SUDDEN-ONSET FATAL ASTHMA - A DISTINCT ENTITY WITH FEW EOSINOPHILS AND RELATIVELY MORE NEUTROPHILS IN THE AIRWAY SUBMUCOSA
SUDDEN-ONSET FATAL ASTHMA - A DISTINCT ENTITY WITH FEW EOSINOPHILS AND RELATIVELY MORE NEUTROPHILS IN THE AIRWAY SUBMUCOSA
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DOI：
10.1164/ajrccm/148.3.713
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发表时间：
1993-09-01
期刊：
影响因子：
--
通讯作者：
GLEICH, GJ
中科院分区：
文献类型：
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作者：
SUR, S;CROTTY, TB;GLEICH, GJ
为探讨突发性哮喘和常见的慢发性哮喘患者气道的组织学差异，我们对7例致死性哮喘患者进行了研究，测定了嗜酸性粒细胞和中性粒细胞的数量，以及它们各自颗粒在气道粘膜和粘膜下层的细胞外沉积，并进行统计学分析。7例患者中有4例为慢发性哮喘发作，发作至死亡的时间间隔超过2.5 h。与此相反，3例患者为突发性哮喘，哮喘发作与死亡之间的时间间隔小于1 h。4例慢发致死性哮喘患者的嗜酸性粒细胞较多（慢发型为34.1 +/- 6.3;突发型为9.7 +/- 3.5; p = 0.002）和中性粒细胞减少（慢发组4.8 ± 2.0;突发组16.8 ± 5.4; p = 0.008）。此外，在慢发型致死性哮喘组中，气道粘膜下层嗜酸性粒细胞超过中性粒细胞（嗜酸性粒细胞>中性粒细胞，p = 0.002）。相反，在突发致死性哮喘组中，中性粒细胞超过嗜酸性粒细胞（中性粒细胞>嗜酸性粒细胞，p = 0.04）。我们认为，突然发作的致命性哮喘是免疫组织学不同于缓慢发作的致命性哮喘，它的特点是相对缺乏的嗜酸性粒细胞在面对过剩的中性粒细胞在气道粘膜下层。这些观察结果提出了一种可能性，即突发性致死性哮喘的气道炎症机制以及气道狭窄机制可能与慢发性致死性哮喘的机制完全不同。
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 and statistically analyzed. Four of the seven patients had slow-onset asthma attacks in which the time interval between onset of asthma and death 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 asthma had more eosinophils (34.1 +/- 6.3 in slow-onset; 9.7 +/- 3.5 in sudden-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 than did patients with sudden-onset fatal asthma. In addition, within the slow-onset fatal asthma group, eosinophils exceeded neutrophils in the airway submucosa (eosinophils > neutrophils, p = 0.002). By contrast, within the sudden-onset fatal asthma group, neutrophils exceeded eosinophils (neutrophils > eosinophils, p = 0.04). We suggest that sudden-onset fatal asthma is immunohistologically distinct from slow-onset fatal asthma and that it is characterized by a relative paucity of eosinophils in the face of an excess of neutrophils in the airway submucosa. These observations raise the possibility that the mechanism of airway inflammation as well as that of airway narrowing in sudden-onset fatal asthma may be quite distinct from those in slow-onset fatal asthma.