出院后配方奶粉对早产儿发育迟缓的预防及治疗

目的 研究配方奶粉(PDF)对早产儿出院后实现追赶生长防止宫外发育迟缓(EUGR)的临床应用价值.方法 以2014年1月至2016年1月深圳市龙华新区人民医院新生儿科200例早产儿为研究对象,按随机数字表分为研究组及对照组各100例,研究组行PDF喂养,对照组母乳喂养(BM)或母乳和足月儿奶粉(TF),比较两组早产儿生长发育指标,并于6个月后比较两组神经行为评分(NBNA)及两组早产儿1年后EUGR的发生率.结果 两组研究对象于生后第1个月、第3个月以及第6个月体重(F=5 562.14,P<0.05)、身长(F=556.38,P<0.05)、头围(F=232.54,P<0.05)经方差分析均有统计学差异(P<0.05),组间两两比较经SNK法分析比较,对照组、研究组生后第1个月体重、身长、头围均无统计学差异(P>0.05);第3个月、第6个月研究组体重、身长均高于同期对照组;同期两组头围比较均无统计学差异(P>0.05);第6个月儿心量表评分中,研究组大动作(t=2.52,P<0.05)、精细动作(t=2.16,P<0.05)、适应能力(t=2.09,P<0.05)、语言(t=0.16,P<0.05)以及社交行为(t=2.58,P<0.05)均优于对照组;研究组1岁时EUGR发生率(24%)低于对照组,有统计学差异(χ2=5.81,P<0.05).结论 早产儿配方奶粉在实现追赶生长及防止EUGR有重要的临床应用价值.     

Metabolic effects of different protein intakes after short term undernutrition in artificially reared infant rats

Background

Early postnatal nutrition is involved in metabolic programming. Small for gestational age and premature babies commonly receive insufficient dietary protein during the neonatal period due to nutrition intolerance, whereas high protein formulas are used to achieve catch up growth. Neither the short term, nor the long term effects of such manipulation of protein intake are known.

Aim

We hypothesized that high or low protein intake during infancy would induce metabolic alterations both during early-life and in adulthood.

Methods

Gastrostomized neonatal rat pups received either 50% (P50%), 100% (P100%), or 130% (P130%) of the normal protein content in rat milk from the 7th to the 15th day of life (D7 to D15), when they were either sacrificed or placed with mothers for the long term study. Glucose tolerance tests (GTT) were performed at D230. Long term rats were sacrificed at D250.

Results

At D15, weight of P50% pups was lower than P100% and P130% pups. Neither liver and kidney mass, nor islet β-cell areas were altered. Brain weight (adjusted to body weight) was higher in P50% vs. P130% (p < 0.05). Insulin/glucose ratio was lower in P50% vs. P130%. Expression of GLUT4 on adipocyte cell membrane and GLUT2 in liver cytosol was significantly enhanced in P50% vs. P130%. Long term, neither GTT results nor body nor organ weights differed between groups.

Conclusion

In neonatal rats, higher protein intakes via the enteral route led to enhanced short term weight gain, insulin resistance, and modified expression of glucose transporters. However, these differences were not sustained.     

Arginine bioavailability and endothelin-1 system in the regulation of vascular function of umbilical vein endothelial cells from intrauterine growth restricted newborns

Background and aims

Intrauterine growth restriction (IUGR) is a major risk factor for perinatal morbidity and mortality, leading to long-term adverse cardiovascular outcomes. The present study aimed to investigate the potential mechanisms in IUGR-associated vascular endothelial dysfunction.

Weight growth velocity of very low birth weight infants: role of gender, gestational age and major morbidities

It's well known that VLBWI fail to thrive, however it's still unclear how gender, GA and morbidities affect growth pattern: aim of this study is to assess the influence of these factors on weight growth.262 VLBWI were selected. Weight was recorded daily up to 28 days, weekly up to discharge and during 7 scheduled follow-up visits up to 2 years of corrected age. Individual profiles were fitted with a mathematical function suitable to model selected growth milestones and mean distance and velocity curves were drawn. Effects of gender, GA, major-morbidities, nutritional and respiratory support on individual weight growth milestones were estimated using a multivariate linear model. Each of these variables acts differently on weight growth pattern mainly modifying velocity curves characteristics.In particular, infants with major morbidities weight growth impairment-seen on distance curves at 2 years of corrected age-depends on poor weight velocity during a critical period ending within 4th month of postnatal age, for SGA or BPD infants, starting from 5th month of postnatal for severely neurologically impaired infants. These critical periods could be the most appropriate to identify risk factors for weight growth impairment in VLBWI.     

