Androgen Excess Clinical Presentation

  • Author: Mohamed Yahya Abdel-Rahman, MD, MSc; Chief Editor: Richard Scott Lucidi, MD   more...
 
Updated: Mar 30, 2012
 

History

Detailed history taking from the patient is the cornerstone in patients with hirsutism. Most of the patients with hirsutism will develop excess hair around puberty or a few years thereafter. Onset of mild hirsutism with a slowly progressive course is usually associated with a functional disturbance. On the other hand, rapid progression of hair growth suggests an androgen secreting tumor.[22]

Location and rate of hair growth

Patients with hirsutism are often most concerned with unwanted hair in their face. However, areas covered by clothes may be less of a concern. Hence, it is important to ask about increased hair growth in other areas, including the upper chest, abdomen, inner aspects of the thighs, and the upper and lower back. The frequency and the method used to remove unwanted hair should be elicited because this often gives some idea of the extent of hair growth.

Rapid virilization associated with hirsutism is suggestive of androgen secreting neoplasm or exogenous androgenic drug use. History should include acne, alopecia, clitoromegaly, deepening of voice, masculinization, breast atrophy, and amenorrhea.

Menstrual abnormalities

Hirsutism is almost always a manifestation of other disease (more than 90% of the time). Because PCOS represents 80% of the etiology, it is important to ask about symptoms of this disorder. Oligomenorrhea or amenorrhea with hirsutism is sufficient to diagnose PCOS according to the revised Rotterdam criteria[23] after exclusion of other causes.

Regular menses, however, do not predict normal androgen status in hirsute women. Although 40% of women with hirsute have regular menses, half of them will be found to have elevated levels of one or more androgens.[24] Other cutaneous manifestations of PCOS like acne, oily skin, androgenic alopecia, seborrhea, and obesity may be present with hirsutism.

Family history

An increased prevalence of hirsutism, acne, and male pattern baldness have been found to run in some families.[25] PCOS often presents with familial clustering. However, it is unclear if this is due to genetic pattern alone or due to environmental factors such as diet.[26] Congenital adrenal hyperplasia also presents with familial clustering. The ethnic differences in hair quantity and distribution should be kept in mind.

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Physical

Focused physical examination is essential for the evaluation of women with hirsutism. The clinician should determine whether hirsutism is truly present, as many women who complain of excess hair growth might not actually have hirsutism, especially those with ethnic and genetic predisposition (South European, and Middle East). Excess hair should be established as villus or terminal. Also, hirsutism should be distinguished from hypertrichosis, where hair growth is not mediated by androgens and hairs are not distributed in an androgen sensitive (male) pattern.[27]

Height, weight, body mass index (BMI), and waist-to-hip ratio (WHR) should be determined. Increased BMI and WHR are associated with PCOS, insulin resistance, and increased risk of coronary artery disease.

Hirsutism

Ferriman and Gallwey[28] published a hirsutism rating scale that is illustrated in the table below. This scale allows the physician to measure a response to therapy objectively. This system is the most widely used and evaluates body areas for absent-to-severe hirsutism with scores of 0-4, respectively. Scores of 8 and higher are consistent with a diagnosis of hirsutism. This scale does not measure the thickness of the hair, which is another way of objectively assessing excess hair.

Scoring systems are a useful aid in quantifying hirsutism and in evaluating treatment response. However, they are somewhat subjective, so the absolute score is not used to define hirsutism. Even with scores >8, the patient determines if she is hirsute. When evaluating treatment response, the patient can determine if he or she notices a difference. Photographs are helpful for documentation and for following the progress of therapy.

Table. Ferriman-Gallwey Scoring System (Open Table in a new window)

Body Area EvaluatedScore



(Graded from 0-4*)



Upper lip
Chin
Upper abdomen
Lower abdomen
Upper arm
Thighs
Upper back
Lower back/buttocks
*0 = No hirsutism, 4 = Severe hirsutism

Other signs of androgen excess

Acne and oily skin are both associated with hirsutism. Androgen acts on the PSU to increase sebum production and has an important role in acne development. However, many cases of acne are not associated with hyperandrogenism.

