseases. [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]

Introduction: Patients with chronic obstructive pulmonary disease (COPD) and emphysema experience malnutrition and pulmonary cachexia. Endoscopic lung volume reduction (ELVR) with endobronchial valves has not only improved lung function, exercise capacity, and quality of life but also influenced body weight. Only a few data are available on body composition changes after ELVR. Methods: This single-center prospective study of patients with advanced COPD investigates body composition before and after endoscopic valve treatment using multifrequency bioelectrical impedance analysis (BIA). The following parameters were evaluated in addition to clinical data and routine tests: body weight, body mass index (BMI), basal metabolic rate, total body water, body fat, cell percentage, phase angle, intracellular water (ICW), extracellular water (ECW), extracellular mass (ECM), body cell mass (BCM), lean body mass (ECM + BCM), and fat-free mass index. Results: A total of 23 patients (mean emphysema index 37.2 ± 7.5%, BMI 23.4 ± 4.3 kg/m2) experienced improvements in lung function and exercise capacity with ELVR. Complete lobar atelectasis was achieved in 39.1% of participants. A non-statistically significant increase in body weight and BMI was observed after ELVR (p = 0.111 and p = 0.102). BIA measurement revealed a worsening of phase angle, cell percentage and ECM/BCM and thus of body composition, but without statistical significance. This is mainly due to a statistically significant increase in ECM, ECW, and ICW (all p < 0.001). Conclusion: ELVR demonstrated no beneficial changes in body composition, although patients tend to gain weight. A larger cohort is warranted to confirm these findings. [ABSTRACT FROM AUTHOR]

Objectives: A prospective, multi-centre study to evaluate concordance of morphologic lung MRI and CT in chronic obstructive pulmonary disease (COPD) phenotyping for airway disease and emphysema. Methods: A total of 601 participants with COPD from 15 sites underwent same-day morpho-functional chest MRI and paired inspiratory-expiratory CT. Two readers systematically scored bronchial wall thickening, bronchiectasis, centrilobular nodules, air trapping and lung parenchyma defects in each lung lobe and determined COPD phenotype. A third reader acted as adjudicator to establish consensus. Inter-modality and inter-reader agreement were assessed using Cohen's kappa (im-κ and ir-κ). Results: The mean combined MRI score for bronchiectasis/bronchial wall thickening was 4.5/12 (CT scores, 2.2/12 for bronchiectasis and 6/12 for bronchial wall thickening; im-κ, 0.04–0.3). Expiratory right/left bronchial collapse was observed in 51 and 47/583 on MRI (62 and 57/599 on CT; im-κ, 0.49–0.52). Markers of small airways disease on MRI were 0.15/12 for centrilobular nodules (CT, 0.34/12), 0.94/12 for air trapping (CT, 0.9/12) and 7.6/12 for perfusion deficits (CT, 0.37/12 for mosaic attenuation; im-κ, 0.1–0.41). The mean lung defect score on MRI was 1.3/12 (CT emphysema score, 5.8/24; im-κ, 0.18–0.26). Airway-/emphysema/mixed COPD phenotypes were assigned in 370, 218 and 10 of 583 cases on MRI (347, 218 and 34 of 599 cases on CT; im-κ, 0.63). For all examined features, inter-reader agreement on MRI was lower than on CT. Conclusion: Concordance of MRI and CT for phenotyping of COPD in a multi-centre setting was substantial with variable inter-modality and inter-reader concordance for single diagnostic key features. Clinical relevance statement: MRI of lung morphology may well serve as a radiation-free imaging modality for COPD in scientific and clinical settings, given that its potential and limitations as shown here are carefully considered. Key Points: • In a multi-centre setting, MRI and CT showed substantial concordance for phenotyping of COPD (airway-/emphysema-/mixed-type). • Individual features of COPD demonstrated variable inter-modality concordance with features of pulmonary hypertension showing the highest and bronchiectasis showing the lowest concordance. • For all single features of COPD, inter-reader agreement was lower on MRI than on CT. [ABSTRACT FROM AUTHOR]

