Background. Asthma associated with sinusitis is supposed to be sustained by bronchoconstrictive reflexes orginating in extrathoracic airway (EA) receptors. The study was designed to evaluate the relationship between extrathoracic airway responsiveness and bronchial responsiveness in sinusitis. Material and methods. We performed histamine inhalation challenge in 61 patients with chronic sinusitis, during disease exacerbation and after treatment with antimirobials and nasal flunisolide for 2 weeks. Forced expiratory volume in 1 second (FEV1) and maximal mid-inspiratory flow (MIF50) were the respective indexes of bronchial and EA narrowing. The histamine concentrations causing a 15% fall in FEV1 (PC15FEV1) and 25% drop in MIF50 (PC25MIF50) were used as thresholds of bronchial and extrathoracic responsiveness. Thresholds of 8 mg/ml or less were assumed to indicate bronchial hyperresponsiveness (B-HR) or EA hyperresponsiveness (EA-HR). Results. During sinusitis exacerbation 49 of 61 patients (80.3%) had extrathoracic airway hyperresponsiveness, which in 32 (65.3%) was associated with bronchial hyperresponsiveness. After treatment extrathoracic airway hyperresponsiveness reversed in 79% of cases. The improvement of EA-HR was closely related to the decrease in neutrophils in nasal lavage. Conclusions: Our findings suggest that in sinusitis, bronchial hyperresponsiveness and so asthma may be sustained by constrictive reflexes originating in extrathoracic airway receptors, made hypersensitive by seeding of the inflammatory process.
Nasosinusal inflammation and extra- and intrathoracic airway responsiveness
BUCCA, Caterina
1997-01-01
Abstract
Background. Asthma associated with sinusitis is supposed to be sustained by bronchoconstrictive reflexes orginating in extrathoracic airway (EA) receptors. The study was designed to evaluate the relationship between extrathoracic airway responsiveness and bronchial responsiveness in sinusitis. Material and methods. We performed histamine inhalation challenge in 61 patients with chronic sinusitis, during disease exacerbation and after treatment with antimirobials and nasal flunisolide for 2 weeks. Forced expiratory volume in 1 second (FEV1) and maximal mid-inspiratory flow (MIF50) were the respective indexes of bronchial and EA narrowing. The histamine concentrations causing a 15% fall in FEV1 (PC15FEV1) and 25% drop in MIF50 (PC25MIF50) were used as thresholds of bronchial and extrathoracic responsiveness. Thresholds of 8 mg/ml or less were assumed to indicate bronchial hyperresponsiveness (B-HR) or EA hyperresponsiveness (EA-HR). Results. During sinusitis exacerbation 49 of 61 patients (80.3%) had extrathoracic airway hyperresponsiveness, which in 32 (65.3%) was associated with bronchial hyperresponsiveness. After treatment extrathoracic airway hyperresponsiveness reversed in 79% of cases. The improvement of EA-HR was closely related to the decrease in neutrophils in nasal lavage. Conclusions: Our findings suggest that in sinusitis, bronchial hyperresponsiveness and so asthma may be sustained by constrictive reflexes originating in extrathoracic airway receptors, made hypersensitive by seeding of the inflammatory process.
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