Computed tomography in pulmonary emphysema

Goddard, P; Nicholson, Elizabeth; László, G.; Watt, Iain

doi:10.1016/s0009-9260(82)80301-2

Cited by 428 publications

(299 citation statements)

References 18 publications

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“…A visual scoring system was used to assess the extent of emphysema according to the modified [16] scoring system of GODDARD et al [17]. Given that automatically calculated parameters, such as LAV, may be a more sensitive technique for the detection and quantification of pulmonary emphysema in vivo, visual assessment of emphysema is a limitation of the present study that could bias the results.…”

Section: Discussionmentioning

confidence: 96%

“…The severity of emphysema was assessed visually by three independent pulmonologists according to the modified [16] scoring system of GODDARD et al [17]; the pulmonologists were blinded to any clinical information regarding the patient. Six images in three slices were analysed in the lungs, including the aortic arch, the carina and 1-2 cm above the highest hemidiaphragm.…”

Section: Lung Computed Tomography Scansmentioning

confidence: 99%

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Functional single nucleotide polymorphisms of theCCL5gene and nonemphysematous phenotype in COPD patients

Hizawa¹,

Makita²,

Nasuhara³

et al. 2008

Eur Respir J

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It was previously reported that the gain-of-function -28 guanine allele of the promoter single nucleotide polymorphism (SNP; cytosine to guanine substitution of nucleotide -28 (-28C.G)) in the CC chemokine ligand 5 gene (CCL5) was associated with susceptibility to late-onset asthma in patients who developed asthma at age o40 yrs. The clinical diagnosis of chronic obstructive pulmonary disease (COPD) includes emphysema and small airway disease, and upregulation of CCL5 has been described in the airways of patients with COPD. It was hypothesised that CCL5 has a genetic impact upon the variable expression of emphysema in patients with COPD.Patients with COPD were studied (n5267). All of the patients underwent pulmonary highresolution computed tomography (CT), and visual scoring (CT score) was performed to determine emphysema severity. Three SNPs of CCL5 were genotyped, including -403G.A, -28C.G and 375T.C.A significant difference was found in CT score according to CCL5 genotype; the -28G allele was inversely associated with CT score. When the analysis was confined to 180 patients with bronchial reversibility of ,15%, even stronger evidence for this association was noted.Functional single nucleotide polymorphisms in the CC chemokine ligand 5 gene were associated with milder emphysema. Together with previous findings, the present study may identify the CC chemokine ligand 5 gene as part of a common pathway in the pathogenesis of lateonset asthma and chronic obstructive pulmonary disease with milder emphysema.

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Section: Discussionmentioning

confidence: 96%

Section: Lung Computed Tomography Scansmentioning

confidence: 99%

Functional single nucleotide polymorphisms of theCCL5gene and nonemphysematous phenotype in COPD patients

Hizawa¹,

Makita²,

Nasuhara³

et al. 2008

Eur Respir J

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“…Visual HRCT score Pulmonary emphysema was visually assessed by an expert chest radiologist, unaware of the clinical and lung function data, as described previously [18][19][20]. On three high-resolution computed tomography (HRCT) slices (at the level of the carina, 5 cm above and 5 cm below the carina), the lung parenchyma was assessed for two aspects of emphysema: severity and extent.…”

Section: Measurement Of Timp-1 and Mmp-9mentioning

confidence: 99%

“…The extent of emphysema using the direct observation method was scored on a four-point scale. The extent score was 1 if ,25% of the lung field was involved; 2 if there was 25-50% involvement; 3 if 50-75% involvement; and 4 if .75% involvement [20]. Severity was graded on a four-point scale: 0, no emphysema; 1, low HRCT attenuation areas ,5 mm in diameter with or without vascular pruning; 2, circumscribed low HRCT attenuation areas .5 mm in diameter, in addition to those ,5 mm in diameter (vascular pruning is present, but with normal lung intervening); and 3, diffuse low-attenuation areas without intervening normal lung, or confluent larger low-attenuation areas with vascular pruning and distortion of the branching pattern of the lung, occupying all or almost all of the involved parenchyma.…”

Section: Measurement Of Timp-1 and Mmp-9mentioning

confidence: 99%

Increased serum concentrations of tissue inhibitor of metalloproteinase-1 in COPD patients

