Vitamin D insufficiency is associated with challenge-proven food allergy in infants - 30/03/13
Abstract |
Background |
Epidemiological evidence has shown that pediatric food allergy is more prevalent in regions further from the equator, suggesting that vitamin D insufficiency may play a role in this disease.
Objective |
To investigate the role of vitamin D status in infantile food allergy.
Methods |
A population sample of 5276 one-year-old infants underwent skin prick testing to peanut, egg, sesame, and cow’s milk or shrimp. All those with a detectable wheal and a random sample of participants with negative skin prick test results attended a hospital-based food challenge clinic. Blood samples were available for 577 infants (344 with challenge-proven food allergy, 74 sensitized but tolerant to food challenge, 159 negative on skin prick test and food challenge). Serum 25-hydroxyvitamin D levels were measured by using liquid chromatography tandem mass spectrometry. Associations between serum 25-hydroxyvitamin D and food allergy were examined by using multiple logistic regression, adjusting for potential risk and confounding factors.
Results |
Infants of Australian-born parents, but not of parents born overseas, with vitamin D insufficiency (≤50 nmol/L) were more likely to be peanut (adjusted odds ratio [aOR], 11.51; 95% CI, 2.01-65.79; P = .006) and/or egg (aOR, 3.79; 95% CI, 1.19-12.08; P = .025) allergic than were those with adequate vitamin D levels independent of eczema status. Among those with Australian-born parents, infants with vitamin D insufficiency were more likely to have multiple food allergies (≥2) rather than a single food allergy (aOR, 10.48; 95% CI, 1.60-68.61 vs aOR, 1.82; 95% CI, 0.38-8.77, respectively).
Conclusions |
These results provide the first direct evidence that vitamin D sufficiency may be an important protective factor for food allergy in the first year of life.
Le texte complet de cet article est disponible en PDF.Key words : Vitamin D, food allergy, peanut allergy, egg allergy, population, oral food challenge, eczema, epigenetic
Abbreviations used : 25(OH)D, aOR, HREC, OFC, OR, sIgE, SPT, UVR
Plan
This study was supported by funding from the National Health and Medical Research Council of Australia, the Ilhan Food Allergy Foundation, AnaphylaxiStop, the Charles and Sylvia Viertel Medical Research Foundation, and the Victorian Government’s Operational Infrastructure Support Program. |
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Disclosure of potential conflict of interest: K. J. Allen is a Viertel Senior Medical Research Fellow and has received payment for lectures from Abbott, Wyeth, and Nutricia. J. J. Koplin is partly supported by a postdoctoral fellowship from a National Health and Medical Research Council Capacity Building Grant in Population Health. A.-L. Ponsonby, L. C. Gurrin, M. Wake, M. Matheson, A. Lowe, and S. C. Dharmage are supported by the National Health and Medical Research Council. D. Tey has received payment for lectures from Merck Sharp & Dohme, Abbott Nutrition, and Alphapharm. P. Martin and T. Dang are Australian Postgraduate Award PhD scholars, and H.-T. Tina Tan is a Malaysian Government PhD scholar. N.J. Osborne is supported by the European Regional Development Fund and the European Social Fund Convergence Programme, has received grants and travel support from the National Health and Medical Research Council, and has received grants from the Australian Egg Corporation. M. Tang is on the advisory board for the Nestlé Nutrition Institute and Nutricia and has received speakers fees from Nutricia, Nestlé Nutrition Institute, and Wyeth. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 131 - N° 4
P. 1109 - avril 2013 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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