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Prenatal diethylstilbestrol exposure and reproductive hormones in premenopausal women

Published online by Cambridge University Press:  20 February 2015

L. A. Wise*
Affiliation:
Slone Epidemiology Center at Boston University, Boston, MA, USA Department of Epidemiology, Boston University School of Public Health, Boston, MA, USA
R. Troisi
Affiliation:
Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA
E. E. Hatch
Affiliation:
Department of Epidemiology, Boston University School of Public Health, Boston, MA, USA
L. J. Titus
Affiliation:
Hood Center for Children and Families, Geisel School of Medicine at Dartmouth, Lebanon, NH, USA
K. J. Rothman
Affiliation:
Department of Epidemiology, Boston University School of Public Health, Boston, MA, USA RTI Health Solutions, Research Triangle Park, NC, USA
B. L. Harlow
Affiliation:
Division of Epidemiology and Community Health, University of Minnesota School of Public Health, Minneapolis, MN, USA
*
*Address for correspondence: L. A. Wise, Slone Epidemiology Center at Boston University, 1010 Commonwealth Avenue, Boston, MA 02215, USA. (Email [email protected])

Abstract

Diethylstilbestrol (DES), a synthetic estrogen widely prescribed to pregnant women in the mid-1900s, is a potent endocrine disruptor. Prenatal DES exposure has been associated with reproductive disorders in women, but little is known about its effects on endogenous hormones. We assessed the association between prenatal DES exposure and reproductive hormones among participants from the Harvard Study of Moods and Cycles (HSMC), a longitudinal study of premenopausal women aged 36–45 years from Massachusetts (1995–1999). Prenatal DES exposure was reported at baseline (43 DES exposed and 782 unexposed). Early follicular-phase concentrations of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and estradiol were measured at baseline and every 6 months during 36 months of follow-up. Inhibin B concentrations were measured through 18 months. We used multivariable logistic and repeated-measures linear regression to estimate odds ratios (OR) and percent differences in mean hormone values (β), respectively, comparing DES exposed with unexposed women, adjusted for potential confounders. DES-exposed women had lower mean concentrations of estradiol (pg/ml) (β=−15.6%, 95% confidence interval (CI): −26.5%, −3.2%) and inhibin B (pg/ml) (β=−20.3%, CI: −35.1%, −2.3%), and higher mean concentrations of FSH (IU/I) (β=12.2%, CI: −1.5%, 27.9%) and LH (IU/I) (β=10.4%, CI: −7.2%, 31.3%), than unexposed women. ORs for the association of DES with maximum FSH>10 IU/I and minimum inhibin B<45 pg/ml – indicators of low ovarian reserve – were 1.90 (CI: 0.86, 4.22) and 4.00 (CI: 0.88–18.1), respectively. Prenatal DES exposure was associated with variation in concentrations of FSH, estradiol and inhibin B among women of late reproductive age.

Type
Original Article
Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2015 

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