Higashimoto

Yamagata²,

Iwata³

et al. 2005

Eur Respir J

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Matrix metalloproteinase (MMP)-9 and tissue inhibitors of metalloproteinase (TIMP)-1 concentrations are increased in the sputum of asthma and chronic bronchitis patients, and are thought to be related to airflow obstruction. However, serum concentrations of these enzymes have not been clearly evaluated in patients with chronic obstructive pulmonary disease (COPD). The aim of this study was to examine the serum concentrations of these enzymes in COPD and asthmatic patients in order to determine their relationship with airway obstruction.Serum samples were obtained from 72 patients with COPD: 66 control subjects and 26 patients with asthma. Smoking histories of control subjects were matched with those of COPD patients. Serum concentrations of TIMP-1 and MMP-9 were determined by ELISA.The circulating TIMP-1 concentration was significantly higher in stable COPD patients than in control and asthmatic subjects, and was significantly negatively correlated with forced expiratory volume in one second/forced vital capacity in COPD patients. The molar ratio between MMP-9 and TIMP-1 was significantly lower in COPD patients than in control subjects. In patients with COPD, the serum TIMP-1 concentration was significantly increased during disease exacerbation.In conclusion, the current findings suggest that serum tissue inhibitors of metalloproteinase-1 concentration can be used as a serum marker of airway obstruction and exacerbation in chronic obstructive pulmonary disease patients.KEYWORDS: Bronchial asthma, chronic obstructive pulmonary disease, exacerbation, metalloproteinases, serum markers, tissue inhibitors of matrix metalloproteinases P ulmonary emphysema, the major contributor to morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD), is characterised by progressive destruction of the extracellular matrix (ECM) of the lung [1-4]. The most widely accepted theory of the pathogenesis of pulmonary emphysema is a proteinase-antiproteinase imbalance. Although a number of studies have demonstrated the important role of increased elastolytic activity derived from neutrophils in emphysema [4,5], recent studies have shown that matrix metalloproteinases (MMPs) play key roles in tissue remodelling of the airways in COPD and asthma patients [2,[6][7][8]. MMPs are a family of structurally related enzymes that are capable of degrading all components of the ECM [9]. Members of the MMP family are selectively inhibited by tissue inhibitors of metalloproteinases (TIMPs). TIMP-1 has been shown to bind to both the active and precursor form of MMP-9, in a 1:1 proportion, and to inhibit its enzymatic activity. Sputum concentrations of MMP-9 and TIMP-1 are increased in patients with COPD and asthma [2,10]. RUSSELL et al. [11] showed that alveolar macrophages from patients with COPD release larger amounts of MMP-9 with greater enzymatic activity than those from healthy smokers. Two recent studies found that the MMP-9/TIMP-1 ratio was correlated with the degree of airway obstruction. BOSSE et al. [12]...

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“…Our ability to detect emphysema changed dramatically in the early 1980s when CT was first exploited to demonstrate subtle parenchymal patterns and to produce objective lung density measurements in Hounsfield units (HU) (10)(11)(12). The widespread adoption of high-resolution scanning has put into everyone's hands the tool to identify anatomic emphysema before there are any clinical manifestations.…”

Section: Ctmentioning

confidence: 99%

Imaging Studies in Emphysema

Friedman¹

2008

Proceedings of the American Thoracic Society

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Definitions of types of emphysema within the framework of chronic obstructive pulmonary disease are given. The classic findings on the chest radiograph are described, and the advances in sensitivity and specificity achieved with computed tomography (CT) scanning are noted. The ''density mask'' and the ''percentile point'' measurements rely on the densitometric property of X-rays, but the scan also shows the severity and distribution of low-attenuation regions that usually represent pathologic emphysema. The alteration of absolute density with changes in lung inflation, CT slice thickness, collimation, and reconstruction algorithm make comparison between CT scans and across studies more difficult. Nevertheless, quantitative CT has superseded subjective scoring of scan appearance by readers as a sensitive way to measure emphysema.

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Computed tomography in pulmonary emphysema

Cited by 428 publications

References 18 publications

Functional single nucleotide polymorphisms of theCCL5gene and nonemphysematous phenotype in COPD patients

Functional single nucleotide polymorphisms of theCCL5gene and nonemphysematous phenotype in COPD patients

Increased serum concentrations of tissue inhibitor of metalloproteinase-1 in COPD patients

Imaging Studies in Emphysema

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