Published ahead of print on December 9, 2005, doi:10.1164/rccm.200508-1305OC
© 2006 American Thoracic Society doi: 10.1164/rccm.200508-1305OC
Progression of Airway Dysplasia and C-Reactive Protein in Smokers at High Risk of Lung CancerDivision of Respirology, Department of Medicine, University of British Columbia; James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research; and the Lung Tumor Group, British Columbia Cancer Agency, Vancouver, British Columbia, Canada Correspondence and requests for reprints should be addressed to Stephen Lam, M.D., British Columbia Cancer Agency, Cancer Imaging Department, 675 West 10th Avenue, Vancouver, BC, Canada V5Z 1L3. 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 mo. Methods: The plasma levels of CRP, interleukins 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 mo 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 dysplastic lesions.
Results: Half of the participants developed progressive dysplastic lesions after 6 mo. The baseline CRP levels in these participants were 64% higher than those without progressive disease (p = 0.027). Only one of eight (13%) participants with CRP Conclusion: Plasma CRP, in concert with lung function and pack-years of smoking, appears to have excellent predictive powers in identifying participants with bronchial dyplastic lesions whose lesions progress to more advanced stages of dysplasia.
Key Words: airway dysplasia C-reactive protein lung inflammation This article has been cited by other articles:
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