Birth defects in the sons and daughters of women who were exposed in utero to diethylstilbestrol (DES)

被引:76
|
作者
Titus-Ernstoff, L. [1 ,2 ,3 ]
Troisi, R. [4 ]
Hatch, E. E. [5 ]
Palmer, J. R. [6 ]
Hyer, M. [7 ]
Kaufman, R. [8 ]
Adam, E. [9 ]
Noller, K. [10 ]
Hoover, R. N. [4 ]
机构
[1] Dartmouth Med Sch, Dept Community & Family Med, Lebanon, NH 03756 USA
[2] Dartmouth Med Sch, Dept Pediat, Lebanon, NH 03756 USA
[3] Hood Ctr Children & Families, Lebanon, NH 03756 USA
[4] NCI, Div Canc Epidemiol & Genet, Bethesda, MD 20892 USA
[5] Boston Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Boston, MA USA
[6] Boston Univ, Slone Epidemiol Unit, Sch Publ Hlth, Brookline, MA USA
[7] Informat Management Serv Inc, Rockville, MD USA
[8] Methodist Hosp, Dept Obstet & Gynecol, Houston, TX 77030 USA
[9] Bayer Coll Med, Dept Virol & Epidemiol, Houston, TX USA
[10] Tufts Univ New England Med Ctr, Dept Obstet & Gynecol, Boston, MA 02111 USA
来源
INTERNATIONAL JOURNAL OF ANDROLOGY | 2010年 / 33卷 / 02期
关键词
birth defects; diethylstilbestrol; epigenetic alterations; maternal exposure; prenatal exposure; PRENATAL EXPOSURE; SEX-HORMONES; FOLLOW-UP; PREGNANCY; TUMORS; RISK; MEN; DESCENDANTS; FERTILITY; CANCER;
D O I
10.1111/j.1365-2605.2009.01010.x
中图分类号
R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
摘要
P>Prenatal exposure to diethylstilbestrol (DES) is associated with adverse health outcomes, including anatomic anomalies of the reproductive tract in women and of the genitourinary tract in men. The mouse model, which replicates many DES-related effects seen in humans, suggests that prenatal DES exposure causes alterations that may affect the next generation of offspring. We asked women participating in a large, multi-centre study of prenatal DES exposure to report birth defects occurring among 4029 sons and 3808 daughters (i.e., the third generation). A subcohort of 793 third generation daughters was also queried for birth defects. We used logistic regression models to generate odds ratio and 95% confidence intervals for the association between prenatal DES exposure in the mother and birth defects in the offspring. Based on the mothers' reports, overall birth defects were elevated in the sons (OR = 1.53; 95% CI = 1.04, 2.23) and in the daughters (OR = 2.35; 95% CI = 1.44, 3.82). Most estimates of association were imprecise, but daughters appeared to have an excess of heart conditions (OR = 4.56; 95% CI = 1.27, 16.34). Our data suggest a possible association between the mother's prenatal DES exposure and birth defects in their offspring, particularly in daughters. We cannot, however, rule-out the possible influence of reporting bias. In particular, the exposed daughters' elevated risk of cardiac defects may be as a result of the underreporting of these conditions by unexposed mothers.
引用
收藏
页码:377 / 383
页数:7
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