Androgenic alopecia is another distressing condition associated with androgen excess. It is characterized by hair loss from the crown of the scalp sparing the frontal and occipital hairline (male pattern baldness).[29]

Acanthosis nigricans is a mucocutaneous condition where velvety hyperpigmentation patches appear mainly in the skin of the nape of the neck, axilla, antecubital fossae, and groin. Acanthosis nigricans is pathognomonic for insulin resistance.[30] In contrast, acanthosis nigricans is rarely seen with androgen secreting tumors.[31]

Virilization

Virilization suggests an androgen secreting tumors. Features of virilization include temporal male pattern balding, laryngeal hypertrophy, loss of feminine body contour and clitoral hypertrophy.[32] Clitoromegaly is diagnosed when the clitoral length times diameter is >35 mm2.

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Causes

A specific underlying cause can be identified in most patients with androgen excess.[33]

Polycystic ovary syndrome (PCOS)

Approximately 80-90% of women with excess androgens have PCOS.[34, 33] PCOS is the most common endocrinological disorder affecting women in their reproductive years. The prevalence in the United States has been estimated at 5-7%[35] and appears to be rising. Approximately 70% of women with PCOS are found to have mildly elevated free testosterone, and 20-30% have mildly elevated dehydroepiandrosterone sulphate (DHEAS).[36]

Hyperandrogenism, insulin resistance, and acanthosis nigricans (HAIR-AN) syndrome

HAIR-AN syndrome is a subset of women with PCOS who present with hyperandrogenism, insulin resistance, acanthosis nigricans, and obesity in the absence of insulin receptor defect.[37] This syndrome is found in 1-3% of hyperandrogenic women.[38] HAIR-AN syndrome is characterized by high levels of post-glucose challenge insulin levels that may reach 300-500 µU/mL.[39]

Ovarian hyperthecosis

Ovarian hyperthecosis is another condition related to PCOS that most often presents in the perimenopausal period. This condition accounts for less than 1% of women with elevated androgens in their reproductive years, but most of the cases of hyperandrogenemia in postmenopausal women.[40]

Ovarian hyperthecosis is described when luteinized theca cell nests are present in the ovarian stroma. Although there is a considerable overlap between hyperthecosis and PCOS, hyperthecosis is associated with a more severe form of hyperandrogenism and virilization. Testosterone levels are much higher than PCOS and may reach levels greater than 200 ng/dL.[41]

Congenital adrenal hyperplasia

Approximately 2% of women with androgen excess are found to have late-onset, nonclassical, congenital adrenal hyperplasia.[34] Congenital adrenal hyperplasia is a group of autosomal recessive disorders resulting from mutations in the genes coding for steroidogenic enzymes. In these disorders, a block in cortisol biosynthesis leads to loss of negative feedback inhibition, increased ACTH secretion, and subsequent excessive adrenal androgen production.[42]

The most common cause of congenital adrenal hyperplasia is 21-hydroxylase deficiency, which accounts for 90-95% of patients with this condition.[42] The remaining patients with congenital adrenal hyperplasia have either 11 β-hydroxylase deficiency or 3 β-hydroxysteroid deficiency.[43]

Cushing syndrome

Cushing syndrome is a rare but important cause of androgen excess, and hirsutism is present in approximately 81% of these patients.[44] Cushing syndrome (also called hypercorticism) is primarily the result of increasing levels of circulating cortisol or exogenous glucocorticoids. This syndrome can present insidiously with a spectrum of classic symptoms including rapid central weight gain (central obesity and “moon face”), abdominal striae, and signs of hyperandrogenemia including hirsutism, acne, and baldness.

Glucocorticoid therapy is currently the most common cause of Cushing syndrome but is unlikely to be associated with signs of increased androgens. In contrast, endogenous Cushing syndrome is often associated with hirsutism. Cushing syndrome can be secondary to an ACTH secreting pituitary tumor, which is called Cushing disease. Other cases of Cushing syndrome are related to autonomous cortisol secretion by the adrenal glands.[45] Adrenal tumors are associated with rapid onset of Cushing syndrome symptoms, often with hirsutism.[46] Rarely, Cushing syndrome is caused by ACTH secretion by other types of tumors such as small cell lung cancer.

Androgen secreting tumors

Androgen secreting tumors of the ovaries or adrenal glands are rare causes of hyperandrogenism that often mimic PCOS. Women with these tumors tend to have sudden onset of symptoms, rapid progression of hyperandrogenism and early development of frank virilization.

The most common virilizing ovarian tumors are Sertoli Leydig cell tumors and account for 0.5% of all ovarian neoplasms.[41] However, any type of ovarian tumor can present with signs of hyperandrogenism.

