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.
Original language | English (US) |
---|---|
Pages (from-to) | 856-865 |
Number of pages | 10 |
Journal | Chest |
Volume | 157 |
Issue number | 4 |
DOIs | |
State | Published - Apr 2020 |
Keywords
- COPD
- COPD epidemiology
- COPD exacerbations
- lung function
- vitamin D
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Critical Care and Intensive Care Medicine
- Cardiology and Cardiovascular Medicine
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In: Chest, Vol. 157, No. 4, 04.2020, p. 856-865.
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TY - JOUR
T1 - Associations Among 25-Hydroxyvitamin D Levels, Lung Function, and Exacerbation Outcomes in COPD
T2 - An Analysis of the SPIROMICS Cohort
AU - SPIROMICS Investigators
AU - Burkes, Robert M.
AU - Ceppe, Agathe S.
AU - Doerschuk, Claire M.
AU - Couper, David J.
AU - Hoffman, Eric A.
AU - Comellas, Alejandro P.
AU - Barr, R. Graham
AU - Krishnan, Jerry A.
AU - Cooper, Christopher
AU - Labaki, Wassim W.
AU - Ortega, Victor E.
AU - Wells, J. Michael
AU - Criner, Gerard J.
AU - Woodruff, Prescott G.
AU - Bowler, Russell P.
AU - Pirozzi, Cheryl S.
AU - Hansel, Nadia N.
AU - Wise, Robert A.
AU - Brown, Todd T.
AU - Drummond, M. Bradley
AU - Alexis, Neil E.
AU - Anderson, Wayne H.
AU - Arjomandi, Mehrdad
AU - Barjaktarevic, Igor
AU - Bateman, Lori A.
AU - Bhatt, Surya P.
AU - Bleecker, Eugene R.
AU - Boucher, Richard C.
AU - Christenson, Stephanie A.
AU - Cooper, Christopher B.
AU - Crystal, Ronald G.
AU - Curtis, Jeffrey L.
AU - Dransfield, Mark T.
AU - Drummond, Brad
AU - Freeman, Christine M.
AU - Galban, Craig
AU - Han, Mei Lan K.
AU - Hastie, Annette T.
AU - Huang, Yvonne
AU - Kaner, Robert J.
AU - Kanner, Richard E.
AU - Kleerup, Eric C.
AU - LaVange, Lisa M.
AU - Lazarus, Stephen C.
AU - Martinez, Fernando J.
AU - Meyers, Deborah A.
AU - Moore, Wendy C.
AU - Newell, John D.
AU - Paine, Robert
AU - Rennard, Stephen I.
N1 - Funding Information: FUNDING/SUPPORT: R. M. B. has received support from the National Institutes of Health, National Heart, Lung, and Blood Institute (NIH-NHLBI) [Grant F32HL143867-01] related to this work. M. B. D. has received support from the NIH-NHLBI [Grant R01HL125432-01A1] related to this work. For SPIROMICS funding, see Acknowledgments.Author contributions: R. M. B. had access to the data and is the guarantor for the content of the manuscript including data and analysis. R. M. B. and M. B. D. had full access to the data and take responsibility for the integrity of the data and accuracy of analysis presented herein. M. B. D. and R. M. B. contributed substantially to the design of the study, data interpretation, and drafting of the manuscript. A. S. C. M. B. D. and R. M. B. contributed to data analysis. D. C. E. A. H. A. P. C. R. G. B. J. A. K. C. C. W. W. L. V. E. O. J. M. W. G. J. C. P. G. W. R. P. B. C. S. P. N. N. H. and M. B. D. contributed to data collection in the SPIROMICS cohort. C. M. D. D. C. E. A. H. A. P. C. R. G. B. J. A. K. C. C. W. W. L. V. E. O. J. M. W. G. J. C. P. G. W. R. P. B. C. S. P. N. N. H. R. A. W. and T. T. B. critically appraised drafts of the manuscript for critically important intellectual content and contributed substantially to revisions of the manuscript. All authors agreed on the manuscript in its final, submitted form. Financial/nonfinancial