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降低儿童生命早期缺铁性脑功能障碍风险的方法。

Approaches for Reducing the Risk of Early-Life Iron Deficiency-Induced Brain Dysfunction in Children.

机构信息

Division of Global Pediatrics, Department of Pediatrics, and Center for Neurobehavioral Development, University of Minnesota, Minneapolis, MN 55455, USA.

Center for Neurobehavioral Development, University of Minnesota, 717 Delaware Street SE, Suite 333, Minneapolis, MN 55414, USA.

出版信息

Nutrients. 2018 Feb 17;10(2):227. doi: 10.3390/nu10020227.

DOI:10.3390/nu10020227
PMID:29462970
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5852803/
Abstract

Iron deficiency is the most common micronutrient deficiency in the world. Women of reproductive age and young children are particularly vulnerable. Iron deficiency in late prenatal and early postnatal periods can lead to long-term neurobehavioral deficits, despite iron treatment. This may occur because screening and treatment of iron deficiency in children is currently focused on detection of anemia and not neurodevelopment. Anemia is the end-stage state of iron deficiency. The brain becomes iron deficient before the onset of anemia due to prioritization of the available iron to the red blood cells (RBCs) over other organs. Brain iron deficiency, independent of anemia, is responsible for the adverse neurological effects. Early diagnosis and treatment of impending brain dysfunction in the pre-anemic stage is necessary to prevent neurological deficits. The currently available hematological indices are not sensitive biomarkers of brain iron deficiency and dysfunction. Studies in non-human primate models suggest that serum proteomic and metabolomic analyses may be superior for this purpose. Maternal iron supplementation, delayed clamping or milking of the umbilical cord, and early iron supplementation improve the iron status of at-risk infants. Whether these strategies prevent iron deficiency-induced brain dysfunction has yet to be determined. The potential for oxidant stress, altered gastrointestinal microbiome and other adverse effects associated with iron supplementation cautions against indiscriminate iron supplementation of children in malaria-endemic regions and iron-sufficient populations.

摘要

缺铁是世界上最常见的微量营养素缺乏症。育龄妇女和幼儿尤其容易受到影响。晚期产前和早期产后的缺铁会导致长期的神经行为缺陷,尽管进行了铁治疗。这可能是因为目前儿童缺铁的筛查和治疗主要集中在检测贫血,而不是神经发育。贫血是缺铁的终末状态。由于可用的铁优先分配给红细胞(RBC)而不是其他器官,因此大脑在出现贫血之前就会出现缺铁。大脑缺铁,与贫血无关,是导致不良神经影响的原因。在贫血前阶段,需要早期诊断和治疗即将发生的大脑功能障碍,以预防神经缺陷。目前可用的血液学指标不是大脑缺铁和功能障碍的敏感生物标志物。非人类灵长类动物模型的研究表明,血清蛋白质组学和代谢组学分析可能更适合这一目的。母体铁补充、延迟脐带夹闭或挤奶以及早期铁补充可以改善高危婴儿的铁状况。这些策略是否能预防缺铁引起的大脑功能障碍尚待确定。与铁补充相关的氧化应激、胃肠道微生物组改变和其他不良反应的潜在风险告诫我们,不应在疟疾流行地区和铁充足的人群中不加选择地对儿童进行铁补充。

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