Androgen-secreting adrenal neoplasms are less common than ovarian neoplasms.[47] Patients with these tumors usually present with mixed picture of Cushing syndrome and virilization.[48]

Hyperprolactinemia

Elevated prolactin levels are found in as many as 6% of women with hirsutism.[49] The exact relationship between elevated prolactin levels and androgen excess is still unclear. Elevated prolactin levels might directly stimulate the adrenal cortex.[50]

Pregnancy

Testosterone rises throughout the normal pregnancy, reaching values around 600-800 ng/dL by term. The increase in SHBG and the placental aromatization of androgens to estrogens protect the mother and her fetus. Placental aromatase enzyme deficiency can cause hyperandrogenemia in both mother and fetus and result in virilization.

Exogenous androgens

Ingestion of androgens or agents with androgenlike activity can result in hirsutism, acne, and virilization. Various anabolic steroids are used by professional athletes, both men and women, to attain a competitive edge or to assist in recovery from injury. These drugs are also used by a large number of noncompetitive body builders for cosmetic purposes and by women to increase libido.

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Contributor Information and Disclosures
Author

Mohamed Yahya Abdel-Rahman, MD, MSc  Research Fellow, Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University Hospitals, Case Western Reserve University

Mohamed Yahya Abdel-Rahman, MD, MSc is a member of the following medical societies: American Institute of Ultrasound in Medicine and American Society for Reproductive Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

William W Hurd, MD, MSc  Professor of Reproductive Biology, Case Western Reserve University School of Medicine; Lilian Hanna Baldwin Chair in Gynecology and Obstetrics, Director, Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University Hospitals Case Medical Center

William W Hurd, MD, MSc is a member of the following medical societies: Alpha Omega Alpha, American Association of Gynecologic Laparoscopists, American College of Obstetricians and Gynecologists, American College of Physician Executives, American College of Surgeons, American Gynecological and Obstetrical Society, American Medical Association, American Society for Reproductive Medicine, Society for Gynecologic Investigation, and Society of Reproductive Surgeons

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Richard S Legro, MD  Professor, Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology, Pennsylvania State University College of Medicine; Consulting Staff, Milton S Hershey Medical Center

Richard S Legro, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Society for Reproductive Medicine, Endocrine Society, Phi Beta Kappa, and Society of Reproductive Surgeons

Disclosure: Korea National Institute of Health and National Institute of Health (Bethesda, MD) Honoraria Speaking and teaching; Greater Toronto Area Reproductive Medicine Society (Toronto, ON, CA) Honoraria Speaking and teaching; American College of Obstetrics and Gynecologists (Washington, DC) Honoraria Speaking and teaching; National Institute of Child Health and Human Development Pediatric and Adolescent Gynecology Research Think Tank Panel (Bethesda, MD) Honoraria Speaking and teaching; University of Illinois (Chicago, IL) Honoraria Speaking and teaching; Georgetown University Hospital (Washington, DC) Honoraria Speaking and teaching; Heilongjiang University (Harbin, China) Speaking and teaching; New England Fertility Society (Nashua, NJ) Honoraria Speaking and teaching; William Beaumont Hospital Division of Reproductive Endocrinology and Infertility (Detroit, MI) Honoraria Speaking and teaching; Wayne State University School of Medicine (Detroit MI) Honoraria Speaking and teaching

Frederick B Gaupp, MD  Consulting Staff, Department of Family Practice, Hancock Medical Center

Frederick B Gaupp, MD is a member of the following medical societies: American Academy of Family Physicians

Disclosure: Nothing to disclose.

Chief Editor

Richard Scott Lucidi, MD  Associate Professor of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Virginia Commonwealth University School of Medicine

Richard Scott Lucidi, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists and American Society for Reproductive Medicine

Disclosure: Nothing to disclose.

References

  1. Adashi EY. The climacteric ovary as a functional gonadotropin-driven androgen-producing gland. Fertil Steril. Jul 1994;62(1):20-7. [Medline].

  2. Gupta M, Chia SY. Ovarian Hormones: Structure, Biosynthesis, Function, Mechanism of Action, and Laboratory Diagnosis. In: T. Falcone and W. Hurd. Clinical Reproductive Medicine and Surgery. Philadelphia, PA: Mosby Inc.; 2007:22.

  3. Davison SL, Bell R. Androgen physiology. Semin Reprod Med. Apr 2006;24(2):71-7. [Medline]. [Full Text].

  4. Baulieu EE. Neurosteroids: a novel function of the brain. Psychoneuroendocrinology. Nov 1998;23(8):963-87. [Medline].

  5. Sherwin BB, Gelfand MM. Differential symptom response to parenteral estrogen and/or androgen administration in the surgical menopause. Am J Obstet Gynecol. Jan 15 1985;151(2):153-60. [Medline].

