Airway structure and inflammatory cells in fatal attacks of asthma

被引:164
作者
Carroll, N
Carello, S
Cooke, C
James, A
机构
[1] SIR CHARLES GAIRDNER HOSP,DEPT PULM PHYSIOL,NEDLANDS,WA 6009,AUSTRALIA
[2] UNIV WESTERN AUSTRALIA,DEPT PATHOL,NEDLANDS,WA 6009,AUSTRALIA
[3] QUEEN ELIZABETH II MED CTR,STATE HLTH LABS,DEPT FORENS PATHOL,PERTH,WA,AUSTRALIA
关键词
fatal asthma; inflammation; morphology;
D O I
10.1183/09031936.96.09040709
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
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.
引用
收藏
页码:709 / 715
页数:7
相关论文
共 38 条
  • [1] ANTO JM, 1993, NEW ENGL J MED, V329, P1807
  • [2] LYMPHOCYTES-T AND ACTIVATED EOSINOPHILS IN AIRWAY MUCOSA IN FATAL ASTHMA AND CYSTIC-FIBROSIS
    AZZAWI, M
    JOHNSTON, PW
    MAJUMDAR, S
    KAY, AB
    JEFFERY, PK
    [J]. AMERICAN REVIEW OF RESPIRATORY DISEASE, 1992, 145 (06): : 1477 - 1482
  • [3] 2 CONSECUTIVE THUNDERSTORM ASSOCIATED EPIDEMICS OF ASTHMA IN THE CITY OF MELBOURNE - THE POSSIBLE ROLE OF RYE GRASS-POLLEN
    BELLOMO, R
    GIGLIOTTI, P
    TRELOAR, A
    HOLMES, P
    SUPHIOGLU, C
    SINGH, MB
    KNOX, B
    [J]. MEDICAL JOURNAL OF AUSTRALIA, 1992, 156 (12) : 834 - 837
  • [4] Cardell BS, 1959, THORAX, V14, P341
  • [5] THE STRUCTURE OF LARGE AND SMALL AIRWAYS IN NONFATAL AND FATAL ASTHMA
    CARROLL, N
    ELLIOT, J
    MORTON, A
    JAMES, A
    [J]. AMERICAN REVIEW OF RESPIRATORY DISEASE, 1993, 147 (02): : 405 - 410
  • [6] CARROLL N, 1993, AM REV RESPIR DIS, V147, pA516
  • [7] CUTZ E, 1978, THORAX, V8, P207
  • [8] DEMONCHY JGR, 1985, AM REV RESPIR DIS, V131, P373
  • [9] A COMPARISON OF QUANTITATIVE ANATOMY OF BRONCHI IN NORMAL SUBJECTS IN STATUS ASTHMATICUS IN CHRONIC BRONCHITIS AND IN EMPHYSEMA
    DUNNILL, MS
    MASSARELLA, GR
    ANDERSON, JA
    [J]. THORAX, 1969, 24 (02) : 176 - +