1,720,984 research outputs found
For whom the "alarm" tolls: how we sense the danger of cigarette smoke and react to it.
No full textEditoria
Is chronic obstructive pulmonary disease a disease of aging?
No full textChronic obstructive pulmonary disease (COPD) is a disease that usually presents clinically at an advanced age, after years of smoking cigarettes. It is usually believed that aging and its biological consequences are important mechanisms in the disease pathogenesis. This concept has maintained the focus of studies on COPD in old-age individuals. Here we analyze the possible role of aging from a different point of view and introduce different concepts that might be considered useful additions to the understanding of the disease. Essentially, we propose and show evidence that COPD is a disease of the young susceptible smoker that progresses over time and manifests in older age because we live longer and not so much because of the effect of aging itself; we examine the concept of cell senescence, the basis of tissue aging, and how stressors like the ones produced by smoking can accelerate cell senescence with all of its untoward consequences in COPD. We thus finally suggest that COPD might accelerate aging rather than be a consequence of it. In conclusion, we suggest that COPD could be considered a disease of the predisposed young individual that manifests clinically in old age because we live longer, with all of its consequences
Pathophysiology of the small airways
No full textAbstract
This review describes, in some detail, the normal structure of the small airways, how this structure is achieved during the development of the bronchial tree from embryogenesis to adulthood, and how the structure determines the function of the airways at different ages and in disease. We then describe the structural abnormalities in small airways in chronic obstructive pulmonary disease (COPD) and their relationship with the disordered pulmonary function found in this disease, as an example of the mechanisms leading to airflow limitation in diseased airways. We address the pathology of small airways in different stages of COPD, summarizing the structural abnormalities associated with the progressive deterioration of pulmonary function from smokers with normal lung function to smokers with severe COPD. The importance of the elastic recoil in the normal and abnormal function of the airways is also highlighted
MORPHOLOGICAL AND CELLULAR BASIS FOR AIR-FLOW LIMITATION IN SMOKERS
No full textAbstract
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 microns 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 (FEV1). 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 FEV1 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 alpha 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
EXTENT OF CENTRILOBULAR AND PANACINAR EMPHYSEMA IN SMOKERS LUNGS - PATHOLOGICAL AND MECHANICAL IMPLICATIONS
No full textAbstract
In order to quantify the extent of centrilobular (CLE) and panacinar (PLE) emphysema and the degree of the possible overlap between the two forms in smokers, the lungs of 25 smokers undergoing lung resection for peripheral lung tumours were studied. The extent of CLE and PLE was assessed by point counting, and the lungs were classified as having pure CLE (C, n = 5), predominant CLE with areas of PLE (CP, n = 7), predominant PLE with features of CLE (PC, n = 7), and pure PLE (P, n = 6) according to the percentage of lung involved by either form. Preoperative pulmonary function tests and the score of inflammation and the diameters of the small airways were also measured. Mean linear intercept (Lm), a measure of mean interalveolar wall distances and forced expiratory volume in one second (FEV1) were similar in the four groups. Small airway pathology was a predominant feature in lungs with CLE, and was significantly decreased in a stepwise fashion as the amount of PLE increased. This was especially so for the amount of muscle in the airway wall and the diameters of the airways. By contrast, lung compliance was higher in panacinar than in centrilobular emphysema.(ABSTRACT TRUNCATED AT 250 WORDS
Immunological aspects of Chronic Obstructive Pulmonary Disease
Full text linkChronic obstructive pulmonary disease (copd) is a major cause of illness and death throughout the world. It affects about 10% of the general population, but its prevalence among heavy smokers can reach 50%.COPD is the fourth leading cause of death in most industrialized countries, and it is projected to be the third leading cause of death worldwide by 2020. Tobacco smoking is the primary risk factor for the development of COPD, but other factors, such as burning biomass fuels for cooking and heating, are important causes of COPD in many developing countries...
Centrilobular and panlobular emphysema in smokers. Two distinct morphologic and functional entities.
