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Interaction between 25‐hydroxyvitamin D and variants at 17q12‐21 on respiratory infections
Author(s) -
Sheen Youn Ho,
Lee Eun,
Kang MiJin,
Yu HoSung,
Ahn Kangmo,
Kim Kyung Won,
Yang SongI,
Jung YoungHo,
Lee KyungJu,
Chang Hyoung Yoon,
Shin Hye Lim,
Choi Kil Yong,
Kim Hyung Young,
Seo JuHee,
Kwon JiWon,
Kim ByoungJu,
Kim HyoBin,
Lee SoYeon,
Suh Dong In,
Yang HyeonJong,
Choi SukJoo,
Oh SooYoung,
Kwon JaYoung,
Kim Soo Hyun,
Won HyeSung,
Kim EunJin,
Lee Jeom Kyu,
Hong SooJong
Publication year - 2016
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.23421
Subject(s) - medicine , respiratory system , respiratory tract infections , intensive care medicine
Summary Objectives 25‐hydroxyvitamin D (25[OH]D) deficiency and genetic variants at the 17q12‐21 locus are independent risk factors for respiratory tract infections (RTIs). We aimed to investigate whether the effect of 25(OH)D at birth and 1 year of age and the polymorphism at the 17q12‐21 locus, or interactions between these two factors, increase susceptibility to RTIs in the first year of life. Methods We tested cord‐blood (CB) 25(OH)D at birth and 1 year of age and genotypes of a variant at the 17q12‐21 locus for associations with RTIs, particularly lower respiratory tract infections (LRTIs), and determined whether there exist interactions between 25(OH)D and 17q12‐21 genotypes in a birth cohort of 473 infants. Results The levels of CB 25(OH)D inversely associate with development of RTIs and LRTIs during the first year of life. There exists an inverse association of 25(OH)D at birth, but not at 1 year, with the risk of acquiring LRTIs in early infancy (adjusted odds ratio [aOR], 2.37; 95% confidence interval [CI]: 1.23–4.60; P = 0.010 and aOR, 0.50; 95%CI: 0.23–1.12; P = 0.094). We have also found a significant interaction between CB 25(OH)D and a variant at the 17q12‐21 locus with respect to the development of early LRTIs, such that associations between a variant at the 17q12‐21 locus and LRTIs are restricted to infants with low CB 25(OH)D concentrations ( P for interaction = 0.013). In addition, when infants with a variant at the 17q12‐21 locus had been exposed to chronic 25(OH)D deficiency over the first year, their risk of LRTIs was increased. Conclusion CB 25(OH)D deficiency during fetal life contribute to the development of LRTIs in genetically susceptible infants. Pediatr Pulmonol. 2016; 51:958–967 . © 2016 Wiley Periodicals, Inc.