6533b821fe1ef96bd127b61d

RESEARCH PRODUCT

Hypothalamic-Pituitary-Adrenal Dysfunction in the Polycystic Ovary Syndrome

Enrico CarminaBulent O. YildizRicardo Azziz

subject

endocrine systemmedicine.medical_specialtybusiness.industrymedicine.drug_classHyperandrogenismStimulationAdrenocorticotropic hormoneMetabolismAndrogenmedicine.diseasePolycystic ovaryPeripheralchemistry.chemical_compoundEndocrinologyDehydroepiandrosterone sulfatechemistryInternal medicineMedicinebusinesshormones hormone substitutes and hormone antagonists

description

Between 20 and 30% of patients with polycystic ovary syndrome (PCOS) demonstrate adrenal androgen (AA) excess, detectable primarily by elevated dehydroepiandrosterone sulfate (DHEAS) levels. Generalized adrenocortical hyperresponsivity to adrenocorticotropic hormone (ACTH) stimulation is also observed and may be the principal mechanism determining AA excess in PCOS. The causes of this abnormality are unclear, but increased peripheral metabolism of cortisol, altered factors regulating glucose-mediated glucose disposal, and perhaps ovarian sex steroids may in different ways contribute to the AA excess in PCOS. Additionally, DHEAS levels and the response of AAs to ACTH are relatively constant over time and may be a genetically determined trait.

yearjournalcountryeditionlanguage
2007-11-07
https://doi.org/10.1007/978-1-59745-179-6_19