Noninvasive evaluation of airway inflammation in asthmatic patients who smoke: implications for application in clinical practice.

Second Respiratory Medicine Department, Medical School, University of Athens, Athens, Greece.

BACKGROUND: Despite the limited pathological data in asthmatic patients who smoke, it is thought that cigarette smoking may modify airway inflammation. OBJECTIVES: To summarize the major clinical studies that have used samples obtained by noninvasive techniques, such as blood, urine, exhaled breath condensate (EBC), fractional exhaled nitric oxide (FeNO), and induced sputum, for the evaluation of airway inflammation and the response to treatment in asthmatic patients who smoke and to evaluate which biomarkers have been adequately validated to be used in routine clinical practice. DATA SOURCES: In this review, we collected the available literature that addressed this topic. We searched the MEDLINE database using a combination of the following keywords: smoking or asthma or inflammation or mechanisms or exhaled nitric oxide or induced sputum or EBC. STUDY SELECTION: We selected the articles that most adequately addressed this topic for inclusion in this review. RESULTS: Smoking significantly influences FeNO and negatively affects its concentration, although FeNO can distinguish steroid-naive asthmatic smokers from nonasthmatic smokers. Sputum neutrophilia is the predominant finding in induced sputum in asthmatic patients who smoke but inflammatory mediators derived either from neutrophils or from a T(H)1 response can also be measured in the supernatants. EBC gives the opportunity to evaluate neutrophil-derived cytokines, airway acidification, and plausible protective mechanisms in smoking asthma. CONCLUSIONS: Despite the encouraging updated results, the introduction of noninvasive techniques in daily clinical practice requires the reworking of some methodologic pitfalls and the identification of a reliable biomarker that is reproducible, possesses normal values, and provides information for the underlying inflammatory process and the response to treatment.

PMID: 18814444 [PubMed - indexed for MEDLINE]