INTRAUTERINE GROWTH-RETARDATION AS AN END-POINT IN MUTATION EPIDEMIOLOGY - AN EVALUATION BASED ON PATERNAL AGE
INTRAUTERINE GROWTH-RETARDATION AS AN END-POINT IN MUTATION EPIDEMIOLOGY - AN EVALUATION BASED ON PATERNAL AGE
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DOI：
10.1016/0165-1218(95)90043-8
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发表时间：
1995-08-01
期刊：
影响因子：
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通讯作者：
SAVITZ, DA
中科院分区：
文献类型：
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作者：
OLSHAN, AF;ANANTH, CV;SAVITZ, DA
Czeizel最近提出，胎儿宫内发育迟缓可能在突变流行病学中作为表型终点有价值。我们假设，如果一些小于胎龄儿(SGA)的出生是由新的生发突变引起的，那么应该与父亲的高龄有关。我们使用来自北卡罗来纳州的大样本出生(n=254892)来评估父亲年龄与SGA、低出生体重和早产的关系。这些分析仅限于20-34岁母亲的出生，并根据母亲的年龄、种族、教育程度、婚姻状况、怀孕和吸烟进行了调整。在任何年龄段的父亲中，SGA、低出生体重和早产的风险都没有发现实质性的增加。例如，SGA的优势比从0.87(50岁或以上的父亲)到1.13(45-49岁的父亲)不等。结果表明，SGA和相关的终点之间没有明显的关系，随着父亲年龄的增加，突变的增加。
Czeizel recently suggested that intrauterine growth retardation might be of value as a phenotypic endpoint in mutation epidemiology. We hypothesized that if some fraction of small-for-gestational age (SGA) births are due to new germinal mutations, then an association with advanced paternal age should be present. We evaluated the relation between paternal age and SGA, low birthweight, and preterm births using a large sample of births (n = 254,892) from North Carolina. The analyses were restricted to births of mothers aged 20-34 years and adjusted for maternal age, race, education, marital status, gravidity, and smoking. No material increase in the risk of SGA, low birthweight, and preterm delivery was found for fathers in any age category. For example, odds ratios for SGA ranged from 0.87 (fathers aged 50 years or greater) to 1.13 (fathers aged 45-49 years). The results indicate no discernable relationship between SGA and related endpoints and the increase in increase of mutations that accompany advanced paternal age.