Source: International Congress 2014 – New mechanisms in the pathogenesis of asthma and other lung diseases
Disease area: Airway diseases

Abstract

BackgroundAsthmatics have a blunted innate immune response to viral airway infections, measured by reduced interferon production, which has been associated with high levels of IgE in vitro, but the clinical significance of this, in a large representative group of adult asthmatics, has not been established.We hypothesized that atopy and high IgE would confer an increased risk of asthma exacerbations in relation to upper airway infections.MethodsAll patients referred consecutively over a 12-months period for specialist assessment of asthma at Bispebjerg Hospital in Copenhagen had total IgE and a skin prick test to 10 aeroallergens measured, and answered the AAAI questionnaire regarding symptoms, including symptoms in relation to colds.ResultsAmong 185 assessed 155 had asthma (57,4% females, mean age 31.1 years) of whom, 56% (n=86) answered yes to the question: "Do you experience colds that 'go to the chest', or take more than 10 days to get over?". These patients had significantly higher IgE than patients who did not report this (Total IgE 309 vs. 128 IU/ml in the two groups respectively (p=0,008). The proportion of patients having at least one positive skin prick tests was not significantly different, but the percentage of subjects with sensitization to house dust mite (HDM) was significantly higher for both derm. pteronyssinus and farinae (40% vs. 22%, p=0.027 & 35% vs. 17%, p=0.018).ConclusionHigh IgE and HDM sensitization are characteristics of asthmatics who report having exacerbations in relation to upper respiratory tract infections, indicating that IgE plays a role in the susceptibility to virus induced exacerbations in adult asthmatics.

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A. Bjerregård, A. Sverrild, V. Backer, C. Porsbjerg (Copenhagen, Denmark). Adult asthma patients reporting exacerbations triggered by upper airway infection have increased total IgE and sensitization to HDM. Eur Respir J 2014; 44: Suppl. 58, 3867

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