  6. Shifren JL, Braunstein GD, Simon JA, Casson PR, Buster JE, Redmond GP, et al. Transdermal testosterone treatment in women with impaired sexual function after oophorectomy. N Engl J Med. Sep 7 2000;343(10):682-8. [Medline].

  7. Appelt H, Strauss B. Effects of antiandrogen treatment on the sexuality of women with hyperandrogenism. Psychother Psychosom. 1984;42(1-4):177-81. [Medline].

  8. Buster JE, Kingsberg SA, Aguirre O, Brown C, Breaux JG, Buch A, et al. Testosterone patch for low sexual desire in surgically menopausal women: a randomized trial. Obstet Gynecol. May 2005;105(5 Pt 1):944-52. [Medline].

  9. Slemenda C, Longcope C, Peacock M, Hui S, Johnston CC. Sex steroids, bone mass, and bone loss. A prospective study of pre-, peri-, and postmenopausal women. J Clin Invest. Jan 1 1996;97(1):14-21. [Medline].

  10. Dimitrakakis C, Zhou J, Wang J, Belanger A, LaBrie F, Cheng C, et al. A physiologic role for testosterone in limiting estrogenic stimulation of the breast. Menopause. Jul-Aug 2003;10(4):292-8. [Medline].

  11. Anderson KE, Sellers TA, Chen PL, Rich SS, Hong CP, Folsom AR. Association of Stein-Leventhal syndrome with the incidence of postmenopausal breast carcinoma in a large prospective study of women in Iowa. Cancer. Feb 1 1997;79(3):494-9. [Medline].

  12. Hofling M, Hirschberg AL, Skoog L, Tani E, Hägerström T, von Schoultz B. Testosterone inhibits estrogen/progestogen-induced breast cell proliferation in postmenopausal women. Menopause. Mar-Apr 2007;14(2):183-90. [Medline].

  13. Bulun SE, Mahendroo MS, Simpson ER. Polymerase chain reaction amplification fails to detect aromatase cytochrome P450 transcripts in normal human endometrium or decidua. J Clin Endocrinol Metab. Jun 1993;76(6):1458-63. [Medline].

  14. Tuckerman EM, Okon MA, Li T, Laird SM. Do androgens have a direct effect on endometrial function? An in vitro study. Fertil Steril. Oct 2000;74(4):771-9. [Medline].

  15. Talbott E, Guzick D, Clerici A, Berga S, Detre K, Weimer K, et al. Coronary heart disease risk factors in women with polycystic ovary syndrome. Arterioscler Thromb Vasc Biol. Jul 1995;15(7):821-6. [Medline].

  16. Ehrmann DA, Schneider DJ, Sobel BE, Cavaghan MK, Imperial J, Rosenfield RL, et al. Troglitazone improves defects in insulin action, insulin secretion, ovarian steroidogenesis, and fibrinolysis in women with polycystic ovary syndrome. J Clin Endocrinol Metab. Jul 1997;82(7):2108-16. [Medline].

  17. Holte J, Gennarelli G, Wide L, Lithell H, Berne C. High prevalence of polycystic ovaries and associated clinical, endocrine, and metabolic features in women with previous gestational diabetes mellitus. J Clin Endocrinol Metab. Apr 1998;83(4):1143-50. [Medline].

  18. Eckardstein A, Wu FC. Testosterone and atherosclerosis. Growth Horm IGF Res. Aug 2003;13 Suppl A:S72-84. [Medline].

  19. Yildiz BO, Bolour S, Woods K, Moore A, Azziz R. Visually scoring hirsutism. Hum Reprod Update. Jan-Feb 2010;16(1):51-64. [Medline].

  20. Lolis MS, Bowe WP, Shalita AR. Acne and systemic disease. Med Clin North Am. Nov 2009;93(6):1161-81. [Medline].

  21. Boyd-Woschinko G, Kushner H, Falkner B. Androgen excess is associated with insulin resistance and the development of diabetes in African American women. J Cardiometab Syndr. Fall 2007;2(4):254-9. [Medline].

  22. Koulouri O, Conway GS. A systematic review of commonly used medical treatments for hirsutism in women. Clin Endocrinol (Oxf). May 2008;68(5):800-5. [Medline].

  23. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS). Hum Reprod. Jan 2004;19(1):41-7. [Medline].

