Moore Lynn L, Bradlee M Loring, Singer Martha R, Rothman Kenneth J, Milunsky Aubrey
Section of Preventive Medicine and Epidemiology, Boston University School of Medicine, Boston, MA 02118, USA.
Am J Epidemiol. 2002 Apr 15;155(8):719-24. doi: 10.1093/aje/155.8.719.
A limited body of data over the past 35 years has suggested that autoimmunity may be responsible for some cases of aneuploidy. The role of diabetes mellitus in the etiology of chromosomal anomalies has been infrequently studied. This study was designed to compare the prevalence of chromosome abnormalities among the offspring of women with gestational diabetes and the offspring of women without it. The authors used data from 7,332 women who underwent amniocentesis in a prospective study of pregnancy outcome (1984-1988) and examined the prevalence of autosomal and sex chromosome defects associated with gestational diabetes. Among the offspring of 231 women with gestational diabetes, the crude prevalence of chromosomal defects was twice as high as that seen in the offspring of 7,101 women without gestational diabetes. These anomalies were predominantly numeric sex chromosome defects. After adjusting for potential confounding by maternal age, body mass index, education, and first-trimester exposures in multiple logistic regression analysis, the authors found that women with gestational diabetes were 7.7 times as likely (95% confidence interval: 2.8, 21.1) to have an infant with a numeric sex chromosome defect as those without gestational diabetes. These results support the theory that some women who develop gestational diabetes may have underlying biochemical changes that induce nondisjunction and the development of chromosomal defects.
过去35年中有限的数据表明，自身免疫可能是某些非整倍体病例的病因。糖尿病在染色体异常病因中的作用鲜有研究。本研究旨在比较妊娠期糖尿病女性后代与非妊娠期糖尿病女性后代中染色体异常的患病率。作者使用了来自7332名接受羊膜穿刺术的女性的数据，这些数据来自一项关于妊娠结局的前瞻性研究（1984 - 1988年），并研究了与妊娠期糖尿病相关的常染色体和性染色体缺陷的患病率。在231名患有妊娠期糖尿病的女性后代中，染色体缺陷的粗患病率是7101名无妊娠期糖尿病女性后代的两倍。这些异常主要是数字性染色体缺陷。在多因素逻辑回归分析中，对母亲年龄、体重指数、教育程度和孕早期暴露等潜在混杂因素进行校正后，作者发现患有妊娠期糖尿病的女性生出数字性染色体缺陷婴儿的可能性是非妊娠期糖尿病女性的7.7倍（95%置信区间：2.8, 21.1）。这些结果支持了这样一种理论，即一些患妊娠期糖尿病的女性可能存在潜在的生化变化，这些变化会导致不分离和染色体缺陷的发生。
