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Original Research: LUNG CANCER |

Surfactant Protein D and Bronchial Dysplasia in Smokers at High Risk of Lung Cancer

Don D. Sin, MD, MPH, FCCP; S. F. Paul Man, MD, FCCP; Annette McWilliams, MD, FCCP; Stephen Lam, MD, FCCP
Author and Funding Information

*From the Department of Medicine, Division of Respirology, University of British Columbia, Vancouver, BC, Canada.

Correspondence to: Don D. Sin, MD, MPH, FCCP, St. Paul's Hospital, 1081 Burrard St, Vancouver, BC, Canada V6Z 1Y6; e-mail: dsin@mrl.ubc.ca

Drs. Sin, Man, and Lam have received research funding from AstraZeneca. Dr. McWilliams has reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.


This research was supported by US Public Health Service grant N01-CN85188 from the National Cancer Institute and The Canadian Institutes of Health Research. Dr. Sin was supported by a Canada Research Chair and a Senior Scholar Award from the Michael Smith Foundation for Health Research.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2008;134(3):582-588. doi:10.1378/chest.08-0600
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Background:  Surfactant dysfunction has been implicated in both lung cancer and COPD. This study evaluated the relationship between surfactant protein D (SP-D) and the progression of bronchial dysplasia in heavy smokers.

Methods:  SP-D and oxidized glutathione levels were determined in samples of BAL fluid from 71 ex-smokers and current heavy smokers who participated in a lung cancer chemoprevention study with inhaled budesonide therapy. Bronchoscopy with biopsies was performed at baseline and was repeated at 6 months. The primary end point was the progression of bronchial dysplasia over 6 months.

Results:  Log-normalized SP-D levels in BAL fluid were significantly associated with the progression of bronchial dysplasia. A 1-U decrease in log-normalized SP-D levels at baseline was associated with a 3.2-fold increase (95% confidence interval, 1.24 to 8.26) in the risk for progression. Reduced FEV1 also predicted the progression of bronchial dysplasia (p < 0.05). Additional reductions in BAL fluid SP-D levels over the 6 months further increased the risk of progression (odds ratio, 1.76 for a 1-U decrease in log-normalized SP-D levels in BAL fluid; p = 0.023). Thirty-seven percent of the variation in SP-D levels in BAL fluid was related positively to the subject's FEV1/FVC ratio, and inversely to their plasma C-reactive protein levels and number of pack-years of smoking.

Conclusion:  Reduced SP-D expression in BAL fluid was associated with the progression of bronchial dysplasia. SP-D levels in BAL fluid may serve as a potential biomarker to identify smokers who are at risk of early lung cancer.

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