SUDDEN-ONSET FATAL ASTHMA - A DISTINCT ENTITY WITH FEW EOSINOPHILS AND RELATIVELY MORE NEUTROPHILS IN THE AIRWAY SUBMUCOSA

Citation
S. Sur et al., SUDDEN-ONSET FATAL ASTHMA - A DISTINCT ENTITY WITH FEW EOSINOPHILS AND RELATIVELY MORE NEUTROPHILS IN THE AIRWAY SUBMUCOSA, The American review of respiratory disease, 148(3), 1993, pp. 713-719
Citations number
28
Categorie Soggetti
Respiratory System
ISSN journal
00030805
Volume
148
Issue
3
Year of publication
1993
Pages
713 - 719
Database
ISI
SICI code
0003-0805(1993)148:3<713:SFA-AD>2.0.ZU;2-2
Abstract
To determine the histologic differences in the airways of patients who died from sudden-onset asthma and the more common slow-onset asthma, we studied seven cases of fatal asthma, The numbers of eosinophils and neutrophils, as well as extracellular deposition of their respective granule contents in the airway mucosa and submucosa, were determined a nd statistically analyzed. Four of the seven patients had slow-onset a sthma attacks in which the time interval between onset of asthma and d eath was more than 2.5 h. In contrast, three patients had sudden-onset asthma in which the time interval between onset of asthma attack and death was less than 1 h. The four patients with slow-onset fatal asthm a had more eosinophils (34.1 +/- 6.3 in slow-onset; 9.7 +/- 3.5 in sud den-onset; p = 0.002) and fewer neutrophils (4.8 +/- 2.0 in slow-onset ; 16.8 +/- 5.4 in sudden-onset; p = 0.008) in the airway submucosa tha n did patients with sudden-onset fatal asthma. In addition, within the slow-onset fatal asthma group, eosinophils exceeded neutrophils in th e airway submucosa (eosinophils > neutrophils, p = 0.002). By contrast , within the sudden-onset fatal asthma group, neutrophils exceeded eos inophils (neutrophils > eosinophils, p = 0.04). We suggest that sudden -onset fatal asthma is immunohistologically distinct from slow-onset f atal asthma and that it is characterized by a relative paucity of eosi nophils in the face of an excess of neutrophils in the airway submucos a. These observations raise the possibility that the mechanism of airw ay inflammation as well as that of airway narrowing in sudden-onset fa tal asthma may be quite distinct from those in slow-onset fatal asthma .