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Original Research: COPD |

Neutrophil Gelatinase-Associated Lipocalin: A Biomarker in COPD

Tomas M. Eagan, MD, PhD; Jan K. Damås, MD, PhD; Thor Ueland, PhD; Marianne Voll-Aanerud, MD, PhD; Tom E. Mollnes, MD, PhD; Jon A. Hardie, MD, PhD; Per S. Bakke, MD, PhD; Pål Aukrust, MD, PhD
Author and Funding Information

From the Department of Thoracic Medicine (Drs Eagan, Voll-Aanerud, Hardie, and Bakke), Haukeland University Hospital, Bergen, Norway; Division of Physiology (Dr Eagan), University of California San Diego, La Jolla, CA; Research Institute for Internal Medicine (Drs Damås, Ueland, and Aukrust) and Section of Clinical Immunology and Infectious Diseases (Dr Damås), Rikshospitalet University Hospital, Oslo, Norway; Department of Infectious Diseases (Dr Damås), St Olavs Hospital, Trondheim, Norway; Section of Endocrinology (Dr Ueland) and Institute of Immunology (Drs Ueland, Mollnes, and Aukrust), Rikshospitalet University Hospital, Oslo, Norway; Faculty of Medicine (Dr Aukrust), University of Oslo, Oslo, Norway; and Section of Pulmonary Medicine (Dr Bakke), Institute of Medicine, University of Bergen, Bergen, Norway.

Correspondence to: Tomas M. Eagan, MD, PhD, Department of Thoracic Medicine, Haukeland University Hospital, Jonas Lies vei 65, 5021 Bergen, Norway; e-mail: tomas.eagan@med.uib.no


Funding/Support: The study was funded by grants from The Foundation for Respiratory Research, University of Bergen, Bergen, Norway, and by grants from Center for Clinical Research, Haukeland University Hospital.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2010 American College of Chest Physicians


Chest. 2010;138(4):888-895. doi:10.1378/chest.09-2718
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Background:  Neutrophil gelatinase-associated lipocalin (NGAL) is an antimicrobial peptide that could be involved in the pathogenesis of COPD. This study aimed to measure the plasma levels of NGAL in a large cohort of patients with COPD and control subjects and examine the levels of NGAL by COPD characteristics.

Methods:  The study included 402 patients with COPD and 229 control subjects aged 40 to 76 years from the Bergen COPD Cohort Study. All patients with COPD had an FEV1/FVC ratio of < 0.7, an FEV1 < 80% predicted, and a smoking history of ≥ 10 pack-years. Plasma levels of NGAL were determined by enzyme immunoassay. Linear regression models were fitted with NGAL as the outcome variable. Confounders examined were sex, age, smoking, Charlson comorbidity score, use of inhaled steroids, neutrophil cell count, plasma creatinine and ferritin, and C-reactive protein.

Results:  Mean ± SD plasma concentrations of NGAL were 75.1 ± 31.8 ng/mL in patients with COPD and 56.5 ± 22.0 ng/mL in control subjects (P < .01). NGAL levels were bivariately associated with age, smoking, body composition, Charlson comorbidity score, neutrophil blood count, creatinine, and C-reactive protein but were significantly elevated in patients with COPD, even after adjustment for confounders. Frequent exacerbations and hypoxemia was associated with higher levels of NGAL, whereas increasing Global Initiative for Chronic Obstructive Lung Disease stage was associated with lower levels of NGAL among patients with COPD.

Conclusions:  Plasma levels of NGAL were significantly higher in patients with COPD compared with control subjects. NGAL was related to important COPD characteristics.

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