Polycystic ovaries in nonobese adolescents and young women with ovarian androgen excess: relation to prenatal growth.
OBJECTIVE
Reduced growth before birth is known to associate with a smaller ovarian volume in adolescents and women without androgen excess. We studied whether prenatal growth relates also to ovarian size and polycystic ovary (PCO) morphology in nonobese adolescents and young women with ovarian androgen excess.


METHODS
A cross-sectional analysis of standardized case notes over a 2-yr period was performed.


METHODS
Nonobese adolescents and young women (age approximately 17 yr; n = 86) seen for ovarian androgen excess, as confirmed by 17-hydroxy-progesterone hyperresponse to a GnRH agonist, were included in the study.


METHODS
Endocrine-metabolic assessment in fasting state, together with a vaginal ultrasound scan to verify the presence or absence of PCO was performed. Birth weight and gestational age were derived from medical records.


RESULTS
PCO prevalence by ultrasound was 38%. Absence of PCO was associated with a shift (P < 0.0005) of the birth weight distribution toward lower values. Patients with a birth weight less than 3.0 kg were 6-fold more likely to have no PCO than to have PCO. Birth weight was across a wide range (1.5-4.0 kg) associated with ovarian volume in hyperandrogenic patients with noncystic ovaries (r = 0.60; P < 0.00001) and was, in a multiple regression analysis, the prime variable linked to ovarian volume (beta = 0.57; P < 0.00001), explaining 32% of its variance.


CONCLUSIONS
The ovarian size and the development of a PCO morphology in nonobese adolescents and young women with ovarian androgen excess relate to prenatal growth. These findings indicate that there are two subgroups of nonobese patients with ovarian androgen excess: one with a normal birth weight distribution and with PCO, and one with lower birth weights and without PCO.
Ibáñez
Lourdes
L
Endocrinology Unit, Hospital Sant Joan de Déu, University of Barcelona, 08950 Esplugues, Barcelona, Spain. libanez@hsjdbcn.org
López-Bermejo
Abel
A
Callejo
Justo
J
Torres
Ana
A
Cabré
Sergi
S
Dunger
David
D
de Zegher
Francis
F
D019326:17-alpha-Hydroxyprogesterone / Q000097:blood; D000293:Adolescent; D000735:Androstenedione / Q000097:blood; D001724:Birth Weight / Q000502:physiology*; D003430:Cross-Sectional Studies; D019314:Dehydroepiandrosterone Sulfate / Q000097:blood; D005260:Female; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D005640:Follicle Stimulating Hormone / Q000097:blood; D006801:Humans; D017588:Hyperandrogenism / Q000097:blood / Q000503:physiopathology*; D007231:Infant, Newborn; D007328:Insulin / Q000097:blood; D007986:Luteinizing Hormone / Q000097:blood; D009929:Organ Size / Q000502:physiology; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000503:physiopathology*; D011446:Prospective Studies; D012044:Regression Analysis; D012189:Retrospective Studies; D013739:Testosterone / Q000097:blood
D007328:Insulin; D013739:Testosterone; D000735:Androstenedione; D019314:Dehydroepiandrosterone Sulfate; D019326:17-alpha-Hydroxyprogesterone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone