Endocrine and cardiometabolic cord blood characteristics of offspring born to mothers with and without polycystic ovary syndrome
Androstenedione concentrations may be increased in the cord blood of offspring of women with polycystic ovary syndrome, which may predispose the offspring to fetal hyperandrogenism.
Volume 107, Issue 1, Pages 261-268
Nadine M.P. Daan, M.D., Ph.D., Maria P.H. Koster, M.D., Ph.D., Regine P. Steegers-Theunissen, M.D., Ph.D., Marinus J.C. Eijkemans, Ph.D., B.C.J.M. Fauser, M.D., Ph.D.
To compare the endocrine and cardiometabolic cord blood characteristics of offspring of mothers with polycystic ovary syndrome (PCOS) with those of healthy controls.
Cross-sectional case control study.
University medical centers.
Offspring from mothers with PCOS (n = 61) and healthy controls (n = 82).
Cord blood withdrawal from neonates.
Main Outcome Measure(s)
Cord blood estradiol, androstenedione, dehydroepiandrosterone sulfate (DHEAS), testosterone, sex hormone-binding globulin, free androgen index (FAI), insulin, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglycerides, c-reactive protein, adiponectin, and leptin.
Androstenedione and leptin concentrations were increased in the offspring of women with PCOS compared with the controls: androstenedione median 2.9 (interquartile range [IQR] 2.3–3.9) nmol/L vs. 2.2 [IQR 1.6–2.7] nmol/L; and leptin median 13.6 [IQR 8.3–22.9] μg/L vs. 9.8 [IQR 6.0–16.5] μg/L. After adjusting for maternal and pregnancy-related confounders (such as maternal age, gestational age, birth weight), androstenedione appeared associated with PCOS in both male (relative change 1.36 [1.04; 1.78]) and female offspring (relative change 1.40 [1.08; 1.82]). Similarly, in male offspring the leptin concentrations appeared associated with PCOS after correction for confounders (relative change 1.55 [1.12; 2.14]). After correction for multiple testing, these associations attenuated.
Observed results suggest that androstenedione concentrations are increased in the cord blood of male and female offspring of women with PCOS, although this requires confirmation. This finding would support the hypothesis that a maternal hyperandrogenic environment during pregnancy in women with PCOS may predispose their offspring to fetal hyperandrogenism. The potential associations between fetal hyperandrogenism and long-term health effects remain to be elucidated.