Normal Ovarian Structure and Function with Normal Glucose Tolerance in Girls with Early Treatment of Classic Congenital Adrenal Hyperplasia - 12/08/11
, Harriet Paltiel 2, Jeanne Chow 2, Julie Ringelheim 3, Catherine M. Gordon 1, 3
Address correspondence to: Amy Fleischman, MD, MMSc, Children’s Hospital Boston, Division of Endocrinology, 333 Longwood Avenue, Boston, MA 02115Abstract |
Hyperandrogenism and hyperinsulinism have both been suggested as etiologic factors behind functional ovarian hyperandrogenism or polycystic ovary syndrome. Females with congenital adrenal hyperplasia provide a clinical model to evaluate the contribution of pre- and post-natal hyperandrogenism on ovarian structure and function.
Study Objective |
To evaluate glucose tolerance, and structure and androgen production of the ovaries in young females with classic congenital adrenal hyperplasia.
Design, Setting, Participants |
Cross-sectional study, including the enrollment of participants, ages 8 to 20 years, recruited from the pediatric endocrinology clinical program of a tertiary pediatric referral center.
Interventions |
Ten participants had oral glucose tolerance testing, adrenal and ovarian androgen measurements, and pelvic ultrasound studies performed.
Main Outcome Measures |
Presence of altered response to glucose challenge, ovarian hyperandrogenism, or presence of polycystic ovaries by ultrasound.
Results |
Measurements of fasting blood glucose, post-challenge glucose, and insulin resistance were normal in this sample. There was no evidence of ovarian hyperandrogenism after adrenal suppression with dexamethasone. All participants had normal ovarian structure without evidence of polycystic ovaries.
Conclusions |
Females with classic congenital adrenal hyperplasia (21-hydroxylase deficiency) and normal glucose tolerance appear to have normal ovarian structure and function during the peripubertal period.
Le texte complet de cet article est disponible en PDF.Key Words : CAH, Ovarian structure, Glucose metabolism, PCOS
Plan
| Funding: This project was supported by an investigator initiated grant from Pfizer, Inc., and the Clinical Investigator Training Program: Harvard-MIT Health Sciences and Technology—Beth Israel Deaconess Medical Center, in collaboration with Pfizer Inc. and Merck & Company, Inc., and Nitt grant M01-RR-2172 from the National Institutes of Health to Children’s Hospital Boston General Clinical Research Center. |
Vol 20 - N° 2
P. 67-72 - avril 2007 Retour au numéro
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