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
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
.