No full textIn order to investigate the hypothesis that different morphologic patterns of disease might correspond to different mechanical properties of the lung in emphysema, pulmonary function tests and lung mechanics were measured in 34 subjects undergoing lung resection for peripheral lung tumors. Using standard microscopic criteria, pure or predominant centrilobular (n = 18) or panlobular (n = 16) emphysema was diagnosed in lungs. The degree of emphysema measured by the mean linear intercept (Lm) was not significantly different between the two groups. However, the coefficient of variation of the interalveolar wall distance (CV) was significantly higher for the same Lm in CLE than in PLE. This indicates that CLE has an uneven pattern of destruction, whereas PLE is more homogeneous. CLE had a higher degree of abnormalities in the small airways (SAD) than did PLE (p less than 0.05) mainly because of significantly higher muscle score (p less than 0.001) and fibrosis. CLE also had a higher proportion of airways less than 400 microns in diameter than did PLE (p less than 0.05). Static compliance, specific compliance, and the exponential constant (K) were significantly lower (p less than 0.005, p less than 0.001, and p less than 0.05, respectively) in CLE than in PLE. FEV1/FVC was significantly correlated with SAD in CLE (r = -0.69, p less than 0.01) but not in PLE (r = 0.29 p greater than 0.05); conversely, FEV1/FVC was significantly correlated with elasticity (K) in PLE (r = -0.72, p less than 0.01) but not in CLE (r = 0.08, p greater than 0.05
Cellularity of the alveolar walls in smokers and its relation to alveolar destruction. Functional implications.
No full textAbstract
Inflammatory cells are believed to play an important role in the pathogenesis of emphysema; however, a relationship between presence of cells in the lung parenchyma and its destruction has never been shown. The aim of this study was to quantitate alveolar septal cellularity in smokers' lungs and to investigate its relationship with parenchymal destruction and lung function. The lungs of 23 smokers (SS) undergoing thoracotomy for localized pulmonary lesions were compared with those of eight nonsmokers (NS) and five smokers (AS) who died suddenly of nonrespiratory causes. Pulmonary function tests were performed within 1 wk of surgery in SS. For each subject, we quantitated alveolar wall cells (CELLS), an index of alveolar wall destruction (DI), and the mean linear intercept (Lm). As no significant differences were found between S and AS with regard to these indices, we combined them (Group S) for comparison with NS. Although Lm was not significantly different between S and NS, (0.331 +/- 0.072 versus 0.288 +/- 0.038), CELLS and DI were higher in S than in NS (48 +/- 8 versus 25 +/- 2 cells/mm, p less than 0.001; 47 +/- 20 versus 17 +/- 5, p less than 0.001, respectively). Further, CELLS and DI were significantly correlated (r = 0.799, p less than 0.001). The number of polymorphonuclear cells (PMN) in S can exceed that in NS by as much as 5-fold; however, PMN were inversely correlated with parenchymal destruction (DI) (r = 0.598, p less than 0.01). Thus, smokers' lungs have alveolar septal hypercellularity, possibly inflammatory, and closely related to destruction involving cells other than the PMN
Loss of alveolar attachments in smokers: an early morphometric correlate of lung function impairment
No full textAbstract
We studied post-mortem 9 nonsmokers' lungs and 9 smokers' lungs as well as 14 surgical smokers' lungs to examine the possible relationship of the number of alveolar attachments with airways inflammation and with lung function. Alveolar attachments are the alveolar walls radially attached to the small airways, and any discontinuity or rupture of these alveolar walls was considered abnormal. Normal and abnormal attachments were counted in nonsmokers and smokers and expressed as number of attachments, distance between attachments, and percentage of abnormal attachments. Although internal small airways diameter and mean linear intercept were not significantly different between smokers of either group and nonsmokers, significant differences in number of attachments (p less than 0.001), distance between attachments (p less than 0.01), and percentage of abnormal attachments (p less than 0.01) were found. The 3 indexes of alveolar attachments correlated significantly with the score for airways inflammation and with the elastic recoil pressure in smokers. No significant correlation with any other lung function test was found. We conclude that smokers have fewer alveolar attachments than do nonsmokers, and that the loss of alveolar attachments represents an early stage in the destruction of lung parenchyma, and is probably linked to inflammation of the small airways. Because of the strategic situation of this lesion, it could be responsible in part for the loss of elastic recoil seen in the initial stages of chronic obstructive pulmonary disease
The yellow brick road
No full textYellow nail syndrome is an uncommon condition characterized by dystrophic yellow nails, lymphedema and respiratory tract involvement. This syndrome typically shows up in middle-aged patients. Although several etiologies have been described, to date, the exact underlying mechanism remains unclear. The most supported pathogenetic hypothesis argues that it results from an abnormal lymphatic drainage. Hereby, we describe the associations of yellow nail syndrome typical features in a 73-year-old man with an acute onset of symptoms. He was admitted to our hospital with acute respiratory failure requiring non-invasive ventilation. Despite our advice, he rapidly relapsed. Taking care of his multiple comorbidities - cardiomyopathy, sleep apnea syndrome and severe obstructive deficit - his symptoms finally improved. Adherence to nocturnal non-invasive ventilation, bronchodilator therapy and pulmonary rehabilitation provided him stability. Acute and critical presentation could mystify the diagnosis of rare syndromes such as the yellow nail syndrome. Its precocious recognition reinforced our approach justifying a detailed screening of the patient's conditions
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