Patterns of development of airflow limitation in smokers with preserved spirometry and air trapping phenotype in COPDGene

Author(s):  
Mehrdad Arjomandi ◽  
Siyang Zeng ◽  
David Lynch ◽  
Russell Bowler
2011 ◽  
Vol 127 (4) ◽  
pp. 1073-1074 ◽  
Author(s):  
Ronald L. Sorkness ◽  
W. Gerald Teague ◽  
Madhuri Penugonda ◽  
Anne M. Fitzpatrick

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jae-Woo Jung ◽  
Jung Suk Oh ◽  
Boram Bae ◽  
Yoon Hae Ahn ◽  
Lucy Wooyeon Kim ◽  
...  

AbstractIn vivo presentation of airway hyper-responsiveness (AHR) at the different time points of the allergic reaction is not clearly understood. The purpose of this study was to investigate how AHR manifests in the airway and the lung parenchyma in vivo following exposure to different stimuli and in the early and late phases of asthma after allergen exposure. Ovalbumin (OVA)-induced allergic asthma model was established using 6-week female BALB/c mice. Enhanced pause was measured with a non-invasive method to assess AHR. The dynamic changes of the airway and lung parenchyma were evaluated with ultra-high-resolution computed tomography (128 multi-detector, 1024 × 1024 matrix) for 10 h. While the methacholine challenge showed no grossly visible changes in the proximal airway and lung parenchyma despite provoking AHR, the OVA challenge induced significant immediate changes manifesting as peribronchial ground glass opacities, consolidations, air-trapping, and paradoxical proximal airway dilatations. After resolution of immediate response, multiple episodes of AHRs occurred with paradoxical proximal airway dilatation and peripheral air-trapping in late phase over a prolonged time period in vivo. Understanding of airflow limitation based on the structural changes of asthmatic airway would be helpful to make an appropriate drug delivery strategy for the treatment of asthma.


2017 ◽  
Vol 12 ◽  
pp. 117727191773030
Author(s):  
Philip E Silkoff ◽  
Dave Singh ◽  
J Mark FitzGerald ◽  
Andreas Eich ◽  
Andrea Ludwig-Sengpiel ◽  
...  

Rationale: Chronic obstructive pulmonary disease (COPD) is a heterogeneous disease, and development of novel therapeutics requires an understanding of pathophysiologic phenotypes. Objectives: The purpose of the Airways Disease Endotyping for Personalized Therapeutics (ADEPT) study was to correlate clinical features and biomarkers with molecular characteristics in a well-profiled COPD cohort. Methods: A total of 67 COPD subjects (forced expiratory volume in the first second of expiration [FEV1]: 45%-80% predicted) and 63 healthy smoking and nonsmoking controls underwent multiple assessments including patient questionnaires, lung function, and clinical biomarkers including fractional exhaled nitric oxide (FENO), induced sputum, and blood. Measurements and main results: The impact of inhaled corticosteroids (ICSs), and to a lesser extent current smoking, was more associated with symptom control, exacerbation rates, and clinical biomarkers, than severity by FEV1. The ICS-treated smoking subjects were most symptomatic, with significantly elevated scores on patient-reported outcomes and more annual exacerbations ( P < .05). Inhaled corticosteroid users had greater airflow obstruction and air trapping compared with non-ICS users, regardless of smoking status. Smoking, regardless of ICS use, was associated with significantly lower FENO ( P < .05). Smoking, in non-ICS users, was associated with an elevated proportion of sputum neutrophils and reduced sputum macrophages. Increased serum C-reactive protein was observed in smokers but not in ICS and nonsmoking ICS users ( P < .05). In contrast, only air trapping and neutrophilic inflammation increased with severity, defined by postbronchodilator FEV1. Conclusions: Compared with COPD severity by FEV1, ICS use and current smoking were better determinants of clinical characteristics and biomarkers. Use of the ADEPT COPD data promises to prove useful in defining biological phenotypes to facilitate personalized therapeutic approaches.


2008 ◽  
Vol 104 (2) ◽  
pp. 394-403 ◽  
Author(s):  
Ronald L. Sorkness ◽  
Eugene R. Bleecker ◽  
William W. Busse ◽  
William J. Calhoun ◽  
Mario Castro ◽  
...  

Five to ten percent of asthma cases are poorly controlled chronically and refractory to treatment, and these severe cases account for disproportionate asthma-associated morbidity, mortality, and health care utilization. While persons with severe asthma tend to have more airway obstruction, it is not known whether they represent the severe tail of a unimodal asthma population, or a severe asthma phenotype. We hypothesized that severe asthma has a characteristic physiology of airway obstruction, and we evaluated spirometry, lung volumes, and reversibility during a stable interval in 287 severe and 382 nonsevere asthma subjects from the National Heart, Lung, and Blood Institute Severe Asthma Research Program. We partitioned airway obstruction into components of air trapping [indicated by forced vital capacity (FVC)] and airflow limitation [indicated by forced expiratory volume in 1 s (FEV1)/FVC]. Severe asthma had prominent air trapping, evident as reduced FVC over the entire range of FEV1/FVC. This pattern was confirmed with measures of residual lung volume/total lung capacity (TLC) in a subgroup. In contrast, nonsevere asthma did not exhibit prominent air trapping, even at FEV1/FVC <75% predicted. Air trapping also was associated with increases in TLC and functional reserve capacity. After maximal bronchodilation, FEV1 reversed similarly from baseline in severe and nonsevere asthma, but the severe asthma classification was an independent predictor of residual reduction in FEV1 after maximal bronchodilation. An increase in FVC accounted for most of the reversal of FEV1 when baseline FEV1 was <60% predicted. We conclude that air trapping is a characteristic feature of the severe asthma population, suggesting that there is a pathological process associated with severe asthma that makes airways more vulnerable to this component.


