Löfqvist Chatarina, Engström Eva, Sigurdsson Jon, Hård Anna-Lena, Niklasson Aimon, Ewald Uwe, Holmström Gerd, Smith Lois E H, Hellström Ann
Pediatric Growth Research Center, Institute for Clinical Sciences, Department of Pediatrics, Sahlgrenska Academy of Göteborg University, Göteborg, Sweden.
Pediatrics. 2006 Jun;117(6):1930-8. doi: 10.1542/peds.2005-1926.
We hypothesized that in premature infants, retinal vascular growth retardation between birth and postmenstrual age of approximately 30 to 32 weeks that initiates retinopathy of prematurity is paralleled by brain growth retardation.
In a prospective longitudinal study, we measured postnatal head growth, retinopathy of prematurity stage, protein and energy intake, severity of illness and serum insulin-like growth factor-1 levels in 58 preterm infants (mean gestational age at birth: 27.6 weeks) from birth until postmenstrual age of approximately 40 weeks.
Premature infant head growth decelerates dramatically after birth until postmenstrual age of approximately 30 weeks. Head growth retardation coincides with retinal vascular growth suppression. Accelerated growth follows between post menstrual ages of approximately 30 to 32 weeks and approximately 40 weeks. The degree of head growth retardation up to postmenstrual age of 31 weeks corresponds to the degree of retinopathy of prematurity and to the degree of suppression of serum levels of insulin-like growth factor-1. At postmenstrual age of 31 weeks, if a child's head circumference SD is below -2.5, then the probability of also developing at least stage 3 retinopathy of prematurity increases fivefold compared with head circumference above -2.5 SD (32% vs 6%) suggesting parallel processes in brain and retina. Serum insulin-like growth factor-1 levels correlate positively with head circumference SD score and with the degree of retinopathy of prematurity.
The correlation between head and retinal growth is consistent with insulin growth factor-1 being one of the postnatal growth factors involved in this multifactorial process and also suggests that factors that contribute to retinopathy of prematurity during this critical period may also affect neurological dysfunction. Additional studies are required to establish this connection.
我们假设，在早产儿中，出生至孕龄约30至32周期间引发早产儿视网膜病变的视网膜血管生长迟缓与脑生长迟缓同时出现。
在一项前瞻性纵向研究中，我们测量了58名早产儿（出生时平均胎龄：27.6周）从出生至孕龄约40周期间的出生后头围生长、早产儿视网膜病变阶段、蛋白质和能量摄入、疾病严重程度以及血清胰岛素样生长因子-1水平。
早产儿出生后直至孕龄约30周时头围生长显著减速。头围生长迟缓与视网膜血管生长抑制同时出现。在孕龄约30至32周与约40周之间头围加速生长。至孕龄31周时的头围生长迟缓程度与早产儿视网膜病变程度以及血清胰岛素样生长因子-1水平的抑制程度相对应。在孕龄31周时，如果儿童的头围标准差低于-2.5，那么与头围高于-2.5标准差相比，发生至少3期早产儿视网膜病变的概率增加五倍（32%对6%），这表明脑和视网膜存在平行过程。血清胰岛素样生长因子-1水平与头围标准差评分以及早产儿视网膜病变程度呈正相关。
头围与视网膜生长之间的相关性与胰岛素生长因子-1作为参与这一多因素过程的出生后生长因子之一相一致，并且还表明在此关键时期导致早产儿视网膜病变的因素可能也会影响神经功能障碍。需要进一步研究来证实这种联系。
