Adrenocortical dysfunction in polycystic ovary syndrome

Introduction: Androgen excess is the most common endocrine disorder of reproductive-aged women, with the majority of patients having a functional abnormality, namely polycystic ovary syndrome (PCOS) (Azziz et al. 2004a). We and others have reported the estimated prevalence of this syndrome to be approximately 6–8% (Knochenhauer et al. 1998, Diamanti-Kandarakis et al. 1999, Asunción et al. 2000, Azziz et al. 2004b), using the 1990 National Institute of Child Health and Human Development (NICHD) conference diagnostic criteria for PCOS (Zawadzki and Dunaif 1992). This conference concluded that the diagnostic criteria of PCOS should include: (1) clinical and/or biochemical signs of hyperandrogenism, (2) oligo-ovulation, and (3) exclusion of other known disorders such as Cushing's syndrome, hyperprolactinemia, and non-classic congenital adrenal hyperplasia (NCAH) (Zawadzki and Dunaif 1992). A recent expert meeting sponsored by the European Society of Human Reproduction and Embryology (ESHRE) and the American Society for Reproductive Medicine (ASRM) expanded this definition, noting that PCOS should be diagnosed when at least two of the following three criteria are present: (1) oligo- and/or anovulation, (2) clinical and/or biochemical signs of hyperandrogenism, or (3) polycystic ovaries on ultrasonography, after the exclusion of related disorders (The Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group 2004a, b). The adrenal androgens (AAs) are primarily secreted by the zonae reticulares of the adrenal cortex, and include dehydroepiandrosterone (DHEA) and its sulfate (DHEAS), Δ5-androstene-3β, 17β-diol (androstenediol), and 11β-hydroxyandrostenedione (11-OHA4).