BACKGROUND: Indirect bronchoprovocation using adenosine monophosphate (AMP) is related to atopic phenotype expression. OBJECTIVE: To evaluate the putative relationship between skin prick allergen sensitization and bronchial hyper-responsiveness to AMP in a retrospective cross-sectional database analysis. METHODS: We retrospectively evaluated two groups of non-smoking asthmatics (forced expiratory volume in 1 s (FEV)1>/=60% predicted) who were reactive (responders) or unreactive (controls) to inhaled AMP. The main outcome measure was the difference in sensitization to individual allergens and the total atopic load according to the presence or absence of bronchial hyper-responsiveness. RESULTS: We initially identified 180 (44%) non-smoking asthmatics with PC20</=200 mg/mL, while 233 (56%) had PC20>/=1600 mg/mL. For those who had a skin prick test, the responders (n=151) and controls (n=151) were found to be matched for age, sex, inhaled corticosteroid dose and number of patients using inhaled corticosteroids. There were significant differences in the number of responders vs. controls in terms of sensitization to house dust mite (77% vs. 62%, P=0.004), aspergillus (19% vs. 9%, P=0.014), cat (61% vs. 48%, P=0.028), total atopic load (493 vs. 380 positive tests, P<0.001) and forced mid-expiratory flow (60% vs. 68% predicted, P<0.001). CONCLUSION: Sensitization to common aeroallergens increased the likelihood of bronchial inflammation as reflected by bronchial hyper-responsiveness to inhaled AMP, independently of both FEV1 or inhaled corticosteroid use. This in turn suggests an association between allergen exposure and AMP responsiveness in asthmatics. Further prospective long-term evaluation is indicated to assess whether allergen avoidance strategies can modify the airway response.
BACKGROUND: Indirect bronchoprovocation using adenosine monophosphate (AMP) is related to atopic phenotype expression. OBJECTIVE: To evaluate the putative relationship between skin prick allergen sensitization and bronchial hyper-responsiveness to AMP in a retrospective cross-sectional database analysis. METHODS: We retrospectively evaluated two groups of non-smoking asthmatics (forced expiratory volume in 1 s (FEV)1>/=60% predicted) who were reactive (responders) or unreactive (controls) to inhaled AMP. The main outcome measure was the difference in sensitization to individual allergens and the total atopic load according to the presence or absence of bronchial hyper-responsiveness. RESULTS: We initially identified 180 (44%) non-smoking asthmatics with PC20</=200 mg/mL, while 233 (56%) had PC20>/=1600 mg/mL. For those who had a skin prick test, the responders (n=151) and controls (n=151) were found to be matched for age, sex, inhaled corticosteroid dose and number of patients using inhaled corticosteroids. There were significant differences in the number of responders vs. controls in terms of sensitization to house dust mite (77% vs. 62%, P=0.004), aspergillus (19% vs. 9%, P=0.014), cat (61% vs. 48%, P=0.028), total atopic load (493 vs. 380 positive tests, P<0.001) and forced mid-expiratory flow (60% vs. 68% predicted, P<0.001). CONCLUSION: Sensitization to common aeroallergens increased the likelihood of bronchial inflammation as reflected by bronchial hyper-responsiveness to inhaled AMP, independently of both FEV1 or inhaled corticosteroid use. This in turn suggests an association between allergen exposure and AMP responsiveness in asthmatics. Further prospective long-term evaluation is indicated to assess whether allergen avoidance strategies can modify the airway response.