Is there agreement on the pathogenesis / pathophysiology of exercise induced asthma?
AbstractPurpose: Exercise Induced Asthma was formally proposed as a concept to the medical profession in 1966. However up to 1990 two different hypotheses were being put forward to explain the mechanism involved. Methods: A literature search of Pubmed, Google Scholar, Ovid and The Cochrane Library was conducted in May 2009 using a combination of controlled vocabulary and truncated text words to capture relevant articles. All relevant randomised controlled trials, case control studies and case series were included in the review. Results: The initial search identified 2361citations. Following the removal of duplicates and the application of selection criteria, a total of 36 articles were included in this review. Two scales were used to assess the data the Jadad Scale and The Scottish Intercollegiate Guidelines Network Grading Review Group guidelines known as SIGN Criteria. Discussion: Within the studies reviewed a particular issue encountered was the definition of EIA itself. Thirteen of the studies gave no definition, ten used FEV1≥10%, seven used FEV1≥15%, four used FEV1≥20% with the remaining two studies using FEV1≥12% and FEV1≥7%. Accordingly pooling of the data for analysis was only possible under the broader headings of the two original hypothesis and two new categories Inflammatory Causative Factors and Emerging Science. Studies into Inflammatory Causative Factors had by far the highest number of studies (15) and participants – with 497 in total. The participants in the McFadden and Emerging Science studies were almost equal at about 180 participants each. While a total of only 63 subjects participated in the Anderson hypothesis studies While the current balance of evidence clearly suggests a more probable relationship with inflammation for asthmatics with EIA. Clearly further work is required to explore the pathogenesis of EIA in non asthmatics. Conclusions: While a number of possible mechanisms involved in the pathogenesis of EIA were evaluated it would still appear that the studies reviewed do not allow any firm conclusions to be drawn. However the evidence appears to be currently weighted in favour of inflammatory causative factors as the basis for EIA.
PublisherUniversity of Chester
TypeThesis or dissertation
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