disclosures: The authors have reported to CHEST the following: R. M. B. has received a grant from the NIH-NHLBI related to this work. C. M. D. has received grants from the NIH and the Department of Defense unrelated to this work. D. C. reports funding from the NIH and the COPD Foundation unrelated to this work. E. A. H. is a founder of and shareholder in VIDA Diagnostics, a company commercializing lung image analysis software developed, in part, at the University of Iowa; activities that are unrelated to this study. A. P. C. reports funds from the NIH-NHLBI, compensated and noncompensated work for VIDA, and personal fees from GlaxoSmithKline (GSK), all unrelated to this work. J. A. K. reports grant funding from the NIH-NHLBI unrelated to this work. C. C. reports working part-time on external scientific engagement and internal medical education for the GSK Global Respiratory Franchise, all unrelated to this work. J. M. W. reports grants from the NIH-NHLBI, NIH-NCATS (National Center for Advancing Translational Sciences), Beyer, Boehringer-Ingelheim, Mereo BioPharma, and financial relationships with Boehringer-Ingelheim, Mereo BioPharma, and PRA, all unrelated to this work. G. J. C. receives grants from Boehringer-Ingelheim, Novartis, Astra Zeneca, Respironics, MedImmune, Actelion, Forest, Pearl, Ikaria, Aeris, PneumRx, Pulmonx, and other fees from HGE Health Care Solutions Inc, Almirall, Boehringer-Ingelheim, and Nuvaira, all unrelated to this work. P. G. W. reports personal fees from Theravance, GSK, NGM Pharmaceuticals, Amgen, Glenmark Pharmaceuticals, Regeneron, Sanofi, Clarus Ventures, 23andMe, Astra Zeneca, all unrelated to this work. R. P. B. served on the advisory boards (GlaxoSmithKline, Boehringer Ingelheim, and Mylan Pharmaceuticals) and received research grants from GSK and Boehringer-Ingelheim, all activities unrelated to this work. N. N. H. reports grants and personal fees from AstraZeneca; grants from Boehringer-Ingelheim, the NIH, and the COPD Foundation; and personal fees from Mylan; all unrelated to this work. R. A. W. reports grants and personal fees from AstraZeneca/Medimmune, Boehringer-Ingelheim, and GSK outside the submitted work. He reports grants from Pearl Therapeutics and Sanofi-Aventis outside the submitted work. He reports personal fees from ContraFect, Pulmonx, Roche, Spiration, Sunovion, Merck, Circassia, Pneuma, Verona, Mylan/Theravance, Propeller Health, AbbVie, and GSK, all unrelated to this work. T. T. B. reports personal fees from Gilead, ViiV, Merck, EMS-Serono, and Theratechnologies, all unrelated to this work. M. B. D. reports grants from the NIH-NHLBI during the conduct of the study related to this work as well as personal fees from Boehringer-Ingelheim, GSK, AstraZeneca, Mylan-Theravance, Novavax, Parion, Midmark, and Philips and grants from the Department of Defense and Boehringer-Ingelheim, unrelated to this work. None declared: A. S. C. R. G. B. W. W. L. V. E. O. and C. S. P. Role of sponsors: Industry sponsors had no role in the design of the study, the collection and analysis of the data, or the preparation of the manuscript. *SPIROMICS collaborators: The authors acknowledge the following current and former investigators of the SPIROMICS sites and reading centers: Neil E. Alexis, MD; Wayne H. Anderson, PhD; Mehrdad Arjomandi, MD; Igor Barjaktarevic, MD, PhD; R. Graham