DHEA, DHEAS and PCOS.pdfVIP

Journal of Steroid Biochemistry Molecular Biology 145 (2015) 213–225 Contents lists available at ScienceDirect Journal of Steroid Biochemistry Molecular Biology journal homepage: www.elsevier .com/ locate / jsbmbReviewDHEA, DHEAS and PCOS Mark O. Goodarzi a, Enrico Carmina b, Ricardo Azziz c,* aCedars-Sinai Medical Center, Los Angeles, CA 90048, USA bUniversity of Palermo, Palermo, Italy cGeorgia Regents University, Office of the President, 120 15th St., AA 311, Augusta, GA 30912, USAA R T I C L E I N F O Article history: Received 26 February 2014 Received in revised form 16 May 2014 Accepted 5 June 2014 Available online 5 July 2014Keywords: Polycystic ovary syndrome Adrenal Androgens Dehydroepiandrosterone (DHEA) Dehydroepiandrosterone sulfate (DHEAS) GeneticsAbbreviations: 11b-HSD1, 11b-hydroxys one; 21-OH, 21-hydroxylase; A4, androsten Reproductive Medicine; AUC, are-under-t Embryology; FSH, follicle stimulating hormo association studies; HOMA-IR, homeostatic premature adrenarche; PCOS, polycystic thiazolidinedione. * Corresponding author. Tel.: +1 7067212 E-mail addresses: razziz@, lsherr /10.1016/j.jsbmb.2014.06.0 0960-0760/? 2014 Elsevier Ltd. All rightsteroid deh edione; A he-curve; ne; FSIGT, model asse ovary sy 301; fax: ouse@gru 03 reserved.A B S T R A C T Approximately 20–30% of PCOS women demonstrate excess adrenal precursor androgen (APA) production, primarily using DHEAS as a marker of APA in general and more specifically DHEA, synthesis. The role of APA excess in determining or causing PCOS is unclear, although observations in patients with inherited APA excess (e.g., patients with 21-hydroxylase deficient congenital classic or non- classic adrenal hyperplasia) demonstrate that APA excess can result in a PCOS-like phenotype. Inherited defects of the enzymes responsible for steroid biosynthesis, or defects in cortisolmetabolism, account for only a very small fraction ofwomen suffering fromhyperandrogenismor APA excess. Rather, womenwith PCOS and APA