Background: Unplanned admissions to hospital represent a hazardous event for older people. Timely identification of high-risk individuals using a prediction tool may facilitate preventive interventions. Aim: To develop and validate an easy-to-use prediction model for unplanned admissions to hospital in community-dwelling older adults using readily available data to allow rapid bedside assessment by GPs. Design and setting: This was a retrospective study using the general practice electronic health records of 243 324 community-dwelling adults aged ≥65 years linked with national administrative data to predict unplanned admissions to hospital within 6 months. Method: The dataset was geographically split into a development (n = 142 791/243 324, 58.7%) and validation (n = 100 533/243 324, 41.3%) sample to predict unplanned admissions to hospital within 6 months. The performance of three different models was evaluated with increasingly smaller selections of candidate predictors (optimal, readily available, and easy-to-use models). Logistic regression was used with backward selection for model development. The models were validated internally and externally. Predictive performance was assessed by area under the curve (AUC) and calibration plots. Results: In both samples, 7.6% (development cohort: n = 10 839/142 791, validation cohort: n = 7675/100 533) had ≥1 unplanned hospital admission within 6 months. The discriminative ability of the three models was comparable and remained stable after geographic validation. The easy-to-use model included age, sex, prior admissions to hospital, pulmonary emphysema, heart failure, and polypharmacy. Its discriminative ability after validation was AUC 0.72 (95% confidence interval = 0.71 to 0.72). Calibration plots showed good calibration. Conclusion: The models showed satisfactory predictive ability. Reducing the number of predictors and geographic validation did not have an impact on predictive performance, demonstrating the robustness of the model. An easy-to-use tool has been developed in this study that may assist GPs in decision making and with targeted preventive interventions. [ABSTRACT FROM AUTHOR]

Background: Patients with chronic lung diseases (CLDs), defined as progressive and life-limiting respiratory conditions, experience a heavy symptom burden as the conditions become more advanced, but palliative referral rates are low and late. Prognostic tools can help clinicians identify CLD patients at high risk of deterioration for needs assessments and referral to palliative care. As current prognostic tools may not generalize well across all CLD conditions, we aim to develop and validate a general model to predict one-year mortality in patients presenting with any CLD. Methods: A retrospective cohort study of patients with a CLD diagnosis at a public hospital from July 2016 to October 2017 was conducted. The outcome of interest was all-cause mortality within one-year of diagnosis. Potential prognostic factors were identified from reviews of prognostic studies in CLD, and data was extracted from electronic medical records. Missing data was imputed using multiple imputation by chained equations. Logistic regression models were developed using variable selection methods and validated in patients seen from January 2018 to December 2019. Discriminative ability, calibration and clinical usefulness of the model was assessed. Model coefficients and performance were pooled across all imputed datasets and reported. Results: Of the 1000 patients, 122 (12.2%) died within one year. Patients had chronic obstructive pulmonary disease or emphysema (55%), bronchiectasis (38%), interstitial lung diseases (12%), or multiple diagnoses (6%). The model selected through forward stepwise variable selection had the highest AUC (0.77 (0.72–0.82)) and consisted of ten prognostic factors. The model AUC for the validation cohort was 0.75 (0.70, 0.81), and the calibration intercept and slope were − 0.14 (-0.54, 0.26) and 0.74 (0.53, 0.95) respectively. Classifying patients with a predicted risk of death exceeding 0.30 as high risk, the model would correctly identify 3 out 10 decedents and 9 of 10 survivors. Conclusions: We developed and validated a prognostic model for one-year mortality in patients with CLD using routinely available administrative data. The model will support clinicians in identifying patients across various CLD etiologies who are at risk of deterioration for a basic palliative care assessment to identify unmet needs and trigger an early referral to palliative medicine. Trial registration: Not applicable (retrospective study). [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease is a common chronic lung disease with an ever-increasing incidence. Despite years of drug research and approvals, we are still not able to halt progress or restore normal lung function. Our previous studies have demonstrated that liver growth factor—LGF has an effect on the repair of the affected tissue in a mouse model of cigarette smoke exposure, but by what pathways it achieves this is unknown. The present study aimed to identify differentially expressed genes between emphysematous mice treated with LGF to identify potential therapeutic targets for the treatment of pulmonary emphysema. The emphysema mouse model was induced by prolonged exposure to cigarette smoke. To determine the gene expression profile of the lung in smokers treated or not with LGF, lung messenger RNA gene expression was assessed with the Agilent Array platform. We carried out differentially expressed gene analysis, functional enrichment and validated in treated mouse lung samples. The treated group significantly improved lung function (~35%) and emphysema level (~20%), consistent with our previous published studies. Microarray analysis demonstrated 290 differentially expressed genes in total (2.0-fold over or lower expressed). Injury repair-associated genes and pathways were further enhanced in the lung of LGF treated mice. The expression trends of two genes (Zscan2 and Bag6) were different in emphysematous lungs treated with LGF compared to untreated lungs. Therefore, Zscan2 and Bag6 genes could play a role in regulating inflammation and the immune response in the lung that undergoes partial lung regeneration. However, further studies are necessary to demonstrate this causal relationship. [ABSTRACT FROM AUTHOR]

