Utility of lung density measurements in the diagnosis of emphysema

Marsh, Suzanne; Aldington, Sarah; Williams, Mathew; Nowitz, Mike; Kingzett-Taylor, Andrew; Weatherall, Mark; Shirtcliffe, Philippa; McNaughton, Amanda; Pritchard, Alison; Beasley, Richard

doi:10.1016/j.rmed.2007.01.002

Cited by 42 publications

(47 citation statements)

References 36 publications

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“…In cases of discordance, the images were viewed together and a consensus decision reached. Only subjects with definite emphysema were included as having macroscopic disease in subsequent analyses (42).…”

Section: Methodsmentioning

confidence: 99%

“…Nevertheless, several studies demonstrate that high-resolution CT is more sensitive and specific than commonly used functional tests for the evaluation of initial emphysema in asymptomatic smokers, despite normal or minimal abnormal changes in spirometry, TL CO , or other variables (41,42). In other words, we speculate that it is probable that the definition of COPD according to current guidelines, and hence assignation of our volunteers to one group, could underestimate the presence of early phases or less obstructive phenotypes of the disease.…”

Section: Figurementioning

confidence: 99%

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Sustained CTL activation by murine pulmonary epithelial cells promotes the development of COPD-like disease

et al. 2009

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Chronic obstructive pulmonary disease (COPD) is a lethal progressive lung disease culminating in permanent airway obstruction and alveolar enlargement. Previous studies suggest CTL involvement in COPD progression; however, their precise role remains unknown. Here, we investigated whether the CTL activation receptor NK cell group 2D (NKG2D) contributes to the development of COPD. Using primary murine lung epithelium isolated from mice chronically exposed to cigarette smoke and cultured epithelial cells exposed to cigarette smoke extract in vitro, we demonstrated induced expression of the NKG2D ligand retinoic acid early transcript 1 (RAET1) as well as NKG2D-mediated cytotoxicity. Furthermore, a genetic model of inducible RAET1 expression on mouse pulmonary epithelial cells yielded a severe emphysematous phenotype characterized by epithelial apoptosis and increased CTL activation, which was reversed by blocking NKG2D activation. We also assessed whether NKG2D ligand expression corresponded with pulmonary disease in human patients by staining airway and peripheral lung tissues from never smokers, smokers with normal lung function, and current and former smokers with COPD. NKG2D ligand expression was independent of NKG2D receptor expression in COPD patients, demonstrating that ligand expression is the limiting factor in CTL activation. These results demonstrate that aberrant, persistent NKG2D ligand expression in the pulmonary epithelium contributes to the development of COPD pathologies.

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Section: Methodsmentioning

confidence: 99%

Section: Figurementioning

confidence: 99%

Sustained CTL activation by murine pulmonary epithelial cells promotes the development of COPD-like disease

et al. 2009

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“…CT scanning CT scans of the chest were performed using a single machine (GE Prospeed; GE Yokogawa Medical Systems, Tokyo, Japan), as described previously [25] (see online supplementary material).…”

Section: Feno Measurementsmentioning

confidence: 99%

Distinct clinical phenotypes of airways disease defined by cluster analysis

Weatherall¹,

Travers²,

Shirtcliffe³

et al. 2009

European Respiratory Journal

218

169

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Airways disease is currently classified using diagnostic labels such as asthma, chronic bronchitis and emphysema. The current definitions of these classifications may not reflect the phenotypes of airways disease in the community, which may have differing disease processes, clinical features or responses to treatment. The aim of the present study was to use cluster analysis to explore clinical phenotypes in a community population with airways disease.A random population sample of 25-75-yr-old adults underwent detailed investigation, including a clinical questionnaire, pulmonary function tests, nitric oxide measurements, blood tests and chest computed tomography. Cluster analysis was performed on the subgroup with current respiratory symptoms or obstructive spirometric results.Subjects with a complete dataset (n5175) were included in the cluster analysis. Five clusters were identified with the following characteristics: cluster 1: severe and markedly variable airflow obstruction with features of atopic asthma, chronic bronchitis and emphysema; cluster 2: features of emphysema alone; cluster 3: atopic asthma with eosinophilic airways inflammation; cluster 4: mild airflow obstruction without other dominant phenotypic features; and cluster 5: chronic bronchitis in nonsmokers.Five distinct clinical phenotypes of airflow obstruction were identified. If confirmed in other populations, these findings may form the basis of a modified taxonomy for the disorders of airways obstruction.

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“…Other studies that classified the COPD phenotype according to HRCT findings found that the cut-off level of the low atten-uation area used to separate non-emphysema from emphysema is quite arbitrary, as it ranges from 0% to 25% (Kasahara et al 2000;Tatsumi et al 2004). Since emphysema can be identified in smokers without airflow limitation on HRCT (Marsh et al 2007), the non-emphysema group in the present study included patients with less than 15% of attenuation area lower than -950 HU at full inspiration. In addition, if a patient showed airflow limitation without evidence of emphysema on HRCT, the patient was categorized into the non-emphysema group, regardless of whether symptoms of chronic bronchitis were present.…”

Section: Discussionmentioning

confidence: 99%

Impaired Colony-Forming Capacity of Circulating Endothelial Progenitor Cells in Patients with Emphysema

Kim

Lee

Jeong

et al. 2012

Tohoku J. Exp. Med.

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Chronic obstructive pulmonary disease (COPD) is classified into emphysema and chronic bronchitis, which are thought to result from different pathophysiological pathways. Smoking-induced lung parenchymal destruction and inadequate repair are involved in the pathogenesis of emphysema. In addition, decreased expression of vascular endothelial growth factor and increased endothelial cell apoptosis in the lung may participate in emphysema pathogenesis. As stem cells, circulating endothelial progenitor cells (EPCs) may play a key role in the maintenance of vascular integrity by replacing and repairing the damaged endothelial cells in the tissues. To determine whether the lack of appropriate repair by circulating EPCs in cases of smoking-induced endothelial cell injury participates in emphysema pathogenesis, we determined the association between the colony-forming or migratory capacity of circulating EPCs and the presence of emphysema in 51 patients with COPD. The patients were divided into emphysema (n = 23) and non-emphysema groups (n = 28) based on high-resolution computed tomography. Twenty-two smokers with normal lung function and 14 normal non-smokers served as controls. Circulating EPCs isolated from patients with emphysema showed significantly lower colony-forming units (CFUs) than those from patients with non-emphysema group, smokers with normal lung function, and normal non-smokers. EPCs from patients with emphysema showed significantly lower migratory capacity than those from normal nonsmoking controls (p < 0.05). On multivariate analysis, the EPC-CFU was independently associated with emphysema (OR 0.944, 95% CI = 0.903-0.987, p = 0.011). Thus, impaired functions of circulating EPCs may contribute to the development of emphysema.

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Utility of lung density measurements in the diagnosis of emphysema

Abstract: CT lung density measurements cannot reliably detect the presence of emphysema in an individual. We recommend further investigation into lung density measurements before their widespread use in clinical practice.

Cited by 42 publications

References 36 publications

Sustained CTL activation by murine pulmonary epithelial cells promotes the development of COPD-like disease

Sustained CTL activation by murine pulmonary epithelial cells promotes the development of COPD-like disease

Distinct clinical phenotypes of airways disease defined by cluster analysis

Impaired Colony-Forming Capacity of Circulating Endothelial Progenitor Cells in Patients with Emphysema

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