Barr, MD, DrPH; Lori A. Bateman, MSc; Surya P. Bhatt, MD; Eugene R. Bleecker, MD; Richard C. Boucher, MD; Russell P. Bowler, MD, PhD; Stephanie A. Christenson, MD; Alejandro P. Comellas, MD; Christopher B. Cooper, MD, PhD; David J. Couper, PhD; Gerard J. Criner, MD; Ronald G. Crystal, MD; Jeffrey L. Curtis, MD; Claire M. Doerschuk, MD; Mark T. Dransfield, MD; Brad Drummond, MD; Christine M. Freeman, PhD; Craig Galban, PhD; MeiLan K. Han, MD, MS; Nadia N. Hansel, MD, MPH; Annette T. Hastie, PhD; Eric A. Hoffman, PhD; Yvonne Huang, MD; Robert J. Kaner, MD; Richard E. Kanner, MD; Eric C. Kleerup, MD; Jerry A. Krishnan, MD, PhD; Lisa M. LaVange, PhD; Stephen C. Lazarus, MD; Fernando J. Martinez, MD, MS; Deborah A. Meyers, PhD; Wendy C. Moore, MD; John D. Newell Jr, MD; Robert Paine III, MD; Laura Paulin, MD, MHS; Stephen P. Peters, MD, PhD; Cheryl Pirozzi, MD; Nirupama Putcha, MD, MHS; Elizabeth C. Oelsner, MD, MPH; Wanda K. O'Neal, PhD; Victor E. Ortega, MD, PhD; Sanjeev Raman, MBBS, MD; Stephen I. Rennard, MD; Donald P. Tashkin, MD; J. Michael Wells, MD; Robert A. Wise, MD; and Prescott G. Woodruff, MD, MPH. The project officers from the Lung Division of the National Heart, Lung, and Blood Institute were Lisa Postow, PhD, and Lisa Viviano, BSN. Other contributions: The authors thank the SPIROMICS participants and participating physicians, investigators, and staff for making this research possible. More information about the study and how to access SPIROMICS data may be found at www.spiromics.org. SPIROMICS was supported by contracts from the NIH/NHLBI [HHSN268200900013C, HHSN268200900014C, HHSN268200900015C, HHSN268200900016C, HHSN268200900017C, HHSN268200900018C, HHSN268200900019C, HHSN268200900020C], by a grant from the NIH/NHLBI [U01 HL137880], and supplemented by contributions made through the Foundation for the NIH and the COPD Foundation from AstraZeneca/MedImmune; Bayer; Bellerophon Therapeutics; Boehringer-Ingelheim Pharmaceuticals, Inc.; Chiesi Farmaceutici S.p.A.; Forest Research Institute, Inc.; GlaxoSmithKline; Grifols Therapeutics, Inc.; Ikaria, Inc.; Novartis Pharmaceuticals Corporation; Nycomed GmbH; ProterixBio; Regeneron Pharmaceuticals, Inc.; Sanofi; Sunovion; Takeda Pharmaceutical Company; and Theravance Biopharma and Mylan. Additional information: The e-Tables can be found in the Supplemental Materials section of the online article. Funding Information: FUNDING/SUPPORT: R. M. B. has received support from the National Institutes of Health , National Heart, Lung, and Blood Institute (NIH-NHLBI) [Grant F32HL143867-01 ] related to this work. M. B. D. has received support from the NIH - NHLBI [Grant R01HL125432-01A1 ] related to this work. For SPIROMICS funding, see Acknowledgments. Publisher Copyright: © 2020 American College of Chest Physicians
PY - 2020/4
Y1 - 2020/4
N2 - 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.
AB - 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.
KW - COPD
KW - COPD epidemiology
KW - COPD exacerbations
KW - lung function
KW - vitamin D
UR - http://www.scopus.com/inward/record.url?scp=85082101954&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85082101954&partnerID=8YFLogxK
U2 - 10.1016/j.chest.2019.11.047
DO - 10.1016/j.chest.2019.11.047
M3 - Article
C2 - 31958447
AN - SCOPUS:85082101954
SN - 0012-3692
VL - 157
SP - 856
EP - 865
JO - Chest
JF - Chest
IS - 4
ER -