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CME

Androgens and Polycystic Ovary Syndrome

  • Authors: Macarena Alpañés, MD; Elena Fernández-Durán, BS; Héctor F. Escobar-Morreale, MD, PhD
  • CME Released: 12/6/2011
  • THIS ACTIVITY HAS EXPIRED
  • Valid for credit through: 12/6/2012
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Target Audience and Goal Statement

This activity is intended for primary care physicians, endocrinologists, obstetrician gynecologists, and other physicians who care for women who may have PCOS.

The goal of this activity is to evaluate the role of androgens in the pathogenesis of PCOS.

Upon completion of this activity, participants will be able to:

  1. Evaluate evidence for hyperandrogenism beginning early in life among women with PCOS
  2. Distinguish diagnostic criteria for PCOS
  3. Analyze the effects of treatment for PCOS on serum androgen levels and clinical manifestations of PCOS
  4. Assess changes in serum androgen levels associated with menopause


Disclosures

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Medscape, LLC, encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content.


Author(s)

  • Macarena Alpañés, MD

    Diabetes, Obesity and Human Reproduction Research Group, Hospital Universitario Ramón y Cajal & Universidad de Alcalá & Instituto Ramón y Cajal de Investigación Sanitaria IRYCIS & CIBER Diabetes y Enfermedades Metabólicas Asociadas CIBERDEM, Madrid, Spain

    Disclosures

    Disclosure: Macarena Alpañés, MD, is supported by grants PI080944 and PI110357 from the Fondo de Investigación Sanitaria, Instituto de Salud Carlos III, Spanish Ministry of Health and Innovation. CIBER Diabetes y Enfermedades Metabólicas Asociadas is also an inititative of Instituto de Salud Carlos III.

  • Elena Fernández-Durán, BS

    Diabetes, Obesity and Human Reproduction Research Group, Hospital Universitario Ramón y Cajal & Universidad de Alcalá & Instituto Ramón y Cajal de Investigación Sanitaria IRYCIS & CIBER Diabetes y Enfermedades Metabólicas Asociadas CIBERDEM, Madrid, Spain

    Disclosures

    Disclosure: Elena Fernández-Durán, BS, is supported by grants PI080944 and PI110357 from the Fondo de Investigación Sanitaria, Instituto de Salud Carlos III, Spanish Ministry of Health and Innovation. CIBER Diabetes y Enfermedades Metabólicas Asociadas is also an inititative of Instituto de Salud Carlos III.

  • Héctor F. Escobar-Morreale, MD, PhD

    Diabetes, Obesity and Human Reproduction Research Group, Hospital Universitario Ramón y Cajal & Universidad de Alcalá & Instituto Ramón y Cajal de Investigación Sanitaria IRYCIS & CIBER Diabetes y Enfermedades Metabólicas Asociadas CIBERDEM, Madrid, Spain

    Disclosures

    Disclosure: Héctor F. Escobar-Morreale, MD, PhD, is supported by grants PI080944 and PI110357 from the Fondo de Investigación Sanitaria, Instituto de Salud Carlos III, Spanish Ministry of Health and Innovation. CIBER Diabetes y Enfermedades Metabólicas Asociadas is also an inititative of Instituto de Salud Carlos III.

Editor(s)

  • Elisa Manzotti

    Editorial Director, Future Science Group, London, United Kingdom

    Disclosures

    Disclosure: Elisa Manzotti has disclosed no relevant financial relationships.

CME Author(s)

  • Charles P. Vega, MD

    Health Sciences Clinical Professor; Residency Director, Department of Family Medicine, University of California, Irvine

    Disclosures

    Disclosure: Charles P. Vega, MD, has disclosed no relevant financial relationships.

CME Reviewer(s)

  • Nafeez Zawahir, MD

    CME Clinical Director, Medscape, LLC

    Disclosures

    Disclosure: Nafeez Zawahir, MD, has disclosed no relevant financial relationships.

  • Sarah Fleischman

    CME Program Manager, Medscape, LLC

    Disclosures

    Disclosure: Sarah Fleischman has disclosed no relevant financial relationships.


Accreditation Statements

    For Physicians

  • This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education through the joint sponsorship of Medscape, LLC and Expert Reviews Ltd. Medscape, LLC is accredited by the ACCME to provide continuing medical education for physicians.

    Medscape, LLC designates this Journal-based CME activity for a maximum of 1.00 AMA PRA Category 1 Credit(s)™ . Physicians should claim only the credit commensurate with the extent of their participation in the activity.

    Medscape, LLC staff have disclosed that they have no relevant financial relationships.