  24. Mehta A, Matwijiw I, Taylor PJ, Salamon EA, Kredentser JV, Faiman C. Should androgen levels be measured in hirsute women with normal menstrual cycles?. Int J Fertil. Nov-Dec 1992;37(6):354-7. [Medline].

  25. Moncada E. Familial study of hirsutism. J Clin Endocrinol Metab. Nov 1970;31(5):556-64. [Medline].

  26. Govind A, Obhrai MS, Clayton RN. Polycystic ovaries are inherited as an autosomal dominant trait: analysis of 29 polycystic ovary syndrome and 10 control families. J Clin Endocrinol Metab. Jan 1999;84(1):38-43. [Medline].

  27. Lowenstein EJ. Diagnosis and management of the dermatologic manifestations of the polycystic ovary syndrome. Dermatol Ther. Jul-Aug 2006;19(4):210-23. [Medline].

  28. Ferriman D, Gallwey JD. Clinical assessment of body hair growth in women. J Clin Endocrinol Metab. Nov 1961;21:1440-7. [Medline].

  29. Cela E, Robertson C, Rush K, Kousta E, White DM, Wilson H, et al. Prevalence of polycystic ovaries in women with androgenic alopecia. Eur J Endocrinol. Nov 2003;149(5):439-42. [Medline].

  30. Kahana M, Grossman E, Feinstein A, Ronnen M, Cohen M, Millet MS. Skin tags: a cutaneous marker for diabetes mellitus. Acta Derm Venereol. 1987;67(2):175-7. [Medline].

  31. Franks S. Polycystic ovary syndrome. N Engl J Med. Sep 28 1995;333(13):853-61. [Medline].

  32. 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. Feb 2009;91(2):456-88. [Medline].

  33. Azziz R, Sanchez LA, Knochenhauer ES, et al. Androgen excess in women: experience with over 1000 consecutive patients. J Clin Endocrinol Metab. Feb 2004;89(2):453-62. [Medline].

  34. Dennedy MC, Smith D, O'Shea D, McKenna TJ. Investigation of patients with atypical or severe hyperandrogenaemia including androgen-secreting ovarian teratoma. Eur J Endocrinol. Feb 2010;162(2):213-20. [Medline].

  35. Carmina E, Lobo RA. Polycystic ovary syndrome (PCOS): arguably the most common endocrinopathy is associated with significant morbidity in women. J Clin Endocrinol Metab. Jun 1999;84(6):1897-9. [Medline].

  36. Landay M, Huang A, Azziz R. Degree of hyperinsulinemia, independent of androgen levels, is an important determinant of the severity of hirsutism in PCOS. Fertil Steril. Aug 2009;92(2):643-7. [Medline].

  37. Flier JS, Eastman RC, Minaker KL, Matteson D, Rowe JW. Acanthosis nigricans in obese women with hyperandrogenism. Characterization of an insulin-resistant state distinct from the type A and B syndromes. Diabetes. Feb 1985;34(2):101-7. [Medline].

  38. Barbieri RL, Ryan KJ. Hyperandrogenism, insulin resistance, and acanthosis nigricans syndrome: a common endocrinopathy with distinct pathophysiologic features. Am J Obstet Gynecol. Sep 1 1983;147(1):90-101. [Medline].

  39. Legro RS. Insulin resistance in polycystic ovary syndrome: treating a phenotype without a genotype. Mol Cell Endocrinol. Oct 25 1998;145(1-2):103-10. [Medline].

  40. Barth JH, Jenkins M, Belchetz PE. Ovarian hyperthecosis, diabetes and hirsuties in post-menopausal women. Clin Endocrinol (Oxf). Feb 1997;46(2):123-8. [Medline].

  41. Lobo RA. Ovarian hyperandrogenism and androgen-producing tumors. Endocrinol Metab Clin North Am. Dec 1991;20(4):773-805. [Medline].

  42. Speiser PW, White PC. Congenital adrenal hyperplasia. N Engl J Med. Aug 21 2003;349(8):776-88. [Medline].

  43. Azziz R, Dewailly D, Owerbach D. Clinical review 56: Nonclassic adrenal hyperplasia: current concepts. J Clin Endocrinol Metab. Apr 1994;78(4):810-5. [Medline].

