Abstract
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 < .001 both comparisons). This was not related to allergen exposure, whereas the total use of ICS and LTRA during the year correlated with the reduction in perennial IgE (P = .030 and P = .013). The decrease in perennial and total IgE correlated significantly with the reduction in FENO (P < .003 and P < .001), and with improvements in ACQ and mAQLQ scores (P < 0.05, all comparisons). We conclude that one year of optimization of treatment with ICS and LTRA in patients with persistent atopic asthma resulted in significant decreases in total IgE and IgE antibodies; these decreases correlated with a reduction in FENO and improvements in asthma control and quality of life. Thus, IgE is reduced by ordinary asthma controller medications and the effect on IgE seems to be clinically important.
Highlights
Asthma is by definition an inflammatory disorder of the airways
The relative change in food Immunoglobulin E (IgE) over one year showed a significant positive correlation with age (Table S5), which indicates that the reduction in food IgE was larger for younger subjects, and a trend toward a similar relationship was seen for total IgE
No significant difference between men and women was found for changes in IgE concentrations (Table S6)
Summary
Asthma is by definition an inflammatory disorder of the airways. Immunoglobulin E (IgE) is often involved in the inflammation, as the majority of asthmatics have atopic asthma, which is most commonly initiated in childhood by sensitization to airborne allergens [1]. Asthma prevalence has been shown to correlate directly with increased levels of total IgE, regardless of proven atopy [2, 3]. The airway inflammation in atopic asthma is recognized as Th2. Parallel reductions of IgE and exhaled nitric oxide lymphocyte-driven and Th2 cytokines modulate the inflammation with, for example, increased IgE concentration, elevated fraction of exhaled nitric oxide (FENO), and recruitment and activation of eosinophilic granulocytes and mast cells [1, 4, 5]. Humanized monoclonal antibodies against IgE are used for treatment of moderate to severe atopic asthma [1, 6]; a reduction of IgE concentration has potential to reduce asthma symptoms and improve management of asthma
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