Parallel reductions of IgE and exhaled nitric oxide after optimized anti‐inflammatory asthma treatment

Immunoglobulin E (IgE) is crucial for the development of airway inflammation in atopic asthma, and inhibition of IgE using monoclonal antibodies is now part of asthma therapy. However, the impact of ordinary anti‐inflammatory treatment on IgE is unclear. The aim of this study was to investigate if o...

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Bibliographic Details
Published in:Immunity, Inflammation and Disease Inflammation and Disease, 2016-06, Vol.4 (2), p.182-190
Main Authors: Syk, Jörgen, Malinovschi, Andrei, Borres, Magnus P., Undén, Anna‐Lena, Andreasson, Anna, Lekander, Mats, Alving, Kjell
Format: Article
Language:English
Subjects:
Allergies
Asthma
asthma control
atopy
breath test
corticosteroid
FENO
immunoglobulin E
Immunoglobulins
Inflammation
leukotriene-receptor antagonist
Medicin och hälsovetenskap
Nitric oxide
Original Research
Primary care
Quality of life
Questionnaires
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Summary:Immunoglobulin E (IgE) is crucial for the development of airway inflammation in atopic asthma, and inhibition of IgE using monoclonal antibodies is now part of asthma therapy. However, the impact of ordinary anti‐inflammatory treatment on IgE is unclear. The aim of this study was to investigate if optimization of treatment with inhaled corticosteroid (ICS) and leukotriene‐receptor antagonist (LTRA) according to symptoms or exhaled nitric oxide (FENO) levels over a one‐year period affects IgE concentrations. Altogether, 158 relatively well‐controlled but multi‐sensitized asthmatics (age 18–65 years), with ongoing ICS treatment at baseline, were included in this post hoc analysis of data from a randomized, controlled trial on FENO‐guided asthma therapy. Asthma control and quality of life (Juniper ACQ and mAQLQ), FENO, and serum IgE were measured at baseline and after one year. Concentrations of IgE antibodies to six common perennial aeroallergens were summed up (perennial IgE). We found that perennial and total IgE decreased by 10.2% and 16.0% (P 
ISSN:2050-4527
2050-4527
DOI:10.1002/iid3.103