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Mold sensitization is common amongst patients with severe asthma requiring multiple hospital admissions |
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| Authors: | B Ronan O'Driscoll Linda C Hopkinson David W Denning |
| Affiliation: | 1. gsf Institute of Epidemiology, GSF National Research Center for Environment and Health, Neuherberg, Germany 2. MDC Gene Mapping Center, Max-Delbrück Center for Molecular Medicine, Berlin, Germany 10. Praxis für Kinderheilkunde, Berlin, Germany 3. LoesGen, Oberb?zberg, Switzerland 4. Praxis für Kinderheilkunde, Ravensburg, Germany 5. FF and K. Zima, Praxis für Kinderheilkunde, Aachen-Laurensberg, germany 6. HJ and M. Barker, Klinik für Kinderheilkunde der RWTH Aachen, Germany 7. JK and W. Leupold, Klinik für Kinder und Jugendliche des Universit?tsklinikums Carl Gustav Carus, Dresden, Germany 8. AK and W. Rebien, Praxis für Kinderheilkunde, Hamburg, Germany 9. Universit?tskinderklinik, Düsseldorf, Germany 11. Praxis für Kinderheilkunde, Homburg, Germany 12. Praxis für Kinderheilkunde, Pfullendorf, Germany 13. Institut für Immunologie, Universit?t Jena, Germany |
| Abstract: | BackgroundAsthma is a complex genetic disease with more than 20 genome-wide scans conducted so far. Regions on almost every chromosome have been linked to asthma and several genes have been associated. However, most of these associations are weak and are still awaiting replication.MethodsIn this study, we conducted a second-stage genome-wide scan with 408 microsatellite markers on 201 asthma-affected sib pair families and defined clinical subgroups to identify phenotype-genotype relations.ResultsThe lowest P value for asthma in the total sample was 0.003 on chromosome 11, while several of the clinical subsets reached lower significance levels than in the overall sample. Suggestive evidence for linkage (p = 0.0007) was found for total IgE on chromosomes 1, 7 and again on chromosome 11, as well as for HDM asthma on chromosome 12. Weaker linkage signals could be found on chromosomes 4 and 5 for early onset and HDM, and, newly described, on chromosome 2 for severe asthma and on chromosome 9 for hay fever.ConclusionsThis phenotypic dissection underlines the importance of detailed clinical characterisations and the extreme genetic heterogeneity of asthma. |
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