Iatrogenic pneumothorax is a relevant complication of computed tomography (CT)-guided percutaneous lung biopsy. The aim of the present study was to analyze the prognostic significance of texture analysis, emphysema score and muscle mass derived from CT-imaging to predict postinterventional pneumothorax after CT-guided lung biopsy. Consecutive patients undergoing CT-guided percutaneous lung biopsy between 2012 and 2021 were analyzed. Multivariate logistic regression analysis included clinical risk factors and CT-imaging features to detect associations with pneumothorax development. Overall, 479 patients (178 females, mean age 65 ± 11.7 years) underwent CT-guided percutaneous lung biopsy of which 180 patients (37.5%) developed pneumothorax including 55 patients (11.5%) requiring chest tube placement. Risk factors associated with pneumothorax were chronic-obstructive pulmonary disease (COPD) (p = 0.03), age (p = 0.02), total lung capacity (p < 0.01) and residual volume (p = 0.01) as well as interventional parameters needle length inside the lung (p < 0.001), target lesion attached to pleura (p = 0.04), and intervention duration (p < 0.001). The combined model demonstrated a prediction accuracy of the occurrence of pneumothorax with an AUC of 0.78 [95%CI: 0.70–0.86] with a resulting sensitivity 0.80 and a specificity of 0.66. In conclusion, radiomics features of the target lesion and the lung lobe CT-emphysema score are predictive for the occurrence of pneumothorax and need for chest insertion after CT-guided lung biopsy. [ABSTRACT FROM AUTHOR]

Reduced skeletal muscle mass and oxidative capacity coexist in patients with pulmonary emphysema and are independently associated with higher mortality. If reduced cellular respiration contributes to muscle atrophy in that setting remains unknown. Using a mouse with genetically induced pulmonary emphysema that recapitulates muscle dysfunction, we found that reduced activity of succinate dehydrogenase (SDH) is a hallmark of its myopathic changes. We generated an inducible, muscle-specific SDH knockout mouse that demonstrates lower mitochondrial oxygen consumption, myofiber contractility, and exercise endurance. Respirometry analyses show that in vitro complex I respiration is unaffected by loss of SDH subunit C in muscle mitochondria, which is consistent with the pulmonary emphysema animal data. SDH knockout initially causes succinate accumulation associated with a down-regulated transcriptome but modest proteome effects. Muscle mass, myofiber type composition, and overall body mass constituents remain unaltered in the transgenic mice. Thus, while SDH regulates myofiber respiration in experimental pulmonary emphysema, it does not control muscle mass or other body constituents. [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]

