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Early postnatal hypoferremia in low birthweight and preterm babies: A prospective cohort study in hospital-delivered Gambian neonates.
EBioMedicine ( IF 11.1 ) Pub Date : 2020-01-22 , DOI: 10.1016/j.ebiom.2019.102613
James H Cross 1 , Ousman Jarjou 1 , Nuredin Ibrahim Mohammed 1 , Santiago Rayment Gomez 2 , Bubacarr J B Touray 1 , Andrew M Prentice 1 , Carla Cerami 1
Affiliation  

BACKGROUND Neonates, particularly those born preterm (PTB) and with low birthweight (LBW), are especially susceptible to bacterial and fungal infections that cause an estimated 225,000 deaths annually. Iron is a vital nutrient for the most common organisms causing septicaemia. Full-term babies elicit an immediate postnatal hypoferremia assumed to have evolved as an innate defence. We tested whether PTB and LBW babies are capable of the same response. METHODS We conducted an observational study of 152 babies who were either PTB (born ≥32 to <37 weeks gestational age) and/or LBW (<2500 g) (PTB/LBW) and 278 term, normal-weight babies (FTB/NBW). Blood was sampled from the umbilical cord vein and artery, and matched venous blood samples were taken from all neonates between 6-24 h after delivery. We measured haematological, iron and inflammatory markers. FINDINGS In both PTB/LBW and FTB/NBW babies, serum iron decreased 3-fold within 12 h of delivery compared to umbilical blood (7·5 ± 4·5 vs 23·3 ± 7·1 ng/ml, P < 0·001, n = 425). Transferrin saturation showed a similar decline with a consequent increase in unsaturated iron-binding capacity. C-reactive protein levels increased over 10-fold (P < 0·001) and hepcidin levels doubled (P < 0·001). There was no difference in any of these responses between PTB/LBW and FTB/NBW babies. INTERPRETATION Premature or low birthweight babies are able to mount a very rapid hypoferremia that is indistinguishable from that in normal term babies. The data suggest that this is a hepcidin-mediated response triggered by acute inflammation at birth, and likely to have evolved as an innate immune response against bacterial and fungal septicaemia. TRIAL REGISTRATION clinicaltrials.gov (NCT03353051). Registration date: November 27, 2017. FUNDING Bill & Melinda Gates Foundation (OPP1152353).

中文翻译:

低出生体重儿和早产儿的早期产后低铁血症:一项针对医院分娩的冈比亚新生儿的前瞻性队列研究。

背景技术新生儿,特别是早产儿(PTB)和低出生体重(LBW)的婴儿特别容易受到细菌和真菌感染的影响,据估计每年导致225,000例死亡。铁是导致败血症的最常见生物的重要营养素。足月婴儿会引起出生后立即发生的低铁血症,该低铁血症被认为是一种先天防御。我们测试了PTB和LBW婴儿是否具有相同的反应能力。方法我们进行了一项观察性研究,对152例PTB(胎龄≥32至<37周胎龄)和/或LBW(<2500 g)(PTB / LBW)的婴儿和278名足月正常体重婴儿(FTB / NBW)进行了观察性研究。 )。从脐带静脉和动脉中抽取血液,并在分娩后6-24小时之间从所有新生儿中抽取匹配的静脉血样品。我们测量了血液学 铁和炎症标志物。结果在PTB / LBW和FTB / NBW婴儿中,分娩后12小时内血清铁与脐带血相比降低了3倍(7·5±4·5与23·3±7·1 ng / ml,P <0 ·001,n = 425)。转铁蛋白饱和度显示出类似的下降,因此不饱和铁结合能力增加。C反应蛋白水平增加了10倍以上(P <0·001),铁调素水平增加了一倍(P <0·001)。这些反应在PTB / LBW和FTB / NBW婴儿之间没有差异。解释早产或低出生体重的婴儿能够发生非常快速的低铁血症,这与正常足月婴儿的高铁血症没有区别。数据表明,这是由铁调素介导的反应,由出生时的急性炎症触发,并可能已发展成针对细菌和真菌败血病的先天免疫反应。试验注册临床试验.gov(NCT03353051)。注册日期:2017年11月27日。资助比尔和梅琳达·盖茨基金会(OPP1152353)。
更新日期:2020-01-23
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