scholarly journals CHARACTERIZATION OF THE AIRWAY WALL COMPLIANCE AFTER TREATMENT WITH BRONCHODILATOR IN COPD PATIENTS

CHEST Journal ◽  
2021 ◽  
Vol 160 (4) ◽  
pp. A2158
Author(s):  
Laura Pini ◽  
Giulia Claudia Ziletti ◽  
Elisa Perger ◽  
Alessandro Pini ◽  
Manuela Ciarfaglia ◽  
...  
2014 ◽  
Vol 307 (7) ◽  
pp. L557-L565 ◽  
Author(s):  
Irene M. J. Eurlings ◽  
Mieke A. Dentener ◽  
Evi M. Mercken ◽  
Rafael de Cabo ◽  
Ken R. Bracke ◽  
...  

Remodeling in chronic obstructive pulmonary disease (COPD) has at least two dimensions: small airway wall thickening and destruction of alveolar walls. Recently we showed comparable alterations of the extracellular matrix (ECM) compounds collagen, hyaluoran, and elastin in alveolar and small airway walls of COPD patients. The aim of this study was to characterize and assess similarities in alveolar and small airway wall matrix remodeling in chronic COPD models. From this comparative characterization of matrix remodeling we derived and elaborated underlying mechanisms to the matrix changes reported in COPD. Lung tissue sections of chronic models for COPD, either induced by exposure to cigarette smoke, chronic intratracheal lipopolysaccharide instillation, or local tumor necrosis factor (TNF) expression [surfactant protein C (SPC)-TNFα mice], were stained for elastin, collagen, and hyaluronan. Furthermore TNF-α matrix metalloproteinase (MMP)-2, -9, and -12 mRNA expression was analyzed using qPCR and localized using immunohistochemistry. Both collagen and hyaluronan were increased in alveolar and small airway walls of all three models. Interestingly, elastin contents were differentially affected, with a decrease in both alveolar and airway walls in SPC-TNFα mice. Furthermore TNF-α and MMP-2 and -9 mRNA and protein levels were found to be increased in alveolar walls and around airway walls only in SPC-TNFα mice. We show that only SPC-TNFα mice show changes in elastin remodeling that are comparable to what has been observed in COPD patients. This reveals that the SPC-TNFα model is a suitable model to study processes underlying matrix remodeling and in particular elastin breakdown as seen in COPD. Furthermore we indicate a possible role for MMP-2 and MMP-9 in the breakdown of elastin in airways and alveoli of SPC-TNFα mice.


Author(s):  
SV Vickerman ◽  
H Zhao ◽  
Y Li ◽  
DA Ngan ◽  
PR Hiebert ◽  
...  

2016 ◽  
Vol 3 (1) ◽  
pp. 29141 ◽  
Author(s):  
Eirunn Waatevik Saure ◽  
Per Sigvald Bakke ◽  
Tomas Mikal Lind Eagan ◽  
Marianne Aanerud ◽  
Robert Leroy Jensen ◽  
...  

Author(s):  
Dilraj Singh ◽  
Katrin Fiebich ◽  
Juergen Dederichs ◽  
Richard Pavkov ◽  
Martina Schulte ◽  
...  
Keyword(s):  

2020 ◽  
Author(s):  
Daryl Cheng ◽  
Siddharth Agarwal ◽  
Joseph Jacob ◽  
John R Hurst

AbstractBackgroundSmoking cessation is the only intervention known to affect disease progression in patients with COPD as measured by the rate of change in forced expiratory volume/1s (FEV1) over time. The need for new drugs to modify the progression of COPD is well recognised. We hypothesised that changes on CT in relation to smoking cessation may relate to changes in response to disease-modifying drugs, and therefore as a novel quantitative biomarker of drug efficacy. CT biomarkers of emphysema and airway wall thickness are increasingly used in research, but there has not been a systematic appraisal of the evidence to assess how these biomarkers evolve with a change in smoking exposure in COPD patients.MethodsWe searched MEDLINE, Embase, the Cochrane Library (Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials (CENTRAL)), and Web of Science to 10th September 2019. We included longitudinal studies of smoking COPD patients who had CT scans before and after smoking cessation. Two review authors (DC, SA) independently screened studies, extracted outcome data and assessed the risk of bias, with a third reviewer (JRH) arbitrating conflicts.ResultsFour studies were included in the final analysis. Three studies measured CT markers of lung density, which all, perhaps counter-intuitively, showed a significant decrease with smoking cessation. One study measured CT markers of airway wall thickness, which also significantly decreased with smoking cessation.Authors’ conclusionsSmoking cessation in COPD patients causes a fall in lung density, but the magnitude of the effect has not been rigorously assessed. One study has reported a decrease in airway wall thickness with smoking cessation. The number of studies is small, with some risk of bias. This question remains important for COPD researchers and requires further studies, in particular to assess whether changes with smoking cessation may model changes in response to novel pharmaceutical agents, and how to handle change in smoking status in relation to longitudinal observational imaging studies in COPD.


Author(s):  
João Simão De Melo Neto ◽  
Ana Elisa Zuliani Stroppa Marques ◽  
Fabiana De Campos Gomes

Introduction: COPD is a major cause of morbidity and mortality, which is preventable, thus studies that discusses the characterization of a given population are important for investment in treatments and prevention. Objective: Characterize individuals with Chronic Obstructive Pulmonary Disease, admitted to a pulmonary rehabilitation center. Method: Retrospective study, exploratory character of medical records of patients with COPD. Sample consisted of 37 patients diagnosed with COPD and age greater than 20 years. The following variables were analyzed: sex, age, marital status, occupation, diagnosis, main complaint, and cardiovascular risk factors presented by patients during admission. Results: Individuals aged >40 years and history of smoking have a higher prevalence in developing COPD. Pulmonary emphysema is a major pathological condition. The most common main complaint was dyspnea and cardiovascular risk factor was present sedentary lifestyle. Moreover, women with COPD were more likely to have depression than men. Conclusion: This study enabled the characterization of COPD patients, providing the possibility of investing in prevention and treatment.


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