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Human Reproduction Update Advance Access originally published online on May 2, 2006
Human Reproduction Update 2006 12(4):351-361; doi:10.1093/humupd/dml017
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© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

The origins and sequelae of abnormal neuroendocrine function in polycystic ovary syndrome

S.K. Blank1,3, C.R. McCartney1,2 and J.C. Marshall1,2

1 The Center for Research in Reproduction and 2 Division of Endocrinology, Department of Internal Medicine, University of Virginia Health System, Charlottesville, VA, USA

3 To whom correspondence should be addressed at: Center for Research in Reproduction, Box 800391, University of Virginia Health System, Charlottesville, VA 22908, USA. E-mail: sek2h{at}virginia.edu

Submitted on December 13, 2005; resubmitted on March 10, 2006; accepted on March 27, 2006

Polycystic ovary syndrome (PCOS) is a common clinical disorder characterized by ovulatory dysfunction and hyperandrogenaemia. A neuroendocrine hallmark of PCOS is persistently rapid LH (GnRH) pulsatility, which favours pituitary synthesis of LH over that of FSH and contributes to the increased LH concentrations and LH : FSH ratios typical of PCOS. Inadequate FSH levels contribute to impaired follicular development, whereas elevated LH levels augment ovarian androgen production. Whereas luteal phase elevations in progesterone normally slow GnRH pulse frequency, women with PCOS do not experience normal progesterone-mediated slowing, due in part to impaired hypothalamic progesterone sensitivity. This reduction in hypothalamic progesterone sensitivity appears to be mediated by elevated androgens because sensitivity can be restored with the androgen receptor blocker flutamide. The ovulatory and hormonal abnormalities associated with PCOS generally present during puberty, typically associated with hyperandrogenaemia. Along with elevated LH concentration and pulsatility, some girls with hyperandrogenaemia have impaired hypothalamic progesterone sensitivity similar to that seen in adult women with PCOS. We propose that peripubertal hyperandrogenaemia may lead to persistently rapid GnRH pulse frequency via impaired hypothalamic feedback inhibition. The subsequent abnormalities in gonadotropin secretion, androgen production and ovulatory function may support progression towards the adult PCOS phenotype.

Key words: androgens / endocrinology / gonadotrophin / polycystic ovaries / progesterone


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