极低出生体重儿宫外生长迟缓及其危险因素分析

【摘要】　目的：回顾极低出生体重儿（Very low birth weight infant, VLBWI）宫外生长迟缓(Extrauterine growth retardation, EUGR)发生情况并分析发生EUGR的相关因素。方法：选择2009年9月至2011年6月在重庆医科大学附属儿童医院新生儿重症监护病房（Neonatal intensive care unit,NICU）住院早产儿进行回顾性分析。入选标准：出生体重<1500g，入院时间<24h且住院天数≥14d，不伴有影响生长发育的先天畸形或遗传代谢性疾病。排除标准：住院天数<14d，住院期间放弃治疗或死亡。将入选病例分为EUGR组和非EUGR组。计数资料比较采用卡方检验，正态分布的计量资料比较用t检验，非正态分布计量资料采用秩和检验，EUGR相关危险因素用二元Logistic回归分析。结果：2009年9月至2011年6月符合纳入标准的VLBWI 87例，其中EUGR为74例(85.1%),非EUGR为13例（14.9%）；与非EUGR组相比，EUGR组宫内生长迟缓（Intrauterine growth retardation，IUGR）发生率高，平均出生胎龄和出院日龄较大，恢复至出生体重时间和开始肠内营养时间较长（P<0.05），而出院时口服热卡较低（P＜0.05）；Logistic回归结果显示IUGR（OR=0.077)、开始肠内营养时间晚(OR=12.081)、出院时口服热卡低(OR=0.003)、恢复至出生体重时间长(OR=48.404)是EUGR发生的危险因素。结论：IUGR、开始肠内营养时间晚、出院时口服热卡低、恢复至出生体重时间长是VLBWI发生EUGR的危险因素。     

357例极低出生体重儿宫外生长迟缓现状调查

目的 调查极低出生体重儿出生时宫内生长迟缓(IUGR)和出院时宫外生长迟缓(EUGR)发生率.方法 以2013版Fenton曲线为标准,对嘉兴市妇幼保健院2013年1月1日至2015年12月31日期间入院并达到出院标准的极低出生体重儿IUGR、EUGR发生率进行回顾性研究,并分层分析不同孕周、不同体重IUGR、EUGR发生率.结果 总共有357例患儿纳入研究,其中89例发生IUGR,发生率为24.9%;186例发生EUGR,发生率为52.1%,其中89例IUGR患儿均发生了EUGR.孕周≤28周、28+1~30周、30+1~32周、>32周,IUGR发生率分别为4.2%、1.8%、3.1%、88.2%,EUGR发生率分别为12.5%、28.3%、48.0%、96.8%,随着孕周的增加,IUGR和EUGR发生率均有增加趋势(χ2值分别为268.857、115.901,均P<0.001).出生体重≤1000g、1001~1250g、>1250g的患儿,IUGR发生率分别为6.1%、21.7%、30.0%,EUGR发生率分别为36.4%、55.0%、52.9%,随着出生体重增加IUGR发生率逐渐增加(χ2=9.656,P=0.008),而EUGR发生率增加趋势不明显(χ2=3.737,P=0.154).结论 其中IUGR患儿更易发生EUGR,需加强干预.     

Notch3 signaling activation in smooth muscle cells promotes extrauterine growth restriction-induced pulmonary hypertension

Background and aimsEarly postnatal life is a critical developmental period that affects health of the whole life. Extrauterine growth restriction (EUGR) causes cardiovascular development problems and diseases, including pulmonary arterial hypertension (PAH). PAH is characterized by proliferation, migration, and anti-apoptosis of pulmonary artery smooth muscle cells (PASMCs). However, the role of PASMCs in EUGR has not been studied. Thus, we hypothesized that PASMCs dysfunction played a role in EUGR-induced pulmonary hypertension.Methods and resultsHere we identified that postnatal nutritional restriction-induced EUGR rats exhibited an elevated mean pulmonary arterial pressure and vascular remodeling at 12 weeks old. PASMCs of EUGR rats showed increased cell proliferation and migration features. In EUGR-induced PAH rats, Notch3 signaling was activated. Relative mRNA and protein expression levels of Notch3 intracellular domain (Notch3 ICD), and Notch target gene Hey1 in PASMCs were upregulated. We further demonstrated that pharmacological inhibition of Notch3 activity by using a γ-secretase inhibitor DAPT, which blocked the cleavage of Notch proteins to ICD peptides, could effectively inhibit PASMC proliferation. Specifically knocked down of Notch3 in rat PASMCs by shRNA restored the abnormal PASMC phenotype in vitro. We found that administration of Notch signaling inhibitor DAPT could successfully reduce mean pulmonary arterial pressure in EUGR rats.ConclusionsThe present study demonstrated that upregulation of Notch3 signaling in PASMCs was crucial for the development of EUGR-induced PAH. Blocking Notch3-Hey1 signaling pathway in PASMCs provides a potential therapeutic target for PAH.     

La nutrition des mille premiers jours : quels enjeux ?

Supplying the ‘raw materials’ required to sustain growth and neurodevelopment has long been considered the sole role of nutrition in the first 1000 days of life. Towards the end of the 20^th century, evidence from epidemiologist David Barker revealed that nutrition received in early life has another, possibly more important role, as it may ‘program’ the risk of developing chronic disease in later adulthood. In utero undernutrition, through impaired fetal amino acid availability, results in intrauterine growth restriction (IUGR), which increases not only perinatal morbi-mortality, but the risk of developing obesity, hypertension, type 2 diabetes, and coronary insufficiency in the future adult. Such evidence led to the emergence of the concept of the developmental origins of health and disease (DOHaD). Its mechanisms, though incompletely understood, likely involve alterations in the growth of specific developing tissues, epigenetic modifications, fetal overexposure to cortisol, the transmission of altered microbiota from mother to child, or the effect of growth trajectory per se. After birth, undernutrition commonly occurs in preterm infants, and results in extra-uterine growth restriction (EUGR), followed by catch-up growth, which may have deleterious long-term effects on adult health. Even before the mechanisms of ‘nutritional programming’ are fully understood, simple nutritional strategies of prevention exist, and include the optimization of nutrition in pregnancy, intensifying nutrition of preterm infants in neonatology units, and the promotion of breastfeeding.