Death in Asthmatics

Cardell, B. S.; Pearson, R. S. Bruce

doi:10.1136/thx.14.4.341

Cited by 107 publications

(32 citation statements)

References 13 publications

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“…Histopathologic analysis of bronchi from patients who died of status asthmaticus showed a pattern similar to that in other cases of asthma but more severe, with extensive mucus plugs in the airway lumen, shedding of the bronchial epithelium, mucus gland hyperplasia, thickening of the basement membrane and infiltration of the airway wall with inflammatory cells (18)(19)(20). Eosinophils were initially the main cells described.…”

Section: Inflammatory Cells In Sa: the Roles Of Eosinophils And Neutrsupporting

confidence: 51%

Inflammatory events in severe acute asthma

Tillie‐Leblond

Gosset

Tonnel

2004

Allergy

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Severe acute asthma can be induced by different triggers, allergens, irritants, viruses, etc., which induce inflammation and provoke acute bronchoconstriction. Inflammatory cells, such as activated eosinophils and neutrophils identified in sputum and bronchial lavages (BL) in severe acute asthma from children and adults are associated with increased levels of IL‐5, IL‐8, and of proinflammatory mediators. Viruses, but also endotoxin or allergen exposure, are able to recruit neutrophils, via an IL‐8 production by activated macrophages or epithelial cells. Together, these inflammatory mediators are responsible for the diffuse bronchial inflammation, which involve large and small airways. Activated T cells may also be related to the pathogenesis of severe asthma. An aberrant CD8+ T lymphocyte response in bronchi, with a cytotoxic activity has been associated with fatal asthma. Moreover, the persistence of inflammatory cells in bronchi, particularly neutrophils, which respond poorly to corticosteroids, could be in part responsible for the epithelial damage, the extensive mucus plugging, and the abnormalities of epithelial and endothelial permeability which are associated with severe acute asthma. Further studies are necessary to better identify the implication of this increased bronchial permeability in the persistence of high levels of airway resistance, particularly in patients with status asthmaticus.

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Section: Inflammatory Cells In Sa: the Roles Of Eosinophils And Neutrsupporting

confidence: 51%

Inflammatory events in severe acute asthma

Tillie‐Leblond

Gosset

Tonnel

2004

Allergy

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“…The epidemiological and clinical data are supported by postmortem studies of the airways in cases of fatal asthma [10][11][12][13][14][15][16][17]. The presence in such cases of extensive bronchial epithelial damage, plugging of the airway lumen with mucus and cellular debris, thickening of the basement membrane, airway smooth muscle hypertrophy and hyperplasia, mucous gland hyperplasia, and infiltration of the airway wall with inflammatory cells, suggests longstanding, persistent airway inflammation and structural change.…”

mentioning

confidence: 75%

Airway structure and inflammatory cells in fatal attacks of asthma

Carroll¹,

Carello²,

Cooke³

et al. 1996

Eur Respir J

203

129

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Fatal attacks of asthma usually occur against a background of chronic persistent symptoms, presumably due to chronic airway inflammation and changes in airway wall structure. Death from asthma is usually attributed to excessive airway narrowing due to a combination of muscle spasm and mucous plugging. To test the hypothesis that airway wall structure and/or the inflammatory cell profile are related to the duration of a fatal attack of asthma, inflammatory cell profiles and airway structure were examined in cases of fatal asthma and related to the duration of the fatal attack.In transverse sections of large and small airways from subjects dying from asthma, the numbers of eosinophils, neutrophils and lymphomononuclear cells were counted. The amount of smooth muscle shortening, the areas of airway wall, smooth muscle, mucous gland and cartilage were measured. Cell counts, airway dimensions and muscle shortening were compared in cases dying within 2 h of the fatal attack (short duration) and those dying more than 5 h after the onset of the fatal attack (long duration).In cases with fatal attacks of short duration, the numbers of neutrophils and the mucous gland area were increased and the numbers of eosinophils were reduced compared to cases with fatal attacks of long duration. Lymphocyte numbers, airway wall thickness, the areas of smooth muscle and cartilage and the amount of smooth muscle shortening were similar in the two groups.These findings suggest fatal attacks of asthma may be triggered by an inflammatory stimulus and suggest that increased production of mucous may contribute to sudden death in such cases.

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“…Increased production of viscid mucus causing airway plugging is known to be a common pathological feature of deaths from asthma [1][2][3][4]16]. On the other hand, there is also heterogeneity in the asthma population, as to the cause of death and postmortem findings.…”

Section: Discussionmentioning

confidence: 99%

Continuity of airway goblet cells and intraluminal mucus in the airways of patients with bronchial asthma

Shimura¹,

Andoh²,

Haraguchi³

et al. 1996

European Respiratory Journal

143

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The aim of this study was to elucidate the mechanism of the formation of the widespread mucous-plugging observed in autopsied lungs from patients with bronchial asthma.We performed morphometric analysis of airways of autopsied lungs from eight patients with bronchial asthma (Group BA), and compared it with those of six chronic bronchitics (Group CB) and four control patients (Control). The following parameters were measured in paraffin sections: volume proportion of bronchial glands to bronchial wall (Gland%); goblet cell granules to total epithelial layer (Goblet%); intraluminal mucus expressed as the mucus occupying ratio (MOR); volume ratio of intraluminal mucus continuous with goblet cells to total intraluminal mucus (Vc/Vtot%); and surface ratio of the contact surface of intraluminal mucus continuous with goblet cells to the total luminal surface (Sc/Stot%).Gland%, Goblet%, and MOR or inflammatory cell numbers in the airway walls both from Group BA and CB were larger than those from the Control group. However, no significant differences were observed between Group BA and CB in Gland%, Goblet%, MOR or inflammatory cell numbers, except for the eosinophil number: i.e. 23±3, 22±3 and 6±2% in Gland%; 22±9, 5±4 and 2±2% in Goblet%; 10±3, 18±3 and 0.3±0.5% in MOR; 199±68, 10±3 and 2±2 cells·mm -2 in eosinophil number of the peripheral airways from Groups BA, CB and Control, respectively. In contrast, marked and significant increases were observed both in Vc/Vtot% and Sc/Stot% in Group BA compared to Groups CB and Control both in central and peripheral airways: i.e. Vc/Vtot% in the peripheral airways was 53±5, 4±3 and 0.8±0.8% from Groups BA, CB and Control, respectively (BA vs CB or BA vs Control, p<0.01 each).These findings suggest that the continuity of goblet cells and intraluminal mucus or lack of full release of mucus, from goblet cells, is peculiar to asthmatic airways, and may contribute to the formation of mucous-plugs.

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Death in Asthmatics

Cited by 107 publications

References 13 publications

Inflammatory events in severe acute asthma

Inflammatory events in severe acute asthma

Airway structure and inflammatory cells in fatal attacks of asthma

Continuity of airway goblet cells and intraluminal mucus in the airways of patients with bronchial asthma

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