Eur Respir J 2010, doi:10.1183/09031936.00146509
K.M. Kunisaki*, D.E. Niewoehner*,#, R.J. Singh¶ and J.E. Connett+
Division of Pulmonary Allergy, Critical Care and Sleep Medicine, University of Minnesota, Minneapolis, MN USA
Pulmonary Section, Minneapolis Veterans Affairs Medical Center Minneapolis, MN USA
Dept of Laboratory Medicine and Pathology Mayo Clinic, Rochester, MN USA
Division of Biostatistics, University of Minnesota Minneapolis, MN USA
CORRESPONDENCE: K.M. Kunisaki, Minneapolis Veterans Affairs Medical Center, Pulmonary, 111N, One Veterans Drive, Minneapolis, MN 55417, E-mail: kunis001 at umn.edu
Low vitamin D blood levels are postulated to be a risk factor for worse lung function, largely based on cross-sectional data. We sought to use longitudinal data to test the hypothesis that baseline plasma 25-hydroxyvitamin D [25(OH)D] is lower in subjects with more rapid lung function decline, compared to those with slow lung function decline.
We conducted a nested, matched case-control study in the Lung Health Study 3 cohort. Cases and controls were continuous smokers with rapid and slow lung function decline, respectively, over approximately 6 years of follow-up. We compared baseline 25(OH)D levels between cases and controls, matching on date of blood draw and clinical center.
Among 196 subjects, despite rapid and slow decliners experiencing strikingly and significantly different rates of decline of forced expiratory volume in one second (–151 vs. –0.28 mL·year–1; p<0.001), there was no significant difference in baseline 25(OH)D levels (25.0 vs. 25.9 ng·mL–1; p=0.54). There was a high prevalence of vitamin D insufficiency (35%) and deficiency (31%); only 4% had a normal 25(OH)D level in the winter.
Although vitamin D insufficiency and deficiency are common among continuous smokers with established mild to moderate COPD, baseline 25(OH)D levels are not predictive of subsequent lung function decline.