Extent of centrilobular and panacinar emphysema in smokers' lungs: pathological and mechanical implications

Saetta, Marina; Kim, W D; Izquierdo, José Luis; Ghezzo, Heberto; Cosio, Manuel G.

doi:10.1183/09031936.94.07040664

Cited by 75 publications

(54 citation statements)

References 13 publications

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“…Conversely, the uneven pattern of lung destruction seen in CLE is associated with more severe abnormalities of the small airways, suggesting that centrilobular destruction is related to airborne factors and intimately related to the airway inflammatory process. The findings of SAETTA et al [48], who investigated the relationship between the inflammation of the small airways and the extent of parenchymal destruction using the destructive index [49] in the lungs of smokers with CLE and with PLE, are in agreement with this hypothesis. In lungs with CLE, a close correlation between inflammation of the airways and parenchymal destruction was evident.…”

Section: The Relationship Of Small Airway Abnormalities and Emphysemasupporting

confidence: 77%

Disease of the airways in chronic obstructive pulmonary disease

Piqueras

Cosio²

2001

European Respiratory Journal

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The pathological hallmarks of chronic obstructive pulmonary disease (COPD) are inflammation of the small airways (bronchiolitis) and destruction of lung parenchyma (emphysema). The functional consequence of these abnormalities is airflow limitation.Airway abnormalities and emphysema interact in a complex fashion in the development of airflow limitation in COPD. In an attempt to improve understanding of the role of the airways in COPD, the morphological counterparts of airflow limitation, the cellular inflammatory infiltrate in the airways and the relationship between emphysema type and airway abnormalities are reviewed.Significant correlation between airway remodelling and functional measurements are found in earlier stages of COPD. In advanced COPD, airflow limitation is reflected by airway narrowing, airway deformity and extent of emphysema. The cellular inflammatory infiltrate is mainly composed of neutrophils in early stages of COPD. However, the presence of CD8z T-cells seems to differentiate smokers with COPD from smokers that would not develop the disease. The inflammatory changes and remodelling found in the airways and their contribution to airflow obstruction might be modulated by the type of emphysema smokers develop, with centrilobular emphysema showing more severe inflammatory changes and narrower airways than panlobular emphysema.In conclusion, the degree of airway involvement in chronic obstructive pulmonary disease can vary greatly for the same degree of airflow obstruction, depending on the type of emphysema smokers develop. If the underlying lung abnormalities in chronic obstructive pulmonary disease vary, as the evidence suggests, the study of cigaretteinduced lung disease as a single entity will further delay understanding of chronic obstructive pulmonary disease. The pathological hallmarks of chronic obstructive pulmonary disease (COPD) are inflammation of the small airways (bronchiolitis) and destruction of lung parenchyma (emphysema). The functional consequence of these abnormalities is airflow limitation.Bronchiolitis contributes to airflow limitation by narrowing and obliterating the airway lumen and by actively constricting the airway. Emphysema, by reducing the elastic recoil of the lung through parenchymal destruction and increase in alveolar size, as well as reducing the elastic load applied to the airways through destruction of alveolar attachments, also contributes to the airflow limitation characteristic of smokers. Although there is increasing evidence that the large airways are inflamed in patients with COPD, this is not believed to contribute directly to the airflow limitation in these patients.It has become apparent that airway abnormalities and emphysema interact in a complex fashion, rather than simply additively in the development of airflow limitation and COPD. The type of emphysema that smokers develop seems to determine, to a great extent, the quantity and possibly type of inflammation and airway remodelling found, suggesting that different pathogenetic mechani...

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Section: The Relationship Of Small Airway Abnormalities and Emphysemasupporting

confidence: 77%

Disease of the airways in chronic obstructive pulmonary disease

Piqueras

Cosio²

2001

European Respiratory Journal

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“…SAETTA and co-workers [22] have extended the observations of KIM et al [21] by precisely assessing the extent of lung involvement by either type of emphysema in smokers. They found that the centrilobular and panlobular emphysemas can be present in pure form or may overlap each other, and that, even in the mixed forms, one type of emphysema is always clearly predominant.…”

Section: Small Airway Abnormalities In Centrilobular Emphysema and Pamentioning

confidence: 85%

“…On the other hand, the uneven pattern of lung destruction seen in centrilobular emphysema is associated with more severe abnormalities in the small airways, suggesting that centrilobular destruction is related to airborne factors and intimately related to the airway inflammatory process. In favour of this hypothesis are the findings of SAETTA and co-workers [22], who investigated the relationship between the inflammation of the small airways and the extent of parenchymal destruction using the destructive index (DI; [19]) in the lungs of smokers with centrilobular and those with panlobular emphysema. In lungs with centrilobular emphysema a close correlation between the inflammation of the airways and the parenchymal destruction was evident.…”

