Steroid hormone metabolism in polycystic ovary syndrome
- Robert L Barbieri, MD
Robert L Barbieri, MD
- Editor-in-Chief — Obstetrics, Gynecology and Women's Health
- Section Editor — General Gynecology and Female Reproductive Endocrinology
- Kate Macy Ladd Professor of Obstetrics, Gynecology and Reproductive Biology
- Harvard Medical School
- Section Editors
- Peter J Snyder, MD
Peter J Snyder, MD
- Editor-in-Chief — Endocrinology
- Section Editor — Pituitary Disease; Male Reproductive Endocrinology
- Professor of Medicine
- University of Pennsylvania School of Medicine
- William F Crowley, Jr, MD
William F Crowley, Jr, MD
- Section Editor — Female Reproductive Endocrinology
- Daniel K Podolsky Professor of Medicine
- Harvard Medical School
Polycystic ovary syndrome (PCOS) is characterized clinically by menstrual dysfunction, including oligo- or anovulation and signs of hyperandrogenism . This review will describe the abnormalities in steroid hormones that are present in this disorder, including the factors responsible for the increase in androgen production. The clinical manifestations of PCOS are discussed separately. (See "Clinical manifestations of polycystic ovary syndrome in adults".)
As a group, women with PCOS have serum concentrations of testosterone, free testosterone, androstenedione, dehydroepiandrosterone (DHEA), and DHEA sulfate (DHEAS) that are significantly elevated compared with ovulatory, nonhirsute women (figure 1) [1,2]. There is, however, significant individual variation, and some women with PCOS may have normal androgen levels when assayed in a single blood specimen . (See "Diagnosis of polycystic ovary syndrome in adults", section on 'Serum androgens'.)
In women, androgens are produced by the adrenal glands and the ovaries, as well as by conversion of less potent to more potent androgens in the periphery. The source of the major androgens in PCOS is shown in the table (table 1). In PCOS, androstenedione and testosterone are secreted primarily by the ovaries and to a lesser degree the adrenals. This pattern differs from that in normal premenopausal women who have approximately equal androstenedione and testosterone production from the ovaries and the adrenals .
Testosterone — Testosterone is the most potent circulating androgen. Its biologic activity is determined by the amount of binding to sex hormone-binding globulin (SHBG), as only the free fraction is active, and by the rate of conversion of testosterone to the potent intracellular androgen, dihydrotestosterone (DHT) (see 'Dihydrotestosterone' below). Serum SHBG concentrations are controlled by androgens (decrease), estrogens (increase), and insulin (decrease) . Thus, hyperandrogenic women with PCOS tend to have low serum SHBG concentrations. This decrease tends to mask the degree of testosterone excess if only serum total testosterone concentration is measured. Thus, a higher proportion of women with PCOS have elevated serum free testosterone concentrations than have elevated serum total testosterone concentrations.
Body mass index (BMI) is positively correlated with serum total testosterone and inversely correlated with SHBG concentrations in women of all reproductive ages.
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- ANDROGEN METABOLISM
- Dehydroepiandrosterone sulfate
- ESTROGEN METABOLISM
- CONTROL OF ANDROGEN PRODUCTION
- Ovarian androgen secretion
- - Role of insulin
- - Role of anti-müllerian hormone (AMH)
- - Other factors
- Adrenal androgen secretion