Robert M Burkes1, Agathe S Ceppe2, Claire M Doerschuk3, David Couper4, Eric A Hoffman5, Alejandro P Comellas6, R Graham Barr7, Jerry A Krishnan8, Christopher Cooper9, Wassim W Labaki10, Victor E Ortega11, J Michael Wells12, Gerard J Criner13, Prescott G Woodruff14, Russell P Bowler15, Cheryl S Pirozzi16, Nadia N Hansel17, Robert A Wise17, Todd T Brown18, M Bradley Drummond3. 1. Division of Pulmonary Diseases and Critical Care Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC. Electronic address: robert.burkes@unchealth.unc.edu. 2. Marsico Lung Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC. 3. Division of Pulmonary Diseases and Critical Care Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC; Marsico Lung Institute, University of North Carolina at Chapel Hill, Chapel Hill, NC. 4. University of North Carolina Gillings School of Global Public Health, Chapel Hill, NC. 5. Department of Radiology, University of Iowa Carver College of Medicine, Iowa City, IA. 6. Division of Pulmonary, Critical Care, and Occupational Medicine, University of Iowa Carver College of Medicine, Iowa City, IA. 7. Department of Epidemiology, Columbia University, New York, NY. 8. Division of Pulmonary, Critical Care, Sleep, and Allergy Medicine, University of Illinois at Chicago, Chicago, IL. 9. Division of Pulmonary and Critical Care Medicine, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, CA. 10. Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, MI. 11. Section of Pulmonary, Critical Care, Allergy, and Immunologic Disease, Wake Forest University, Winston-Salem, NC. 12. Division of Pulmonary, Allergy, and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL. 13. Division of Thoracic Medicine and Surgery, Temple University, Philadelphia, PA. 14. Division of Pulmonary Critical Care, Allergy, and Sleep Medicine, University of California, San Francisco, San Francisco, CA. 15. Division of Pulmonary, Critical Care, and Sleep Medicine, National Jewish Health, Denver, CO. 16. Division of Pulmonary and Critical Care Medicine, University of Utah, Salt Lake City, UT. 17. Division of Pulmonary and Critical Care Medicine, Johns Hopkins University, Baltimore, MD. 18. Division of Endocrinology, Diabetes, and Metabolism, Johns Hopkins University, Baltimore, MD.
Abstract
BACKGROUND: The relationship between 25-hydroxyvitamin D (25-OH-vitamin D) and COPD outcomes remains unclear. Using the Subpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS), we determined associations among baseline 25-OH-vitamin D and cross-sectional and longitudinal lung function and COPD exacerbations. METHODS: Serum 25-OH-vitamin D level was measured in stored samples from 1,609 SPIROMICS participants with COPD. 25-OH-vitamin D levels were modeled continuously and dichotomized as deficient (< 20 ng/mL) vs not deficient (≥ 20 ng/mL). Outcomes of interest included % predicted FEV1 (current and 1-year longitudinal decline) and COPD exacerbations (separately any and severe, occurring in prior year and first year of follow-up). RESULTS: Vitamin D deficiency was present in 21% of the cohort and was more prevalent in the younger, active smokers, and blacks. Vitamin D deficiency was independently associated with lower % predicted FEV1 (by 4.11%) at enrollment (95% CI, -6.90% to -1.34% predicted FEV1; P = .004), 1.27% predicted greater rate of FEV1 decline after 1 year (95% CI, -2.32% to -0.22% predicted/y; P = .02), and higher odds of any COPD exacerbation in the prior year (OR, 1.32; 95% CI, 1.00-1.74; P = .049). Each 10-ng/mL decrease in 25-OH-vitamin D was associated with lower baseline lung function (-1.04% predicted; 95% CI, -1.96% to -0.12% predicted; P = .03) and increased odds of any exacerbation in the year before enrollment (OR, 1.11; 95% CI, 1.01-1.22; P = .04). CONCLUSIONS: Vitamin D deficiency is associated with worse cross-sectional and longitudinal lung function and increased odds of prior COPD exacerbations. These findings identify 25-OH-vitamin D levels as a potentially useful marker of adverse COPD-related outcomes.
BACKGROUND: The relationship between 25-hydroxyvitamin D (25-OH-vitamin D) and COPD outcomes remains unclear. Using the Subpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS), we determined associations among baseline 25-OH-vitamin D and cross-sectional and longitudinal lung function and COPD exacerbations. METHODS: Serum 25-OH-vitamin D level was measured in stored samples from 1,609 SPIROMICS participants with COPD. 25-OH-vitamin D levels were modeled continuously and dichotomized as deficient (< 20 ng/mL) vs not deficient (≥ 20 ng/mL). Outcomes of interest included % predicted FEV1 (current and 1-year longitudinal decline) and COPD exacerbations (separately any and severe, occurring in prior year and first year of follow-up). RESULTS:Vitamin D deficiency was present in 21% of the cohort and was more prevalent in the younger, active smokers, and blacks. Vitamin D deficiency was independently associated with lower % predicted FEV1 (by 4.11%) at enrollment (95% CI, -6.90% to -1.34% predicted FEV1; P = .004), 1.27% predicted greater rate of FEV1 decline after 1 year (95% CI, -2.32% to -0.22% predicted/y; P = .02), and higher odds of any COPD exacerbation in the prior year (OR, 1.32; 95% CI, 1.00-1.74; P = .049). Each 10-ng/mL decrease in 25-OH-vitamin D was associated with lower baseline lung function (-1.04% predicted; 95% CI, -1.96% to -0.12% predicted; P = .03) and increased odds of any exacerbation in the year before enrollment (OR, 1.11; 95% CI, 1.01-1.22; P = .04). CONCLUSIONS:Vitamin D deficiency is associated with worse cross-sectional and longitudinal lung function and increased odds of prior COPD exacerbations. These findings identify 25-OH-vitamin D levels as a potentially useful marker of adverse COPD-related outcomes.
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