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Original Research: COPD |

Serum Bilirubin and Disease Progression in Mild COPDBilirubin and Disease Progression in COPD

Scott Apperley, MD; Hye Yun Park, MD; Daniel T. Holmes, MD; S. F. Paul Man, MD; Donald Tashkin, MD; Robert A. Wise, MD; John E. Connett, PhD; Don D. Sin, MD, FCCP
Author and Funding Information

From the Department of Medicine, Pulmonary Division (Drs Apperley, Man, and Sin), and the Department of Pathology (Dr Holmes), University of British Columbia, Vancouver, BC, Canada; the UBC James Hogg Research Centre and the Institute for Heart and Lung Health (Drs Park, Man, and Sin), St. Paul’s Hospital, Vancouver, BC, Canada; the Division of Pulmonary and Critical Care Medicine (Dr Park), Department of Medicine, Samsung Medical Center, Seoul, South Korea; the Division of Pulmonary and Critical Care Medicine (Dr Tashkin), David Geffen School of Medicine at UCLA, Los Angeles, CA; the Division of Pulmonary and Critical Care Medicine (Dr Wise), Johns Hopkins University School of Medicine, Baltimore, MD; and the Division of Biostatistics (Dr Connett), School of Public Health, University of Minnesota, Minneapolis, MN.

CORRESPONDENCE TO: Don D. Sin, MD, FCCP, St. Paul’s Hospital, 1081 Burrard St, Vancouver, BC, V6Z 1Y6, Canada; e-mail: don.sin@hli.ubc.ca


FUNDING/SUPPORT: The LHS Biomarker Study was in part funded by the Canadian Respiratory Research Network, which is supported by grants from the Canadian Institutes of Health Research-Institute of Circulatory and Respiratory Health; Canadian Lung Association/Canadian Thoracic Society; British Columbia Lung Association; and industry partners Boehringer-Ingelheim Canada Ltd, AstraZeneca Canada Inc, and Novartis Canada Ltd. The original LHS was funded by the US National Heart, Lung, and Blood Institute. Dr Sin is a Canada Research Chair in COPD.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;148(1):169-175. doi:10.1378/chest.14-2150
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BACKGROUND:  COPD is a chronic inflammatory disorder associated with oxidative stress. Serum bilirubin has potent antioxidant actions, and higher concentrations have been shown to protect against oxidative stress. The relation between serum bilirubin and COPD progression is unknown.

METHODS:  Serum bilirubin was measured in 4,680 smokers aged 35 to 60 years old with mild to moderate airflow limitation. The relationship of serum bilirubin to postbronchodilator FEV1 and rate of FEV1 decline over 3 to 9 years was determined using regression modeling. Total and disease-specific mortality were also ascertained.

RESULTS:  Serum bilirubin was positively related to FEV1 (P < .001). Serum bilirubin was also negatively related to the annual decline in FEV1 when adjusted for baseline demographics, pack-years smoked, and baseline measures of lung function (P = .01). Additionally, serum bilirubin was negatively associated with risk of death from coronary heart disease (P = .03); however, the relationships between bilirubin and other mortality end points were not statistically significant (P > .05).

CONCLUSIONS:  Bilirubin is inversely related to COPD disease severity and progression. Higher serum bilirubin concentration was associated with a higher FEV1 and less annual decline in FEV1. Bilirubin was also associated with less coronary heart disease mortality. These data support the hypothesis that bilirubin has a protective effect on COPD disease progression, possibly through its antioxidant actions. Bilirubin may prove useful as an easily accessible and readily available blood-based COPD biomarker.

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