The adrenal and polycystic ovary syndrome

Bulent O. Yildiz, Ricardo Azziz

Research output: Contribution to journalReview article

66 Citations (Scopus)

Abstract

Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders characterized by androgen excess, oligo-ovulation and polycystic ovaries. Although ovaries are the main source of increased androgens in the syndrome, between 20 and 30% of patients with PCOS have adrenal androgen (AA) excess, detectable primarily by elevated dehydroepiandrosterone sulfate (DHEAS) levels. Patients with PCOS demonstrate a generalized hypersecretion of adrenocortical products, basally and in response to ACTH stimulation. The mechanisms of these abnormalities are unclear although AA excess in PCOS is likely a complex trait, modulated by both intrinsic and acquired factors. To date, no specific genetic defects have been identified. The production of AAs in response to ACTH appears to be closely related to altered factors regulating glucose-mediated glucose disposal, increased peripheral metabolism of cortisol, and to a less extent to the effects of extra-adrenal androgens, insulin resistance, hyperinsulinemia or obesity. Finally, DHEAS levels and the response of AAs to ACTH are relatively constant over time and are closely correlated between PCOS patients and their siblings suggesting that this abnormality is an inherited trait in PCOS.

Original languageEnglish (US)
Pages (from-to)331-342
Number of pages12
JournalReviews in Endocrine and Metabolic Disorders
Volume8
Issue number4
DOIs
StatePublished - Dec 1 2007

Fingerprint

Polycystic Ovary Syndrome
Androgens
Adrenocorticotropic Hormone
Dehydroepiandrosterone Sulfate
Ovary
Glucose
Intrinsic Factor
Hyperinsulinism
Ovulation
Insulin Resistance
Hydrocortisone
Siblings
Obesity

Keywords

  • Adrenal
  • Cortisol
  • DHEA
  • Heritability
  • Hyperandrogenism
  • PCOS

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

The adrenal and polycystic ovary syndrome. / Yildiz, Bulent O.; Azziz, Ricardo.

In: Reviews in Endocrine and Metabolic Disorders, Vol. 8, No. 4, 01.12.2007, p. 331-342.

Research output: Contribution to journalReview article

Yildiz, Bulent O. ; Azziz, Ricardo. / The adrenal and polycystic ovary syndrome. In: Reviews in Endocrine and Metabolic Disorders. 2007 ; Vol. 8, No. 4. pp. 331-342.
@article{681ef70d86134d88a55e5ad68b5f53f0,
title = "The adrenal and polycystic ovary syndrome",
abstract = "Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders characterized by androgen excess, oligo-ovulation and polycystic ovaries. Although ovaries are the main source of increased androgens in the syndrome, between 20 and 30{\%} of patients with PCOS have adrenal androgen (AA) excess, detectable primarily by elevated dehydroepiandrosterone sulfate (DHEAS) levels. Patients with PCOS demonstrate a generalized hypersecretion of adrenocortical products, basally and in response to ACTH stimulation. The mechanisms of these abnormalities are unclear although AA excess in PCOS is likely a complex trait, modulated by both intrinsic and acquired factors. To date, no specific genetic defects have been identified. The production of AAs in response to ACTH appears to be closely related to altered factors regulating glucose-mediated glucose disposal, increased peripheral metabolism of cortisol, and to a less extent to the effects of extra-adrenal androgens, insulin resistance, hyperinsulinemia or obesity. Finally, DHEAS levels and the response of AAs to ACTH are relatively constant over time and are closely correlated between PCOS patients and their siblings suggesting that this abnormality is an inherited trait in PCOS.",
keywords = "Adrenal, Cortisol, DHEA, Heritability, Hyperandrogenism, PCOS",
author = "Yildiz, {Bulent O.} and Ricardo Azziz",
year = "2007",
month = "12",
day = "1",
doi = "10.1007/s11154-007-9054-0",
language = "English (US)",
volume = "8",
pages = "331--342",
journal = "Reviews in Endocrine and Metabolic Disorders",
issn = "1389-9155",
publisher = "Springer Netherlands",
number = "4",

}

TY - JOUR

T1 - The adrenal and polycystic ovary syndrome

AU - Yildiz, Bulent O.

AU - Azziz, Ricardo

PY - 2007/12/1

Y1 - 2007/12/1

N2 - Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders characterized by androgen excess, oligo-ovulation and polycystic ovaries. Although ovaries are the main source of increased androgens in the syndrome, between 20 and 30% of patients with PCOS have adrenal androgen (AA) excess, detectable primarily by elevated dehydroepiandrosterone sulfate (DHEAS) levels. Patients with PCOS demonstrate a generalized hypersecretion of adrenocortical products, basally and in response to ACTH stimulation. The mechanisms of these abnormalities are unclear although AA excess in PCOS is likely a complex trait, modulated by both intrinsic and acquired factors. To date, no specific genetic defects have been identified. The production of AAs in response to ACTH appears to be closely related to altered factors regulating glucose-mediated glucose disposal, increased peripheral metabolism of cortisol, and to a less extent to the effects of extra-adrenal androgens, insulin resistance, hyperinsulinemia or obesity. Finally, DHEAS levels and the response of AAs to ACTH are relatively constant over time and are closely correlated between PCOS patients and their siblings suggesting that this abnormality is an inherited trait in PCOS.

AB - Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders characterized by androgen excess, oligo-ovulation and polycystic ovaries. Although ovaries are the main source of increased androgens in the syndrome, between 20 and 30% of patients with PCOS have adrenal androgen (AA) excess, detectable primarily by elevated dehydroepiandrosterone sulfate (DHEAS) levels. Patients with PCOS demonstrate a generalized hypersecretion of adrenocortical products, basally and in response to ACTH stimulation. The mechanisms of these abnormalities are unclear although AA excess in PCOS is likely a complex trait, modulated by both intrinsic and acquired factors. To date, no specific genetic defects have been identified. The production of AAs in response to ACTH appears to be closely related to altered factors regulating glucose-mediated glucose disposal, increased peripheral metabolism of cortisol, and to a less extent to the effects of extra-adrenal androgens, insulin resistance, hyperinsulinemia or obesity. Finally, DHEAS levels and the response of AAs to ACTH are relatively constant over time and are closely correlated between PCOS patients and their siblings suggesting that this abnormality is an inherited trait in PCOS.

KW - Adrenal

KW - Cortisol

KW - DHEA

KW - Heritability

KW - Hyperandrogenism

KW - PCOS

UR - http://www.scopus.com/inward/record.url?scp=38049054091&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=38049054091&partnerID=8YFLogxK

U2 - 10.1007/s11154-007-9054-0

DO - 10.1007/s11154-007-9054-0

M3 - Review article

C2 - 17932770

AN - SCOPUS:38049054091

VL - 8

SP - 331

EP - 342

JO - Reviews in Endocrine and Metabolic Disorders

JF - Reviews in Endocrine and Metabolic Disorders

SN - 1389-9155

IS - 4

ER -