Section: Small Airway Abnormalities In Centrilobular Emphysema and Pamentioning

confidence: 99%

Morphological and cellular basis for airflow limitation in smokers

Saetta¹,

Finkelstein²,

Mg³

1994

Eur Respir J

Self Cite

100

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M Mo or rp ph ho ol lo og gi ic ca al l a an nd d c ce el ll lu ul la ar r b ba as si is s f fo or r a ai ir rf fl lo ow w l li im mi it ta at ti io on n i in n s sm mo ok ke er rs s ABSTRACT: Airflow limitation has two well-defined components, increased resistance, which is found predominantly in the small airways, and loss of elastic recoil. Small airways contribute to the increased resistance to flow by the narrowing of the airway lumen. Morphometric studies have shown that smokers have increased epithelial abnormalities, cellular inflammatory infiltrates in the airway wall, increased muscle and fibrosis, when compared with nonsmokers. Along with these anatomical changes, an increased percentage of airways <400 µm in diameter is found. In addition to the measured changes, other nonmeasurable, dynamic events occur in the airways of smokers, which further decrease lumen diameter. There is ample evidence to show that the airways of smokers react to nonspecific stimuli by constricting, which results in increased resistance and decreased forced expiratory volume in one second (FEV 1 ). The pathological changes found in smokers, that could be responsible for active muscle constriction and airway narrowing include: 1) airway epithelial damage, resulting in increased permeability and impairment of other epithelial function; 2) chronic airway inflammation; 3) structural changes in the airway wall; and 4) loss of alveolar attachments.However, not all smokers develop the abovementioned airway abnormalities. We describe how smokers could develop either centrilobular emphysema (CLE), or panlobular emphysema (PLE). We have found that smokers with CLE have more abnormal and narrower small airways, and flow limitation is correlated with the small airway abnormalities and not with loss of recoil. In contrast, smokers with PLE have much less severe airway abnormalities, diffuse emphysema that can be detected microscopically at a stage when FEV 1 might be only mildly abnormal, and early changes in elastic recoil as evidenced by the changes in the pressure-volume curve of the lung. Furthermore, in PLE, airflow limitation is correlated with loss of recoil but not with abnormalities in the small airways.We believe that the mechanisms involved in the pathogenesis of the two types of emphysema in smokers are different; an airborne mechanism for CLE, possibly related to airway hyperresponsiveness, and a bloodborne mechanism for PLE, which may be related to dysfunction of α 1 -antiproteases. We conclude that the separation of smokers based on their emphysema type is essential if we are to understand the pathogenesis of chronic obstructive pulmonary disease (COPD) in these subjects.

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“…Emphysema in usual COPD may be relatively pure CAE or PAE, but is more often a mixture of both forms of emphysema [5]. The emphysema in a 1 -AT-COPD is predominantly PAE.…”

Section: Emphysemamentioning

confidence: 99%

Report of a workshop: quantitative computed tomography scanning in longitudinal studies of emphysema

Newell

Hogg²,

Snider³

2004

Eur Respir J

156

138

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It has been reported that quantitative computed tomography (CT) scanning of the lungs showed decreased progression of emphysema in a randomised clinical trial in patients with severe a 1 -antitrypsin (a 1 -AT) deficiency receiving monthly intravenous augmentation therapy with human a 1 -AT. Comparable results were not obtained using rate of decline of forced expiratory volume in one second.Accordingly, the Alpha-1 Foundation convened a workshop to explore the feasibility of using quantitative CT data as a primary outcome variable in trials of drugs for treating a 1 -AT deficiency.This report reviews the following: the principles for the use of modern CT scanners for quantifying emphysema; the methods and data on validation by comparison with measurements of severity of emphysema in inflation-fixed specimens of lungs; and the possibility of decreasing radiation dosage from CT to make it safe and ethically possible to use CT in longitudinal studies.The workshop concluded that it is feasible, safe and ethically possible to use computed tomography in longitudinal studies of emphysema. It recommended that the primary end-point should be a significant shift in the 15th percentile of lung density. Eur Respir J 2004; 23: 769-775.

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Extent of centrilobular and panacinar emphysema in smokers' lungs: pathological and mechanical implications

Cited by 75 publications

References 13 publications

Disease of the airways in chronic obstructive pulmonary disease

Disease of the airways in chronic obstructive pulmonary disease

Morphological and cellular basis for airflow limitation in smokers

Report of a workshop: quantitative computed tomography scanning in longitudinal studies of emphysema

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