摘要
目的分析高危因素包括出生体重、胎龄及其他高危因素对新生儿17α-OHP水平分布,为新生儿肾上腺皮质增生症(CAH)筛查切值的优化提供参考。方法对苏州市新生儿疾病筛查中心2010年8月至2014年1月CAH筛查资料进行回顾性分析。运用非参数检验Wilcoxon检验比较性别、胎龄和体重各组之间的统计学差异,通过同时固定性别、胎龄和体重三因素,分析其他高危因素对新生儿17α-OHP水平的影响。结果新生儿17α-OHP水平呈正偏态分布,高危新生儿17α-OHP水平(中位数为8.52nmol/L)显著高于正常新生儿17α-OHP水平(中位数为6.27 nmol/L),Wilcoxon=1.43×108,P=0.000。男性新生儿17α-OHP水平(中位数为6.81 nmol/L)显著高于女性新生儿17α-OHP水平(中位数为6.33 nmol/L),Wilcoxon=3.77×108,P=0.000,但不是独立影响因素。早产新生儿17α-OHP水平(中位数为11.40 nmol/L)显著高于足月新生儿17α-OHP水平(中位数为6.36 nmol/L),Wilcoxon=4.40×108,P=0.000;通过对是否高危、性别和体重同时分层比较表明早产新生儿17α-OHP水平均显著高于足月新生儿17α-OHP水平。不同出生体重新生儿17α-OHP水平不同,极低出生体重新生儿17α-OHP水平(中位数为13.15 nmol/L)显著高于低出生体重新生儿17α-OHP水平(中位数为10.60 nmol/L),Wilcoxon=2.42×105,P=0.000;低出生体重新生儿17α-OHP水平显著高于正常出生体重新生儿17α-OHP水平(中位数为6.43 nmol/L),Wilcoxon=6.77×108,P=0.000;正常出生体重新生儿17α-OHP水平显著高于巨大出生体重新生儿17α-OHP水平(中位数为6.25 nmol/L),Wilcoxon=4.25×107,P=0.000,出生体重对新生儿17α-OHP水平的作用可能受到性别的影响。男性和女性正常体重足月的高危新生儿17α-OHP水平均高于男性和女性正常新生儿17α-OHP水平,Wilcoxon=1.43×108,P=0.000和Wilcoxon=1.24×108,P=0.000。巨大出生体重足月的高危新生儿17α-OHP水平也显著高于巨大出生体重足月的非高危新生儿17α-OHP水平,Wilcoxon=2.20×106,P=0.000。结论高危因素包括体重、孕周及其他高危因素可以作为优化新生儿肾上腺皮质增生症筛查Cut-off值的参考因素。
Objective： To analyze the distribution of 17α-OHP in high-risk newborns including low weight, Gestational age, and the others, and provide a reference for revising cut-off value of newborn for screening congenital adrenal hyperplasia （CAH） . Methods： The retrospective CAH screening data during 2010.8-2014.1 from Suzhou municipal hospital newborn screening center were investigated. The source data was composed of all normal newborns and high risk newborns born in Suzhou municipal hospital with gender, gestational week, and weight registered. Compare difference groups in terms of gender, gestafional week, and weight using Wilcoxon nonparametric test. Analyze the high risk factors effect on 17α-OHP level in newborn by layering gender, gestational week, and weight simultaneously. Results： Neonatal 17α-OHP level was positively skewed distribution. The high-risk newborns 17α-OHP level median was 9.07 nmol/L, significantly higher than 6.64 nmol/L in normal newborns, Wilcoxon= 1.43 x 108, P= 0.000. The male newborns 17α-OHP levels level median was 6.81nmol/L, significantly higher than 6.33nmol/L in female newborns, Wilcoxon=3.77x108, P=0.000, however gender was not an independent factor. The preterm birth 17α-OHP level median was 11.40 nmol/L, significantly higher than 6.36nmol/L in term birth, Wilcoxon=4.40x 108, P=0.000. Furthermore, all the preterm birth 17α-OHP levels were significantly higher in terms birth, layering high-risk, gender, and weight simultaneously. Neonatal 17α-OHP levels had significant difference in weight terms. Very low birth weight 17α-OHP level median was 13.15nmol/L, significantly higher than 10.60 nmol/L in low birth weight, Wilcoxon=2.42x 105, P=0.000. Low birth weight 17α-OHP level median was significantly higher than 6.43 nmol/L in normal birth weight, Wilcoxon=6.77x 108, P=0.000. Normal birth weight 17α-OHP level median was significantly higher than 6.25nmol/L in macrosomia, Wilcoxon=4.25 x 107, P=0.000, however weight was not an independent factor. Male and female normal weight and term newborns at high risk 17α-OHP levels were respectively higher than males and females normal newborn 17α-OHP levels, Wilcoxon = 1.43 x 108, P=0.000 and Wilcoxon = 1.24 x 108, P= 0.000. Macrosomia at high risk 17α-OHP level was 6.72nmol/ L, significantly higher than 6.18nmol/L in normal newborn, Wilcoxon=2.20x 106, P=0.000. Conclusions： High-risk factors including gestational age, low weight, and the others, were considered as reference factors for optimizing CAH screening cut-off value.
出处
《中国优生与遗传杂志》
2014年第9期119-123,共5页
Chinese Journal of Birth Health & Heredity