    Contact This Provider

For questions regarding the content of this activity, contact the accredited provider for this CME/CE activity noted above. For technical assistance, contact [email protected]


Instructions for Participation and Credit

There are no fees for participating in or receiving credit for this online educational activity. For information on applicability and acceptance of continuing education credit for this activity, please consult your professional licensing board.

This activity is designed to be completed within the time designated on the title page; physicians should claim only those credits that reflect the time actually spent in the activity. To successfully earn credit, participants must complete the activity online during the valid credit period that is noted on the title page. To receive AMA PRA Category 1 Credit™, you must receive a minimum score of 70% on the post-test.

Follow these steps to earn CME/CE credit*:

  1. Read the target audience, learning objectives, and author disclosures.
  2. Study the educational content online or printed out.
  3. Online, choose the best answer to each test question. To receive a certificate, you must receive a passing score as designated at the top of the test. Medscape Education encourages you to complete the Activity Evaluation to provide feedback for future programming.

You may now view or print the certificate from your CME/CE Tracker. You may print the certificate but you cannot alter it. Credits will be tallied in your CME/CE Tracker and archived for 6 years; at any point within this time period you can print out the tally as well as the certificates by accessing "Edit Your Profile" at the top of your Medscape homepage.

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CME

Androgens and Polycystic Ovary Syndrome

Authors: Macarena Alpañés, MD; Elena Fernández-Durán, BS; Héctor F. Escobar-Morreale, MD, PhDFaculty and Disclosures
THIS ACTIVITY HAS EXPIRED

CME Released: 12/6/2011

Valid for credit through: 12/6/2012

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Abstract and Introduction

Abstract

Polycystic ovary syndrome (PCOS) is a mainly hyperandrogenic disorder and is possibly the most frequent endocrinopathy in premenopausal women. Androgen excess is the primary defect in PCOS, because ovarian theca cells secrete increased amounts of androgens even after several passes in primary culture. Excessive androgen amounts might favor the visceral deposition of body fat in affected women, resulting in insulin resistance, compensatory hyperinsulinism and further androgen excess. This vicious circle starts early during life in women with PCOS, even during fetal development, manifests clinically during puberty and does not end after menopause. All the steps in the vicious circle contribute to the association of PCOS with metabolic dysfunction and cardiovascular risk factors. Fortunately, most, if not all, of the therapeutic strategies currently in use for the management of PCOS, including lifestyle modification and diet, oral contraceptives, antiandrogens and insulin sensitizers, may ameliorate androgen excess and its long-term consequences.

Introduction

Polycystic ovary syndrome (PCOS) is possibly the most prevalent endocrinopathy in premenopausal women,[1] affecting approximately 6–8% of this population.[2–4] The complete PCOS phenotype is characterized by clinical and/or biochemical hyperandrogenism, ovulatory dysfunction and polycystic morphology of the ovaries,[5] and is frequently associated with insulin resistance and obesity.[6]

Current understanding of the etiology of PCOS is incomplete, yet the association of PCOS with several predisposing and protective genetic variants suggests a complex multigenic inheritance upon which several environmental factors exert a major influence.[7]

Although androgen excess is the central pathophysiologic characteristic of PCOS,[5,8] the frequent association of PCOS with insulin resistance, leading to compensatory hyperinsulinism, may further contribute to androgen excess because insulin facilitates androgen synthesis at the adrenals and at the ovaries.[9] In fact, reputed authors consider PCOS as another manifestation of the metabolic syndrome in women, and suggest that insulin resistance is the key mechanism leading to androgen excess in these women.[10]

On the contrary, our present hypothesis[6] is that androgen excess facilitates a predominantly visceral deposition of fat in women with PCOS, and visceral fat dysfunction further facilitates androgen secretion by the adrenals and the ovaries – directly through the endocrine effects of several adipokines, and indirectly through insulin resistance and compensatory hyperinsulinism – closing a vicious circle that may start as early as fetal life in affected women (Figure 1).

Figure 1.

Enlarge

Unifying Hypothesis Explaining the Interplay Between the Polycystic Ovary Syndrome and Abdominal Adiposity. This interplay is the result of a vicious circle represented by the solid arrows: androgen excess favors the abdominal deposition of body fat, and visceral fat facilitates androgen excess of ovarian and/or adrenal origin by the direct effects (dashed arrow) of several autocrine, paracrine and endocrine mediators, or indirectly by the induction of insulin resistance and hyperinsulinism.
Reproduced from[6], with permission. © Elsevier (2007).

In the present article, we will review the role of androgen excess throughout the life cycle of women with PCOS, highlighting the metabolic and cardiovascular consequences of hyperandrogenism and the importance of androgen excess as a target for successful long-term management of these patients.