OVARIAN AND ADRENAL HYPERANDROGENISM

Because in normal women androgens are secreted in almostequal quantities by both adrenals and ovaries, for many years many studieshave tried to distinguish the source of androgen excess. However, inthe last 10–15 years, the diagnoses of ovarian or adrenal hyperandrogenismhave almost disappeared. This is due to the lack of specificityof dynamic tests as well as to the emphasis given on clinical informationand ovarian sonography for the diagnosis of hyperandrogenic syndromes.However, determination of the source of increased androgens may still beuseful for improving the classification and the understanding of androgenexcess disorders. The aim of this review is to examine the source ofandrogen excess in the three more common androgen excess disorders:polycystic ovary syndrome (PCOS), idiopathic hyperandrogenism; andnonclassic 21-hydroxylase deficiency (NCAH). The ovary is the main androgensource in PCOS and idiopathic hyperandrogenism while adrenalandrogen secretion is prevalent in NCAH. However, androgen secretionfrom more than one source is common in all main forms of hyperandrogenismas is the case in 70–80% of patients with NCAH, in 35% ofwomenwith PCOS, and in 50% of patients with idiopathic hyperandrogenism.SecondaryPCOSis the main cause of ovarian androgen excess in nonclassic21-hydroxylase deficiency while adrenal hyperandrogenism in PCOSand idiopathic hyperandrogenism is probably the consequence of multiplefactors including hyperinsulinemia, altered cortisol metabolism, andincreased ovarian steroid production. The clinical image is not generallyaffected by the source of androgen excess. However, hyperandrogenic patientswith increased dehydroepiandrosterone sulfate (DHEAS) tend tohave lower body weight and insulin levels and a better metabolic profile.