Relevance of specific IgE antibody titer to the prevalence, severity, and persistence of asthma among 19-year-olds in northern Sweden - 18/04/17
Abstract |
Background |
Although sensitization to indoor allergens is strongly associated with asthma, there are questions as to how this relates to asthma symptoms.
Objective |
We sought to study the relevance of IgE antibodies to cat and dog allergens in an area in which (1) the climate discourages cockroach, fungal, and mite growth and (2) dander allergens are known to be present in schools and houses without animals.
Methods |
IgE to 8 allergens was tested in 963 sera from a population-based study on 19-year-olds, and associations with asthma symptoms, diagnosis, and treatment were examined. In positive sera IgE to specific cat and dog allergens was also assayed.
Results |
IgE specific for animal dander had the highest prevalence and strongest relationship to asthma diagnosis. Furthermore, asthma severity, as judged by the frequency of symptoms and use of treatment, was directly associated with the titer of IgE antibodies to animal dander. Among the 103 subjects who had current asthma at age 19 years, 50 had asthma before age 12 years. Among those 50, the odds ratios for asthma related to any IgE antibodies to animal dander or high-titer IgE antibodies (≥17.5 IU/mL) were 9.2 (95% CI, 4.9-17) and 13 (95% CI, 6.9-25), respectively. In multivariable analysis IgE antibodies to Fel d 1 and Can f 5 were each associated with current asthma.
Conclusion |
High-titer IgE antibodies to cat and dog allergens were strongly associated with the diagnosis, severity, and persistence of asthma; however, a large proportion of patients with current asthma did not live in a house with a cat or dog.
Le texte complet de cet article est disponible en PDF.Key words : IgE titer, IgE antibodies, mammalian allergen, asthma severity, cat ownership
Plan
| Supported by National Institutes of Health grants R01-AI-20565 and U19-AI-070364 to T.A.E.P.-M., as well as P30-ES-09089 to M.S.P., and grants to E.R. from the Swedish Heart-Lung Foundation, the Swedish Research Council, the Swedish Asthma-Allergy Foundation, the Swedish Foundation for Health Care Science and Allergy Research (Vårdal), Visare Norr, Umeå University, and Norrbotten County Council. Phadia/Thermo Fisher provided unrestricted support for IgE assays. Additional funding was provided by GlaxoSmithKline World Wide Epidemiology and ALK-Abelló (Hörsholm, Denmark). |
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| Disclosure of potential conflict of interest: E. Ronmark has received research support from the Swedish Heart-Lung Foundation, the Swedish Asthma-Allergy Foundation, the Swedish Research Council, Umeå University, Visare Norr, Norrbotten County Council, and GlaxoSmithKline. B. Lundback has received research support from the Swedish Heart-Lung Foundation, the Swedish Asthma-Allergy Foundation, the Swedish Research Council, Umeå University, Visare Norr, Norrbotten County Council, GlaxoSmithKline, and AstraZeneca and has participated in the advisory boards for and received lecture fees from AstraZeneca, GlaxoSmithKline, and Novartis. T. A. E. Platts-Mills has received research support from Thermo Fisher/Phadia. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 138 - N° 6
P. 1582-1590 - décembre 2016 Retour au numéro
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