2016 ◽  
Vol 2 (2) ◽  
pp. 00100-2015 ◽  
Author(s):  
Jantina C. de Groot ◽  
Huib Storm ◽  
Marijke Amelink ◽  
Selma B. de Nijs ◽  
Edwin Eichhorn ◽  
...  

Adult-onset eosinophilic asthma is increasingly recognised as a severe and difficult-to-treat subtype of asthma. In clinical practice, early recognition of patients with this asthma subtype is important because it may have treatment implications. Therefore, physicians need to know the distinct characteristics of this asthma phenotype. The objective of the present study was to determine the characteristic profile of patients with adult-onset eosinophilic asthma.130 patients with adult-onset (>18 years of age) asthma and high blood eosinophil counts (≥0.3×109 L−1) were compared with 361 adult-onset asthma patients with low (<0.3×109 L−1) blood eosinophils. Measurements included a series of clinical, functional and imaging parameters.Patients with high blood eosinophils were more often male, had less well controlled asthma and higher exacerbation rates, despite the use of higher doses of inhaled corticosteroids. They had higher levels of total IgE without more sensitisation to common inhaled allergens. In addition, these patients had worse lung function, and more often showed fixed airflow limitation, air trapping, nasal polyposis and abnormalities on sinus computed tomography scanning. Chronic rhinosinusitis, air trapping and male sex were three independent factors associated with blood eosinophilia (adjusted OR 3.8 (95% CI 1.7–8.1), 3.0 (95% CI 1.1–8.1) and 2.4 (95% CI 1.3–4.4), respectively).Patients with adult-onset asthma with elevated blood eosinophils exhibit a distinct profile, which can readily be recognised in clinical practice.


2019 ◽  
Vol 9 (14) ◽  
pp. 2842 ◽  
Author(s):  
Nilakash Das ◽  
Kenneth Verstraete ◽  
Marko Topalovic ◽  
Jean-Marie Aerts ◽  
Wim Janssens

Spirometry is the gold standard to detect airflow limitation, but it does not measure airway resistance, which is one of the physiological factors behind airflow limitation. In this study, we describe the dynamics of forced expiration in spirometry using a deflating balloon and using this model. We propose a methodology to estimate ζ (zeta), a dimensionless and effort-independent parameter quantifying airway resistance. In N = 462 (65 ± 8 years), we showed that ζ is significantly (p < 0.0001) greater in COPD (2.59 ± 0.99) than healthy smokers (1.64 ± 0.18), it increased significantly (p < 0.0001) with the severity of airflow limitation and it correlated significantly (p < 0.0001) with airway resistance (r = 0.55) and specific conductance (r = −0.60) obtained from body-plethysmography. ζ also showed significant associations (p < 0.001) with diffusion capacity (r = −0.64), air-trapping (r = 0.68), and CT densitometry of emphysema (r = 0.40 against % below −950 HU and r = −0.34 against 15th percentile HU). Moreover, simulation studies demonstrated that an increase in ζ resulted in lower airflows from baseline. Therefore, we conclude that ζ quantifies airway resistance from forced expiration in spirometry—a method that is more abundantly available in primary care than traditional but expensive methods of measuring airway resistance such as body-plethysmography and forced oscillation technique.


1997 ◽  
Vol 36 (2) ◽  
pp. 235
Author(s):  
Jung Hwa Hwang ◽  
Chull Hee Cha ◽  
Jai Soung Park ◽  
Young Beom Kim ◽  
Hae Kyung Lee ◽  
...  

Respiration ◽  
2021 ◽  
pp. 1-10
Author(s):  
Marina Aiello ◽  
Marianna Ghirardini ◽  
Laura Marchi ◽  
Annalisa Frizzelli ◽  
Roberta Pisi ◽  
...  

<b><i>Background:</i></b> Alpha-1 antitrypsin deficiency (AATD) is a hereditary disorder involving lungs, characterized by low serum concentration of the protein alpha-1 antitrypsin (AAT) also called proteinase inhibitor (PI). Asthma is common in AATD patients, but there are only few data on respiratory function in asthmatic patients with AATD. <b><i>Objectives:</i></b> The aim of the study was to evaluate lung function in asthmatic outpatients with mutation in the <i>SERPINA1</i> gene coding for AAT versus asthmatic subjects without mutation. <b><i>Methods:</i></b> We performed the quantitative analysis of the serum concentration of AAT in 600 outpatients affected by mild to moderate asthma from the University Hospital of Parma, Italy. Fifty-seven of them underwent the genetic analysis subsequently; they were subdivided into mutated and non-mutated subjects. All the mutated patients had a heterozygous genotype, except 1 (PI*SS). We assessed the lung function through a flow-sensing spirometer and the small airway parameters through an impulse oscillometry system. <b><i>Results:</i></b> The values of forced vital capacity (% predicted) and those of the residual volume to total lung capacity ratio (%) were, respectively, lower and higher in patients mutated versus patients without mutation, showing a significantly greater air trapping (<i>p =</i> 0.014 and <i>p =</i> 0.017, respectively). Moreover, patients with mutation in comparison to patients without mutation showed lower forced expiratory volume in 3 s (% predicted) and forced expiratory volume in 6 s (L) spirometric values, reflecting a smaller airways contribution. <b><i>Conclusions:</i></b> In asthmatic patients, heterozygosity for AAT with PI*MZ and PI*MS genotypes was associated with small airway dysfunction and with lung air trapping.


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