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Is Vitamin D’s “Moment in the Sun” Behind Us (nope) – Jan 2014

Chest. 2014;145(1):5-6. doi:10.1378/chest.13-2049
Editorial: David M. Mannino, MD, FCCP

Comment by VitaminDWiki This editorial was based on the results of a single COPD Clinical Trial – which did not have enough participants to make the observed 28% reduction in COPD exacerbations to be statistically significant – less than 7% of the participants had > 30ng of vitamin D


This editorial relates to: No Association of 25-Hydroxyvitamin D With Exacerbations in Primary Care Patients With COPD (Chest. 2014;145(1):37-43.)

Vitamin D has been the focus of a great deal of chronic disease research in recent years.1 The number of publications with vitamin D as part of the title increased nearly 10-fold over 23 years from 224 in 1990 to nearly 2,000 in 2012. Traditionally, vitamin D has been linked as an important micronutrient to musculoskeletal health and the development of rickets in children.2 Over the past few years, the interest in vitamin D has expanded to include chronic diseases such as diabetes mellitus,3 cardiovascular disease,4 and multiple sclerosis.5 In the respiratory field, vitamin D deficiency has been linked to asthma,6 COPD,7 lung function decline,8 and respiratory infections.9 In addition, there has been a movement from a focus on vitamin D deficiency (25-hydroxyvitamin D level < 10 ng/dL [25 nmol/L]) to vitamin D inadequacy (25-hydroxyvitamin D level < 30 ng/dL [75 nmol/L]).10 This movement has some critics who note that evidence supporting supplementation to increase levels of vitamin D in individuals without a deficiency is not supported adequately.10,11


No Association of 25-Hydroxyvitamin D With Exacerbations in Primary Care Patients With COPD

Chest. 2014;145(1):37-43. doi:10.1378/chest.13-1296
Milo A. Puhan, MD, PhD; Lara Siebeling, MD; Anja Frei, PhD; Marco Zoller, MD; Heike Bischoff-Ferrari, MD, DrPH; Gerben ter Riet, MD, PhD

Background: Cross-sectional studies suggest an association of 25-hydroxyvitamin D with exacerbations in patients with COPD, but longitudinal evidence from cohort studies is scarce. The aim of this study was to assess the association of serum 25-hydroxyvitamin D with exacerbations and mortality in primary care patients with COPD.

Methods: In the main analysis, we included 356 patients with COPD (GOLD [Global Initiative for Chronic Obstructive Lung Disease] stages II-IV, free from exacerbations for ≥ 4 weeks) from a prospective cohort study in Dutch and Swiss primary care settings. We used negative binomial and Cox regression to assess the association of 25-hydroxyvitamin D with (centrally adjudicated) exacerbations and mortality, respectively.

Results: Baseline mean ± SD serum 25-hydroxyvitamin D concentration was 15.5 ± 8.9 ng/dL, and 274 patients (77.0%) had 25-hydroxyvitamin D deficiency (< 20 ng/dL). Compared with patients with severe 25-hydroxyvitamin D deficiency (< 10 ng/dL, n = 106 [29.8%]), patients with moderately deficient (10-19.99 ng/dL, n = 168 [47.2%]) and insufficient (20-29.99 ng/dL, n = 58 [16.3%]) concentrations had the same risk for exacerbations (incidence rate ratio, 1.01 [95% CI, 0.77-1.57] vs 1.00 [95% CI, 0.62-1.61], respectively).

In patients with desirable concentrations (> 30 ng/dL, n = 24 [6.7%]), the risk was lower, although not significantly (incidence rate ratio, 0.72 [95% CI, 0.37-1.42]). In patients taking vitamin D supplements, using different cutoffs for 25-hydroxyvitamin D or competing risk models did not materially change the results. We did not find a statistically significant association of 25-hydroxyvitamin D concentration with mortality.

Conclusions: This longitudinal study in a real-world COPD population that carefully minimized misclassification of exacerbations and the influence of confounding did not show an association of 25-hydroxyvitamin D with exacerbations and mortality.

Trial registry: ClinicalTrials.gov; No.: NCT00706602; URL: www.clinicaltrials.gov.


See also VitaminDWiki


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