Mannose‐binding protein in preterm infants: developmental profile and clinical significance
Mannose‐binding protein in preterm infants: developmental profile and clinical significance
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早产儿甘露糖结合蛋白：发育概况和临床意义
DOI：
10.1111/j.1365-2249.1995.tb03866.x
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发表时间：
1995
影响因子：
4.6
通讯作者：
J. Karlberg
中科院分区：
文献类型：
--
作者：
Y. Lau;S. Chan;M. Turner;J. Fong;J. Karlberg
本研究的目的是确定早产儿甘露糖结合蛋白（MBP）的发育特征。从168名早产儿中纵向收集了885份血清样本，测量MBP，并对其中63份MBP基因中的密码子54突变进行了基因分型。MBP水平/密码子54基因分型也分别测定了146/123名足月婴儿和138/123名成人的脐带血。将早产儿、足月儿和成人分为“低”和“高"MBP组的最佳MBP临界值分别为400 ng/ml（55例低，113例高）、700 ng/ml（35例低，111例高）和750 ng/ml（33例低）。105高），分别通过根据密码子54突变实现最少数量的错误分类。早产儿、足月儿和成人的54号密码子突变的相对危险度“低”组与“高”组相比分别为42.4、67.9和22.9（P KO 00001）。168例早产儿中，MBP“低”组（n = 55）和“高”组（n= 113）的胎龄和出生体重分别为29.5 ± 2.8周、30.5±2.8周（p=0.03）和1230± 317 g、1277± 289 g（p = 0.35）。分别两组早产儿MBP水平在各年龄段均有显著性差异（P<0.001）。作为一个整体，MBP水平从妊娠25周时的平均500 ng/ml上升到足月后20周时的1700 ng/ml。早产儿“低”和“高”MBP组的死亡率分别为22%和12%（p-0.113）。这种差异的死亡率是由于胎龄和出生体重标准差评分（SDS）调整后的妊娠期和性别（p = 0.0001），而不是低MBP水平（p = 0.65）。MBP水平与出生体重SDS评分无相关性（P = 0.26）。平均值± SD。未发生54密码子突变的早产儿、足月儿和成人的MBP水平分别为1225 ±701 ng/ml（n = 45）、2064 ± 829 ng/ml（n= 88）和2473 ± 1395 ng/ml（n = 95）; 54位密码子突变的相应值分别为130 ±275 ng/ml（n= 18）、533 ±665 ng/ml（n = 35）和330± 225 ng/ ml（n= 28）。早产儿宫内生长迟缓不影响MBP水平。对于那些没有密码子54突变的人，三个年龄组之间的MBP水平存在显著差异。对于具有密码子54突变的那些，早产儿和足月儿之间存在显著差异，但足月儿和成人之间没有显著差异。我们的结论是，有一个成熟的MBP水平的早产儿，和一个适度低的MBP表型不影响生存。我们不能排除MBP水平显著降低的影响（密码子54突变纯合子个体的特征），因为本研究中未发现此类早产儿。
The aim of this study was to determine the developmental profile of mannose‐binding protein (MBP) in preterm infants. MBP was measured in 885 longitudinally collected serum samples from 168 preterm infants, and 63 were genotyped with respect to the codon 54 mutation in the MBP gene. MBP level/codon 54 genotyping were also determined on the cord blood of 146/123 term infants and 138/123 adults, respectively. The best cut‐off values of MBP for dividing preterm, term infants and adults into ‘low’ and ‘high’ M BP groups were 400 ng/ml (55 low, 113 high), 700 ng/ml (35 low, 111 high) and 750 ng/ml (33 low. 105 high), respectively, by achieving the least number of misclassifications according to the codon 54 mutation. The relative risk of the ‘low’ groups for presence of the codon 54 mutation compared with ‘high’ groups were 42 4, 67–9 and 22–9 for preterm, term infants and adults, respectively (P KO 00001). The gestational age and birth weight of the ‘low’(n = 55) and ‘high’(n= 113) MBP groups of the 168 preterm infants were 29.5 ± 2.8 weeks, 30.5±2.8 weeks (p=0.03) and 1230±317g, 1277±289g (p = 0.35). respectively. The mean MBP levels of these two groups of preterm infants were different (P<0001) at all ages measured. As a whole group, the MBP level rose from a mean of 500 ng/ml at 25 weeks gestation to 1700ng/ml at 20 weeks post full‐term. The mortality rates of ‘low’ and ‘high’ MBP groups of preterm infants were 22% and 12%, respectively (p‐0.113). This difference in mortality was due to gestational age and birth weight standard deviation score (SDS) after adjusting for length of gestation and gender (p = 0.0001) rather than to low MBP levels (p = 0 65). MBP levels were not related to birthweight SDS score (P = 0 26). The mean ± sd. MBP levels for preterm, term infants and adults without the codon 54 mutation were 1225 ±701 ng/ml (n = 45), 2064 ± 829 ng/ml (n= 88) and 2473 ± 1395ng/ml (n = 95), respectively; the corresponding values for those with the codon 54 mutation were 130 ±275 ng/ml (n= 18), 533 ±665 ng/ml (n = 35)and 330±225ng/ ml (n= 28), respectively. Intra‐uterine growth retardation in preterm infants does not influence MBP levels. For those without the codon 54 mutation, there is a significant difference in MBP level between the three age groups. For those with the codon 54 mutation, there is a significant difference between preterm and term infants, but not between term infants and adults. We conclude that there is a maturation in MBP levels for preterm infants, and that a moderately low MBP phenotype does not affect survival. We cannot exclude an effect of profoundly reduced MBP levels (characteristic of individuals homozygous for the codon 54 mutation), since no such preterm infant was identified in this study.