Carter R Colin, Jacobson Joseph L, Molteno Christopher D, Dodge Neil C, Meintjes Ernesta M, Jacobson Sandra W
Division of Pediatric Emergency Medicine, Morgan Stanley Children's Hospital of New York, Columbia University Medical Center, New York, New York;
Departments of Psychiatry and Mental Health, and Human Biology, University of Cape Town Faculty of Health Sciences, Cape Town, South Africa; and Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine, Detroit, Michigan.
Pediatrics. 2016 Aug;138(2). doi: 10.1542/peds.2016-0775. Epub 2016 Jul 8.
Although both fetal and long-term growth restriction are well documented in fetal alcohol spectrum disorders, effects on pattern of growth trajectory have not been characterized. Furthermore, the degree to which growth trajectories are related to fetal alcohol-related neurocognitive deficits is unknown.
Ninety-three heavy drinking pregnant women and 64 controls were recruited at initiation of prenatal care in Cape Town, South Africa. Small for gestational age (SGA) was defined as birth weight <10th percentile. Length/height, weight, and head circumference were measured at 6.5 and 12 months and 5, 9, and 13 years. Four growth trajectories were identified: SGA with long-term postnatal growth restriction (length/height-for-age <10th percentile through 13 years); SGA with catch-up growth; no SGA or postnatal growth restriction; and late-onset postnatal stunting. IQ was assessed at 5 and 10 years, and learning, memory, and executive function at 10 years.
Children born SGA with postnatal growth restriction were most heavily exposed. Exposure was intermediate for those born SGA with catch-up growth and lowest for those without prenatal or postnatal growth restriction. Effects on neurocognition were strongest in children with both prenatal and long-term growth restriction, more moderate in those with fetal growth restriction and postnatal catch-up, and weakest in those without growth restriction.
These findings validate the use of growth restriction in the diagnosis of fetal alcohol spectrum disorders and identify growth trajectory as a biomarker of which heavily exposed children are at greatest risk for cognitive developmental deficits.
尽管胎儿酒精谱系障碍中胎儿生长受限和长期生长受限均有充分记录,但对生长轨迹模式的影响尚未得到描述。此外,生长轨迹与胎儿酒精相关神经认知缺陷的相关程度尚不清楚。
在南非开普敦,93名重度饮酒孕妇和64名对照者在产前检查开始时被招募。小于胎龄(SGA)定义为出生体重<第10百分位数。在6.5个月和12个月以及5岁、9岁和13岁时测量身长/身高、体重和头围。确定了四种生长轨迹:伴有长期出生后生长受限的SGA(至13岁时身长/身高-年龄<第10百分位数);伴有追赶生长的SGA;无SGA或出生后生长受限;以及迟发性出生后发育迟缓。在5岁和10岁时评估智商,在10岁时评估学习、记忆和执行功能。
出生时为SGA且出生后生长受限的儿童暴露程度最高。对于出生时为SGA且有追赶生长的儿童,暴露程度中等,对于无产前或产后生长受限的儿童,暴露程度最低。对神经认知的影响在产前和长期生长受限的儿童中最强,在有胎儿生长受限和出生后追赶生长的儿童中较中等,在无生长受限的儿童中最弱。
这些发现证实了生长受限在胎儿酒精谱系障碍诊断中的应用,并确定生长轨迹是一种生物标志物,暴露严重的儿童认知发育缺陷风险最大。