Published ahead of print on December 9, 2005, doi:10.1164/rccm.200508-1305OC Am. J. Respir. Crit. Care Med., Volume 173, Number 5, March 2006, 535-539 A more recent version of this article appeared on March 1, 2006
Submitted on August 22, 2005 Progression of Airway Dysplasia and C-reactive Protein in Smokers at High Risk of Lung CancerDon D Sin1,1 Department of Medicine (Division of Respirology), University of British Columbia, Vancouver, BC, Canada; Department of Medicine, James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research, Vancouver, BC, Canada, 2 Department of Medicine, British Columbia Cancer Agency (Lung Tumor Group), Vancouver, BC, Canada, 3 Department of Medicine, James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research, Vancouver, BC, Canada; Department of Medicine, British Columbia Cancer Agency (Lung Tumor Group), Vancouver, BC, Canada * To whom correspondence should be addressed. E-mail: slam{at}bccancer.bc.ca.
Rationale : Chronic inflammation has been implicated in the development of airway dysplasia and lung cancer. It is unclear whether circulating biomarkers of inflammation could be used to predict progression of airway dysplasia.
Objective: We determined whether circulating levels of C-reactive protein (CRP) or other inflammatory biomarkers could predict progression of bronchial dysplasia in smokers over 6 months.
Methods: The plasma levels of CRP, interleukin (IL)-6, and 8 and monocyte chemoattractant protein-1 were measured at baseline in 65 ex-and current smokers who had at least one site of bronchial dysplasia > 1.2 mm in size. Additional bronchial biopsies were taken after 6 months from the same sites where dysplastic lesions were discovered at baseline. Progressive dysplastic lesions were defined as worsening of the dysplastic lesion by at least two grades or development of new dsyplastic lesions.
Results: Half of the participants developed progressive dysplastic lesions after 6 months. The baseline CRP levels in these participants were 64% higher than those without progressive disease (P=0.027). Only 1 out of 8 (13%) participants with CRP Key words: C-reactive protein, airway dysplasia, lung inflammation
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0.5 mg/L developed progressive disease, while 31 out of 57 (54%) participants with CRP > 0.5 mg/L developed progressive disease (p=0.011). The odds of developing progressive disease were 9.6 fold higher in the latter than in the former group.
Conclusion: Plasma CRP, in concert with lung function, and pack-years of smoking, appear to have excellent predictive powers in identifying participants with bronchial dyplastic lesions whose lesions progress to more advanced stages of dysplasia.
