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Polycystic Ovary Syndrome pp 102–116Cite as

Adrenocortical Dysfunction in the Polycystic Ovary Syndrome

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Abstract

While the majority of patients with hyperandrogenism demonstrate an ovarian source for their high androgen secretion, approximately one half also display excessive adrenocortical production. Dehydroepiandrosterone-sulfate (DHS) was found to be elevated in over 50% of patients with the polycystic ovary syndrome (PCOS) (1–3). Using selective catheterization of the adrenal and ovarian vessels, between 12% and 42% of hyper-androgenic women demonstrated significant adrenal androgen hypersecretion, including androstenedione (A4), dehydroepiandrosterone (DHA), and ∆5-androstenediol (ADIOL) (4–6). The type(s) of adreno-cortical dysfunction resulting in the adrenocortical excess and the mech-anism(s) responsible for this dysfunction in women with PCOS have yet to be elucidated. In this chapter we detail some of our investigations into the nature of the adrenocortical abnormality and the possible factors responsible for it.

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Authors
  1. Ricardo Azziz
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Editors and Affiliations

  1. Department of Obstetrics and Gynecology, School of Medicine, University of California, Davis, 95816, Sacramento, CA, USA

    R. Jeffrey Chang M.D.

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© 1996 Springer-Verlag New York, Inc.

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Azziz, R. (1996). Adrenocortical Dysfunction in the Polycystic Ovary Syndrome. In: Chang, R.J. (eds) Polycystic Ovary Syndrome. Serono Symposia USA. Springer, New York, NY. https://doi.org/10.1007/978-1-4613-8483-0_7

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  • DOI: https://doi.org/10.1007/978-1-4613-8483-0_7

  • Publisher Name: Springer, New York, NY

  • Print ISBN: 978-1-4613-8485-4

  • Online ISBN: 978-1-4613-8483-0

  • eBook Packages: Springer Book Archive

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