Book contents
- Polycystic Ovary Syndrome
- Polycystic Ovary Syndrome
- Copyright page
- Contents
- Contributors
- Chapter 1 Introduction to and History of Polycystic Ovary Syndrome
- Chapter 2 Polycystic Ovary Syndrome: From Phenotype to Genotype
- Chapter 3 The Epidemiology of Polycystic Ovary Syndrome
- Chapter 4 Ovarian Ultrasonography in Polycystic Ovary Syndrome
- Chapter 5 The Classification of Polycystic Ovary Syndrome Informed by the International Guideline 2018
- Chapter 6 The Relevance of the Anti-Müllerian Hormone in Polycystic Ovary Syndrome Diagnosis and Management
- Chapter 7 Origins of Polycystic Ovary Syndrome In Utero
- Chapter 8 Adrenal and Polycystic Ovary Syndrome
- Chapter 9 Polycystic Ovary Syndrome and Environmental Toxins
- Chapter 10 Lifestyle in Polycystic Ovary Syndrome
- Chapter 11 Ovulation Induction in Polycystic Ovary Syndrome
- Chapter 12 Ovarian Surgery for Ovulation Induction
- Chapter 13 In Vitro Fertilization and Assisted Reproductive Technologies in Polycystic Ovary Syndrome
- Chapter 14 Pregnancy Complications and Children Outcomes in Patients with Polycystic Ovarian Syndrome
- Chapter 15 The Role of In Vitro Maturation in Polycystic Ovary Syndrome
- Chapter 16 The Treatment of Obesity in Polycystic Ovary Syndrome
- Chapter 17 Mood Disorders in Polycystic Ovary Syndrome
- Chapter 18 The Long-Term Health Consequences of Polycystic Ovary Syndrome
- Chapter 19 Polycystic Ovary Syndrome
- Chapter 20 Cancer and Polycystic Ovary Syndrome
- Index
- References
Chapter 8 - Adrenal and Polycystic Ovary Syndrome
Published online by Cambridge University Press: 13 May 2022
- Polycystic Ovary Syndrome
- Polycystic Ovary Syndrome
- Copyright page
- Contents
- Contributors
- Chapter 1 Introduction to and History of Polycystic Ovary Syndrome
- Chapter 2 Polycystic Ovary Syndrome: From Phenotype to Genotype
- Chapter 3 The Epidemiology of Polycystic Ovary Syndrome
- Chapter 4 Ovarian Ultrasonography in Polycystic Ovary Syndrome
- Chapter 5 The Classification of Polycystic Ovary Syndrome Informed by the International Guideline 2018
- Chapter 6 The Relevance of the Anti-Müllerian Hormone in Polycystic Ovary Syndrome Diagnosis and Management
- Chapter 7 Origins of Polycystic Ovary Syndrome In Utero
- Chapter 8 Adrenal and Polycystic Ovary Syndrome
- Chapter 9 Polycystic Ovary Syndrome and Environmental Toxins
- Chapter 10 Lifestyle in Polycystic Ovary Syndrome
- Chapter 11 Ovulation Induction in Polycystic Ovary Syndrome
- Chapter 12 Ovarian Surgery for Ovulation Induction
- Chapter 13 In Vitro Fertilization and Assisted Reproductive Technologies in Polycystic Ovary Syndrome
- Chapter 14 Pregnancy Complications and Children Outcomes in Patients with Polycystic Ovarian Syndrome
- Chapter 15 The Role of In Vitro Maturation in Polycystic Ovary Syndrome
- Chapter 16 The Treatment of Obesity in Polycystic Ovary Syndrome
- Chapter 17 Mood Disorders in Polycystic Ovary Syndrome
- Chapter 18 The Long-Term Health Consequences of Polycystic Ovary Syndrome
- Chapter 19 Polycystic Ovary Syndrome
- Chapter 20 Cancer and Polycystic Ovary Syndrome
- Index
- References
Summary
Polycystic ovary syndrome (PCOS) is characterized by clinical or biochemical hyperandrogenism, oligo-anovulation and polycystic ovarian morphology on ultrasound. Although the ovaries are the primary source of hyperandrogenism in PCOS, between 20% and 30% of patients with PCOS demonstrate adrenal androgen (AA) excess, as reflected by the circulating dehydroepiandrosterone sulfate (DHEAS) levels. The contribution of AA excess to the development or phenotypic expression of PCOS is not fully understood. Women with PCOS, particularly those with hyperandrogenic subphenotypes, show generalized hypersecretion of adrenocortical products, basally and in response to adrenocorticotropic hormone (ACTH). Alterations in adrenocortical biosynthesis, an exaggeration in the responsivity to ACTH, defects in cortisol metabolism and extra-adrenal factors, including obesity, insulin and glucose levels, and ovarian secretions play a limited role in increased AA production observed in PCOS. Adrenal androgen (AA) levels and their response to ACTH stimulation are highly individualized and relatively constant over time, suggesting that AA hypersecretion may be an inherited trait. Familial aggregation of AA excess in both brothers and sisters of patients with PCOS also supports heritability. However, studies to date have failed to identify specific genetic defects in adrenocortical dysfunction of PCOS due to the genetic and phenotypic heterogeneity of the syndrome and the lack of insufficiently large cohorts.
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- Polycystic Ovary Syndrome , pp. 67 - 79Publisher: Cambridge University PressPrint publication year: 2022
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