OVARIAN AND ADRENAL HYPERANDROGENISM

Because in normal women androgens are secreted in almost equal quantities by both adrenals and ovaries, for many years many studies have tried to distinguish the source of androgen excess. However, in the last 10–15 years, the diagnoses of ovarian or adrenal hyperandrogenism have almost disappeared. This is due to the lack of specificity of dynamic tests as well as to the emphasis given on clinical information and ovarian sonography for the diagnosis of hyperandrogenic syndromes. However, determination of the source of increased androgens may still be useful for improving the classification and the understanding of androgen excess disorders. The aim of this review is to examine the source of androgen excess in the three more common androgen excess disorders: polycystic ovary syndrome (PCOS), idiopathic hyperandrogenism; and nonclassic 21-hydroxylase deficiency (NCAH). The ovary is the main androgen source in PCOS and idiopathic hyperandrogenism while adrenal androgen secretion is prevalent in NCAH. However, androgen secretion from more than one source is common in all main forms of hyperandrogenism as is the case in 70–80% of patients with NCAH, in 35% ofwomen with PCOS, and in 50% of patients with idiopathic hyperandrogenism. SecondaryPCOSis the main cause of ovarian androgen excess in nonclassic 21-hydroxylase deficiency while adrenal hyperandrogenism in PCOS and idiopathic hyperandrogenism is probably the consequence of multiple factors including hyperinsulinemia, altered cortisol metabolism, and increased ovarian steroid production. The clinical image is not generally affected by the source of androgen excess. However, hyperandrogenic patients with increased dehydroepiandrosterone sulfate (DHEAS) tend to have lower body weight and insulin levels and a better metabolic profile.