Vitamin D insufficiency in neonatal hypoxic-ischemic encephalopathy.
Vitamin D insufficiency in neonatal hypoxic-ischemic encephalopathy.
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DOI:
10.1038/pr.2017.13
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发表时间:
2017-07
影响因子:
3.6
通讯作者:
Jenkins D
中科院分区:
文献类型:
--
作者:
Lowe DW;Hollis BW;Wagner CL;Bass T;Kaufman DA;Horgan MJ;Givelichian LM;Sankaran K;Yager JY;Katikaneni LD;Wiest D;Jenkins D
Vitamin D has neuroprotective and immunomodulatory properties, and deficiency is associated with worse stroke outcomes. Little is known about effects of hypoxia-ischemia or hypothermia treatment on vitamin D status in neonates with hypoxic-ischemic encephalopathy (HIE). We hypothesized vitamin D metabolism would be dysregulated in neonatal HIE altering specific cytokines involved in Th17 activation, which might be mitigated by hypothermia. We analyzed short term relationships between 25(OH) and 1,25(OH)2 vitamin D, vitamin D binding protein, and cytokines related to Th17 function in serum samples from a multicenter randomized controlled trial of hypothermia 33°C for 48h after HIE birth versus normothermia in 50 infants with moderate to severe HIE. Insufficiency of 25(OH) vitamin D was observed after birth in 70% of infants, with further decline over the first 72h, regardless of treatment. 25(OH) vitamin D positively correlated with antiinflammatory cytokine IL-17E in all HIE infants. However, Th17 cytokine suppressor IL-27 was significantly increased by hypothermia, negating the IL-27 correlation with vitamin D observed in normothermic HIE infants. Serum 25(OH) vitamin D insufficiency is present in the majority of term HIE neonates and is related to lower circulating anti-inflammatory IL-17E. Hypothermia does not mitigate vitamin D deficiency in HIE.
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