Volume 126, Issue 1 , Pages 52-58.e5, July 2010
Serum vitamin D levels and severe asthma exacerbations in the Childhood Asthma Management Program study
Background
Asthma exacerbations, most often caused by respiratory tract infections, are the leading causes of asthma morbidity and comprise a significant proportion of asthma-related costs. Vitamin D status might play a role in preventing asthma exacerbations.
Objectives
We sought to assess the relationship between serum vitamin D levels and subsequent severe asthma exacerbations.
Methods
We measured 25-hydroxyvitamin D levels in sera collected from 1024 children with mild-to-moderate persistent asthma at the time of enrollment in a multicenter clinical trial of children randomized to receive budesonide, nedocromil, or placebo (as-needed β-agonists): the Childhood Asthma Management Program. Using multivariable modeling, we examined the relationship between baseline vitamin D levels and the odds of any hospitalization or emergency department visit over the 4 years of the trial.
Results
Thirty-five percent of all subjects were vitamin D insufficient, as defined by a level of 30 ng/mL or less 25-hydroxyvitamin D. Mean vitamin D levels were lowest in African American subjects and highest in white subjects. After adjusting for age, sex, body mass index, income, and treatment group, insufficient vitamin D status was associated with a higher odds of any hospitalization or emergency department visit (odds ratio, 1.5; 95% CI, 1.1-1.9; P = .01).
Conclusion
Vitamin D insufficiency is common in this population of North American children with mild-to-moderate persistent asthma and is associated with higher odds of severe exacerbation over a 4-year period.
Key words: Asthma, vitamin D, inhaled corticosteroids, asthma exacerbations
Abbreviations used: AMP, Antimicrobial protein, BMI, Body mass index, CAMP, Childhood Asthma Management Program, ED, Emergency department, PAR, Population attributable risk
We acknowledge the Childhood Asthma Management Program (CAMP) investigators and research team, supported by the National Heart, Lung, and Blood Institute, for collection of CAMP Genetics Ancillary Study data. All work on data collected from the CAMP Genetics Ancillary Study was conducted at the Channing Laboratory of the Brigham and Women's Hospital under appropriate CAMP policies and human subject's protections. The CAMP Genetics Ancillary Study is supported by U01 HL075419, U01 HL65899, P01 HL083069, R01 HL086601, and T32 HL07427 from the National Heart, Lung, and Blood Institute(NHLBI)/National Institutes of Health. We also acknowledge the Asthma Clinical Research Network (ACRN) investigators and research teams supported by U01 HL51510, U01 HL51834, U01 HL51831, U01 HL51845, U01 HL 51843, M01 RR00079, and M01 RR03186 from the NHLBI. This work was also supported by National Institutes of Health grant R21HL089842.
Disclosure of potential conflict of interest: A. L. Fuhlbrigge is on an advisory board for and has given talks for Merck and has received continuing medical education from Advanced Health Media, funded through GlaxoSmithKline. B. W. Hollis has consulted for DiaSorin and has received research support from the National Institutes of Health. R. S. Zeiger has consulted for AstraZeneca, Aerocrine, Genentech, Novartis, Merck, Schering-Plough, and MedImmune and has received indirect research support from Aerocrine, Genentech, GlaxoSmithKline, Merck, AstraZeneca, and TEVA Pharmaceuticals. A. A. Litonjua has received research support from the National Institutes of Health. The rest of the authors have declared that they have no conflict of interest.
PII: S0091-6749(10)00657-3
doi:10.1016/j.jaci.2010.03.043
© 2010 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
Volume 126, Issue 1 , Pages 52-58.e5, July 2010
