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Clinical Investigations: ASTHMA |

The Effect of Cigarette Smoking on Exhaled Nitric Oxide in Mild Steroid-Naive Asthmatics*

Geert M. Verleden, PhD; Lieven J. Dupont, MD; Ann C. Verpeut, MD; Maurits G. Demedts, PhD
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*From the Department of Respiratory Diseases, University Hospital Gasthuisberg, Leuven, Belgium.

Correspondence to: Geert M. Verleden, PhD, Department of Respiratory Diseases, University Hospital Gasthuisberg, 49, Herestraat, B-3000 Leuven, Belgium; e-mail: geert.verleden@uz.kuleuven.ac.be



Chest. 1999;116(1):59-64. doi:10.1378/chest.116.1.59
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Study objectives: It has been demonstrated previously that exhaled nitric oxide (eNO) is increased in steroid-naive asthmatics and that inhaled steroids reduce eNO in these patients. Cigarette smoking has also been reported to reduce the eNO in healthy volunteers. Recently a correlation has been demonstrated between eNO and airway hyperresponsiveness in steroid-naive, mild asthmatics. We hypothesized that cigarette smoking would reduce the eNO level in steroid-naive asthmatics and might, therefore, affect the correlation between eNO and airway hyperresponsiveness.

Design: Comparison of eNO in healthy smoking and nonsmoking volunteers with the level of eNO in steroid-naive and steroid-treated asthmatics. Correlate the eNO level with the provocative concentration of histamine causing a 20% fall in FEV1 (PC20hist) in the asthmatic smoking and nonsmoking patients.

Setting: University outpatient asthma clinic.

Patients and methods: eNO levels and PC20hist were measured in three different asthmatic patient groups (group A = 29 steroid-naive, nonsmoking asthmatics; group B = 19 steroid-treated, nonsmoking asthmatics; and group C = 13 smoking, steroid-naive asthmatics) and in two healthy volunteer groups (group D = 18 nonsmoking; and group E = 16 smoking).

Results: eNO in group A was significantly increased compared with the values in groups B and D (21.8 ± 12.7, 12.8 ± 4.9, and 10.6 ± 2.2 parts per billion[ ppb], respectively). Cigarette smoking decreased eNO in healthy volunteers (7.4 ± 1.8 ppb, group E) as well as in steroid-naive asthmatics (12.7 ± 5.1 ppb, group C). There was a significant correlation between eNO and PC20hist in group A (r = −0.45, p < 0.05); this correlation was, however, lost in both groups B and C.

Conclusion: Cigarette smoking and inhaled steroids reduce the eNO in patients with mild asthma to a comparable extent. Because the correlation between eNO and airway hyperresponsiveness was lost in steroid-treated and smoking, steroid-naive asthmatics, we question the value of eNO as a marker of airway inflammation, at least in mild asthmatics who are already being treated with inhaled steroids or who are currently smoking.

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