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1 West Australian Sleep Disorders Research Institute, Sir Charles Gairdner Hospital, Nedlands, 2 School of Medicine and Pharmacology, University of West Australia, Perth, 3 Dept of Epidemiology and Preventive Medicine, Central and Eastern Clinical School, Monash University, Melbourne, and 4 Cardio-Respiratory Research Group, University of Tasmania, Hobart, Australia.
CORRESPONDENCE: A. L. James, West Australian Sleep Disorders Research Institute, Sir Charles Gairdner Hospital, Nedlands, Western Australia 6009, Australia. Fax: 08 93462034. E-mail: ajames@it.net.au
Keywords: Airway inflammation, fatal asthma, remodelling, salbutamol
Received: December 21, 2004
Accepted June 2, 2005
Fatal asthma is characterised pathologically by airway wall remodelling, eosinophil and neutrophil infiltration, accumulation of mucus in the airway lumen and smooth muscle shortening. The durations of fatal attacks of asthma show a clear bimodal distribution. Airway smooth muscle contraction and the accumulation of luminal mucus may contribute to death from asthma and relate to time to death.
The current authors have examined these two components in uninflated lung tissue in cases of fatal asthma from the second Victorian asthma mortality study. Based on time from onset of symptoms to death, cases fell into two distinct groups: short course <3 (1.5±0.6 mean±SD) h; and long course >8 (12.3±5.9) h.
Short course cases had more muscle shortening, higher levels of salbutamol and higher ratios of neutrophils to eosinophils than long course cases, who tended to have more mucus in the lumen.
In conclusion, this study confirms the dichotomy of both time to death and the eosinophil/neutrophil ratio in cases of fatal asthma. It suggests that in short course cases acute airway narrowing is due, predominantly, to bronchoconstriction despite higher blood levels of salbutamol. Mucus accumulation may be more important in long course cases.
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