Introduction: Although long-term macrolide antibiotics could reduce the recurrent exacerbation of chronic obstructive pulmonary disease (COPD), the side effect of bacterial resistance and the impact on the microbiota remain concerning. We investigated the influence of long-term erythromycin treatment on the airway and gut microbiota in mice with emphysema and patients with COPD. Methods: We conducted 16S rRNA gene sequencing to explore the effect of erythromycin treatment on the lung and gut microbiota in mice with emphysema. Liquid chromatography-mass spectrometry was used for lung metabolomics. A randomized controlled trial was performed to investigate the effect of 48-week erythromycin treatment on the airway and gut microbiota in COPD patients. Results: The mouse lung and gut microbiota were disrupted after cigarette smoke exposure. Erythromycin treatment depleted harmful bacteria and altered lung metabolism. Erythromycin treatment did not alter airway or gut microbial diversity in COPD patients. It reduced the abundance of pathogens, such as Burkholderia, in the airway of COPD patients and increased levels of symbiotic bacteria, such as Prevotella and Veillonella. The proportions of Blautia, Ruminococcus, and Lachnospiraceae in the gut were increased in COPD patients after erythromycin treatment. The time to the first exacerbation following treatment was significantly longer in the erythromycin treatment group than in the COPD group. Conclusion: Long-term erythromycin treatment reduces airway and gut microbe abundance in COPD patients but does not affect microbial diversity and restores microbiota balance in COPD patients by reducing the abundance of pathogenic bacteria. [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]

Alexis Dupuis,1 Aurore Thierry,2 Jeanne-Marie Perotin,1,3 Julien Ancel,1,3 Valérian Dormoy,3 Sandra Dury,1 Gaëtan Deslée,1,3 Claire Launois1,3 1Department of Respiratory Diseases, University Hospital of Reims, Reims, France; 2Université de Reims Champagne-Ardenne, VieFra, CHU Reims, Unité d’Aide Méthodologique, Reims, F-51100, France; 3University of Reims Champagne-Ardenne (URCA), Inserm UMR-S 1250, SFR Cap-Santé, Reims, FranceCorrespondence: Claire Launois, Service des Maladies Respiratoires, 45, Rue Cognacq Jay, Reims Cedex, Reims, 51092, France, Tel +33 3 26 78 76 14, Fax +33 3 26 06 03 19, Email claunois@chu-reims.frBackground: The role of obesity on dyspnea in chronic obstructive pulmonary disease (COPD) patients remains unclear. We aimed to provide an assessment of dyspnea in COPD patients according to their Body Mass Index (BMI) and to investigate the impact of obesity on dyspnea according to COPD severity.Methods: One hundred and twenty seven COPD patients with BMI ≥ 18.5 kg/m² (63% male, median (interquartile range) post bronchodilator forced expiratory volume of 1 second (post BD FEV1) at 51 (34– 66) % pred) were consecutively included. Dyspnea was assessed by mMRC (Modified medical research council) scale. Lung function tests were recorded, and emphysema was quantified on CT-scan (computed tomography-scan).Results: Twenty-five percent of the patients were obese (BMI ≥ 30kg/m²), 66% of patients experienced disabling dyspnea (mMRC ≥ 2). mMRC scores did not differ depending on BMI categories (2 (1– 3) for normal weight, 2 (1– 3) 1 for overweight and 2 (1– 3) for obese patients; p = 0.71). Increased mMRC scores (0– 1 versus 2– 3 versus 4) were associated with decreased post BD-FEV1 (p < 0.01), higher static lung hyperinflation (inspiratory capacity/total lung capacity (IC/TLC), p < 0.01), reduced DLCO (p < 0.01) and higher emphysema scores (p < 0.01). Obese patients had reduced static lung hyperinflation (IC/TLC p < 0.01) and lower emphysema scores (p < 0.01) than non-obese patients. mMRC score increased with GOLD grades (1– 2 versus 3– 4) in non-obese patients but not in obese patients, in association with a trend towards reduced static lung hyperinflation and lower emphysema scores.Conclusion: By contrast with non-obese patients, dyspnea did not increase with spirometric GOLD grades in obese patients. This might be explained by a reduced lung hyperinflation related to the mechanical effects of obesity and a less severe emphysema in severe COPD patients with obesity.Keywords: chronic obstructive pulmonary disease, obesity, dyspnea, lung function, pulmonary emphysema