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Phenotypes, Risk Factors, and Mechanisms of Adult-Onset Asthma

Ilmarinen, Pinja; Tuomisto, Leena E; Kankaanranta, Hannu (2015)

 
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Ilmarinen, Pinja
Tuomisto, Leena E
Kankaanranta, Hannu
2015

Mediators of Inflammation 2015 -
514868
Lääketieteen yksikkö - School of Medicine
This publication is copyrighted. You may download, display and print it for Your own personal use. Commercial use is prohibited.
doi:10.1155/2015/514868
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Julkaisun pysyvä osoite on
https://urn.fi/URN:NBN:fi:uta-201607132087

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Copyright © 2015 Pinja Ilmarinen et al. This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Tiivistelmä
Asthma is a heterogeneous disease with many phenotypes, and age at disease onset is an important factor in separating the phenotypes. Genetic factors, atopy, and early respiratory tract infections are well-recognized factors predisposing to childhoodonset asthma. Adult-onset asthma is more often associated with obesity, smoking, depression, or other life-style or environmental factors, even though genetic factors and respiratory tract infections may also play a role in adult-onset disease. Adult-onset asthma is characterized by absence of atopy and is often severe requiring treatment with high dose of inhaled and/or oral steroids. Variety of risk factors and nonatopic nature of adult-onset disease suggest that variety of mechanisms is involved in the disease pathogenesis and that these mechanisms differ from the pathobiology of childhood-onset asthma with prevailing Th2 airway inflammation. Recognition of the mechanisms andmediators that drive the adult-onset disease helps to develop novel strategies for the treatment. The aim of this review was to summarize the current knowledge on the pathogenesis of adult-onset asthma and to concentrate on the mechanisms and mediators involved in establishing adult-onset asthma in response to specific risk factors.We also discuss the involvement of these mechanisms in the currently recognized phenotypes of adult-onset asthma.
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