To determine the prevalence of airway hyperresponsiveness to inhaled mannitol in healthy smokers compared to nonsmokers and COPD patients and to longitudinally assess whether airway hyperresponsiveness to mannitol improves after smoking cessation.
Airway hyperresponsiveness to inhaled mannitol was determined in smokers (n=42), COPD patients (n=20) and healthy controls (n=45). In smokers, mannitol test was repeated three months after smoking cessation. Demographics including age, lung function and atopy status were similar for smokers and controls (p=ns).
Airway hyperresponsiveness to mannitol (= 15% fall in FEV1) was significantly more common among smokers (26.2%) and COPD-patients (45%) as compared to controls (2,2%) (p<0.01 for both)(see figure 1). The response-dose-ratio (% fall in FEV1/cumulative dose) was significantly higher in smokers (0.0231 ± 0.293) as compared to controls (0.0085 ± 0.234), respectively (p<0.01). After successful smoking cessation, response to mannitol became negative in all but one patient (p=0.021) and response-dose-ratio decreased in all cases (p=0.012)(see figure 2). None of the patients with a negative mannitol test turned positive, irrespective of the outcome of smoking cessation.
Bronchial hyperresponsiveness to mannitol is markedly increased in smokers and in COPD patients as compared to controls. Airway hyperresponsiveness positivity rate and response-dose-ratio to mannitol significantly decrease after short-term smoking cessation.
As increased AHR affects survival in COPD, particularly in smokers, early diagnose of AHR in smokers could have prognostic implications concerning COPD development. Moreover, evidence of AHR may act as a further motivation for asymptomatic smokers to quit, specially if this finding is likely to be influenced by giving up smoking.
Daiana Stolz, None.