ERJ
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (6)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by James, A. L.
Right arrow Articles by Walters, E. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by James, A. L.
Right arrow Articles by Walters, E. H.
Eur Respir J 2005; 26:429-434
Copyright ©ERS Journals Ltd 2005

Time to death, airway wall inflammation and remodelling in fatal asthma

A. L. James1,2,§, J. G. Elliot1,§, M. J. Abramson3 and E. H. Walters4

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.




This article has been cited by other articles:


Home page
Eur Respir JHome page
A. L. James and S. Wenzel
Clinical relevance of airway remodelling in airway diseases
Eur. Respir. J., July 1, 2007; 30(1): 134 - 155.
[Abstract] [Full Text] [PDF]


Home page
Eur Respir JHome page
P. Bradding
Mast cell regulation of airway smooth muscle function in asthma
Eur. Respir. J., May 1, 2007; 29(5): 827 - 830.
[Full Text] [PDF]


Home page
ChestHome page
F. H. Y. Green, J. C. Butt, A. L. James, and N. G. Carroll
Abnormalities of the bronchial arteries in asthma.
Chest, October 1, 2006; 130(4): 1025 - 1033.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2005 by the European Respiratory Society.