Abstract
Context: The association between early menopause and vascular disease as a possible causative factor has recently received attention. Preeclampsia (PE) is associated with future cardiovascular risk factors, and this premature vascular aging potentially modifies the ovarian aging process. Objective: The purpose of this study was to assess whether women with a history of PE have lower anti-Müllerian hormone (AMH) levels than women with normotensive pregnancies. Design: This was a retrospective cohort study. Setting: The study was conducted in a tertiary referral center. Patients: Clinical data and blood samples of participants in the Preeclampsia Risk EValuation in FEMales study were used (336 women with a history of PE and 329 women after a normotensive pregnancy). Interventions: There were no interventions. Main Outcome Measures: The relative decrease in AMH levels was assessed after a median follow- up of 10.5 years. Results: The meanAMHlevel was 2.00 ± 1.87μg/L in the PE group compared with 2.26 ± 2.56μg/L in the reference group. Linear regression analysis with censoring for undetectable AMH levels, adjusted for age, smoking, and hormonal contraceptive use, showed a relative reduction in AMH levels of 20.9% at any age (fold change 0.79, 95% confidence interval, 0.67-0.94). Conclusions:Wedemonstrate that women with a history of PE have significantly lowerAMHlevels than women with normotensive pregnancies. Calculations based on a reference population indicate advancement of reproductive age of approximately 1.5 years. Because PE is considered a manifestation of impaired vascular health, these results support the hypothesis that compromised vascular health could act as a causative mechanism in early ovarian aging. Copyright © 2014 by the Endocrine Society.
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CITATION STYLE
Yarde, F., Maas, A. H. E. M., Franx, A., Eijkemans, M. J. C., Drost, J. T., Van Rijn, B. B., … Broekmans, F. J. M. (2014). Serum AMH levels in women with a history of preeclampsia suggest a role for vascular factors in ovarian aging. Journal of Clinical Endocrinology and Metabolism, 99(2), 579–586. https://doi.org/10.1210/jc.2013-2902
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