POLYCYSTIC-OVARY-SYNDROME AS A FORM OF FUNCTIONAL OVARIAN HYPERANDROGENISM DUE TO DYSREGULATION OF ANDROGEN SECRETION

In 1935, Stein and Leventhal (1) reported the association of polycystic ovaries in women with amenorrhea, hirsutism, and obesity. Morphological and histological studies of the ovaries from these patients revealed a thickened tunica albuginea, hyperplasia of the theca interna and cortical stroma, and multiple subcapsular follicles that were in various stages of atresia (1). Subsequently, the heterogeneity of both the ovarian histology and clinical findings in women with polycystic ovaries was recognized and led to the establishment of the term polycystic ovary syndrome (PCOS) (2, 3). Indeed, patients with the severest cases may have hyperthecosis, a form in which there are no cysts (2, 4, 5), and those with milder ovarian dysfunction tend to have normal ovarian morphology (6). Later, increased concentrations of serum LH or an increase in the ratio of LH to FSH were shown to be characteristic (7) and became common diagnostic criteria in lieu of biopsy evidence of polycystic ovaries. More recently, hyperandrogenemia was shown to be typical (8), and improvements in imaging techniques have made it possible to noninvasively demonstrate polycystic ovaries (9). © 1995 by The Endocrine Society.