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Polycystic Ovary Syndrome

Article information

Kosin Med J. 2015;30(2):109-114
Publication date (electronic) : 2015 January 20
doi : https://doi.org/10.7180/kmj.2015.30.2.109
Yong-Il Ji1,, Min Jeong Kim2
1Department of Obstetrics and Gynecology, College of Medicine, Inje Universtiy, Haeundae Pik Hospital, Busan, Korea
2Department of Neurology, College of Medicine, Kosin Universtiy, Busan, Korea
Corresponding Author: Yong-Il Ji, Department of Obstetrics and Gynecology, Inje University, Haeunade Paik Hospital, 875, Haeun-daero, Haeundae-gu, Busan 48108, Korea Phone: +82-51-797-2020, Fax: +82-51-797-2030, E-mail: jyimdog@paik.ac.kr
Received 2012 February 13; 2012 February 13; Accepted 2012 February 13.

Abstract

Abstract

Polycystic ovary syndrome affects 6%-7% of reproductive-aged women, making it the most common endocrine disorder in this population. It is characterized by chronic anovulation and hyperandrogenism. Affected women may present with reproductive manifestations such as irregular menses or infertility, or cutaneous manifestations, including hirsutism, acne, or male-pattern hair loss. Over the past decade, several serious metabolic complications also have been associated with polycystic ovary syndrome including type 2 diabetes mellitus, metabolic syndrome, sleep apnea, and possibly cardiovascular disease and nonalcoholic fatty liver disease. In addition to treating symptoms by regulating menstrual cycles and improving hyperandrogenism, it is imperative that clinicians recognize and treat metabolic complications. Lifestyle therapies are first-line treatment in women with polycystic ovary syndrome, particularly if they are overweight. Pharmacological therapies are also available and should be tailored on an individual basis. This article reviews the diagnosis, clinical manifestations, metabolic complications, and treatment of the syndrome.

Keywords: Anovulation; Diabetes mellitus; Hirsutism; Insulin resistance; Polycystic ovary syndrome

PCOS definitions 1990–20093

Posssible pathogenesis of polycystic ovary syndrome4

Laboratory testing to evaluate for metabolic complications of polycystic ovary syndrome1

Summary of recommendations for addressing reproductive, cosmetic, metabolic, and psychological complications of polycystic ovary syndrome1

References

1. Setji TL, Brown AJ. Polycystic ovary syndrome: diagnosis and treatment. Am J Med 2007;120:128–32.
2. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and longterm health risks related to polycystic ovary syndrome. Fertil Steril 2004;81:19–25.
3. Roe AH, Dokras A. The diagnosis of polycystic ovary syndrome in adolescents. Rev Obstet Gynecol 2011;4:45–51.
4. American Association of Clinical Endocrinologists Polycystic Ovary Syndrome Writing Committee. American Association of Clinical Endocrinologists Position Statement on Metabolic and Cardiovascular Consequences of Polycystic Ovary Syndrome. Endocr Pract 2005;11:126–34.
5. Badawy A, Elnashar A. Treatment options for polycystic ovary syndrome. Int J Womens Health 2011;3:25–35.
6. Lord JM, Flight IH, Norman RJ. Insulin-sensitising drugs (metformin, troglitazone, rosiglitazone, pioglitazone, D-chiro-inositol) for polycystic ovary syndrome. Cochrane Database Syst Rev 2003. CD003053.
7. Zimmermann S, Phillips RA, Dunaif A, Finegood DT, Wilkenfeld C, Ardeljan M, et al. Polycystic ovary syndrome: lack of hypertension despite profound insulin resistance. J Clin Endocrinol Metab 1992;75:508–13.
8. Azziz R, Carmina E, Dewailly D, Diamanti-Kandarakis E, Escobar-Morreale HF, Futterweit W, et al. The Androgen Excess and PCOS Society criteria for the polycystic ovary syndrome: the complete task force report. Fertil Steril 2009;91:456–88.

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Copyright © 2015 Kosin University School of Medicine Proceedings

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Table 1.

PCOS definitions 1990–20093

PCOS definition Clinical hyperandrogenism (Ferriman-Gallwey score ≥8) or biochemical hyperandrogenism (elevated total/free testosterone) Oligomenorrhea (less than 6–9 menses per year) or oligo-ovulation Polycystic ovaries on ultrasound (≥12 antral follicles in one ovary or ovarian volume ≥10cm3)
NICHD(1990)7 Yes Yes No
Rotterdam (2003)2 Yes Yes Yes
    2 of 3 criteria  
AE-PCOS Society8 Yes Yes Yes
(2009)   1 of 2 criteria  

PCOS, polycystic ovary syndrome; NICHD, Eunice Kennedy Shriver National Institute of Child Health and Human Development; AE-PCOS,

Table 2.

Posssible pathogenesis of polycystic ovary syndrome4

1. Hypothalamic-pituitary axis abnormalities cause abnormal secretion of gonadotropin releasing hormone and luteinizing hormone, resulting in increased ovarian androgen production.
2. An enzymatic defect of ovarian (± adrenal) steroidogenesis favors excess androgen production.
3. Insulin resistance drives the metabolic and reproductive abnormalities in polycystic ovary syndrome.

Table 3.

Laboratory testing to evaluate for metabolic complications of polycystic ovary syndrome1

Laboratory Test Evaluation for: Comment
2-hr oral glucose tolerance Impaired glucose tolerance, Consider this in all women with polycystic ovary
test type 2 diabetes syndrome, particularly those with a body mass
    index >25 kg/m2 or other risk factors for type 2
    diabetes such as a positive family history.
Fasting lipid profile Dyslipidemia Hypertriglyceridemia and decreased high-density
    lipoprotein are relatively common in women with
    polycystic ovary syndrome. Elevations in
    low-density lipoprotein have also been noted.
    Thus, periodic screening is recommended.
Alanine aminotransferase Hepatic steatosis Consider checking transaminases in women with
and aspartate   other risk factors for nonalcoholic fatty liver
aminotransferase   disease.

Table 4.

Summary of recommendations for addressing reproductive, cosmetic, metabolic, and psychological complications of polycystic ovary syndrome1

  Assess diabetes and cardiovascular disease risk
Metabolic Assess risk for nonalcoholic fatty liver disease
  Discuss lifestyle therapies such as nutrition and physical activity
  Assess bleeding pattern and risk for endometrial hyperplasia
Cycle control Provide therapies to prevent endometrial hyperplasia: estrogen-progestin therapy (oral
  contraceptives, patch, or vaginal ring) or cyclic progestin (every 1–3 months)
  Address body image and eating behaviors
Psychosocial Screen for depression Discuss stress management
  Provide nonjudgmental support
  Discuss use of estrogen-containing oral contraceptives to suppress androgens if no
  contraindications
Cosmetic Consider spironolactone 50–100 mg twice daily for refractory hirsutism or acne
  Discuss use of enflornithine hydrochloride 13.9% cream, laser therapy, and electrolysis
  Discuss over-the-counter topical minoxidil for male-pattern scalp hair loss
  Discuss fertility goals
Ovulation Discuss therapies to increase ovulation frequency: weight loss, metformin
  Consider referral to Reproductive Endocrinology for assisted reproductive technologies
Sleep apnea Screen for sleep apnea Refer for sleep study if indicated