  44. Howlett TA, Rees LH, Besser GM. Cushing's syndrome. Clin Endocrinol Metab. Nov 1985;14(4):911-45. [Medline].

  45. Reyss AC, Dewailly D. Cushing's Syndrome, Acromegaly, and Androgen Excess. In: Azziz R, Dewailly D. Contemporary Endocrinology: Androgen Excess Disorders in Women:Polycystic Ovary Syndrome and Other Disorders. 2nd. Totowa, NJ: Humana Press Incorp; 2006:87-7.

  46. Orth DN. Cushing's syndrome. N Engl J Med. Mar 23 1995;332(12):791-803. [Medline].

  47. Derksen J, Nagesser SK, Meinders AE, Haak HR, van de Velde CJ. Identification of virilizing adrenal tumors in hirsute women. N Engl J Med. Oct 13 1994;331(15):968-73. [Medline].

  48. Latronico AC, Chrousos GP. Extensive personal experience: adrenocortical tumors. J Clin Endocrinol Metab. May 1997;82(5):1317-24. [Medline].

  49. Wu CH. Plasma androgens, progestins, and prolactin in hirsutism. Eur J Obstet Gynecol Reprod Biol. Sep 1982;13(6):377-87. [Medline].

  50. Hagag P, Hertzianu I, Ben-Shlomo A, Weiss M. Androgen suppression and clinical improvement with dopamine agonists in hyperandrogenic-hyperprolactinemic women. J Reprod Med. Jul 2001;46(7):678-84. [Medline].

  51. Martin KA, Chang RJ, Ehrmann DA, Ibanez L, Lobo RA, Rosenfield RL, et al. Evaluation and treatment of hirsutism in premenopausal women: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. Apr 2008;93(4):1105-20. [Medline].

  52. The evaluation and treatment of androgen excess. Fertil Steril. Nov 2006;86(5 Suppl 1):S241-7. [Medline].

  53. Somani N, Harrison S, Bergfeld WF. The clinical evaluation of hirsutism. Dermatol Ther. Sep-Oct 2008;21(5):376-91. [Medline].

  54. Escobar-Morreale HF, Carmina E, Dewailly D, et al. Epidemiology, diagnosis and management of hirsutism: a consensus statement by the Androgen Excess and Polycystic Ovary Syndrome Society. Hum Reprod Update. Mar 2012;18(2):146-70. [Medline].

  55. [Guideline] ACOG technical bulletin. Evaluation and treatment of hirsute. Int J Gynaecol Obstet. 1995;49:341-6. [Medline].

  56. Hoffman DI, Klove K, Lobo RA. The prevalence and significance of elevated dehydroepiandrosterone sulfate levels in anovulatory women. Fertil Steril. Jul 1984;42(1):76-81. [Medline].

  57. Hunter MH, Carek PJ. Evaluation and treatment of women with hirsutism. Am Fam Physician. Jun 15 2003;67(12):2565-72. [Medline].

  58. Azziz R, Hincapie LA, Knochenhauer ES, Dewailly D, Fox L, Boots LR. Screening for 21-hydroxylase-deficient nonclassic adrenal hyperplasia among hyperandrogenic women: a prospective study. Fertil Steril. Nov 1999;72(5):915-25. [Medline].

  59. Benacerraf BR, Finkler NJ, Wojciechowski C, Knapp RC. Sonographic accuracy in the diagnosis of ovarian masses. J Reprod Med. May 1990;35(5):491-5. [Medline].

  60. Blake MA, Holalkere NS, Boland GW. Imaging techniques for adrenal lesion characterization. Radiol Clin North Am. Jan 2008;46(1):65-78, vi. [Medline].

  61. American Association of Clinical Endocrinologists Position Statement on Metabolic and Cardiovascular Consequences of Polycystic Ovary Syndrome. Endocr Pract. Mar-Apr 2005;11(2):126-34. [Medline].

  62. Salley KE, Wickham EP, Cheang KI, Essah PA, Karjane NW, Nestler JE. Glucose intolerance in polycystic ovary syndrome--a position statement of the Androgen Excess Society. J Clin Endocrinol Metab. Dec 2007;92(12):4546-56. [Medline].

  63. International Expert Committee report on the role of the A1C assay in the diagnosis of diabetes. Diabetes Care. Jul 2009;32(7):1327-34. [Medline].

  64. Waldstreicher J, Santoro NF, Hall JE, Filicori M, Crowley WF Jr. Hyperfunction of the hypothalamic-pituitary axis in women with polycystic ovarian disease: indirect evidence for partial gonadotroph desensitization. J Clin Endocrinol Metab. Jan 1988;66(1):165-72. [Medline].

  65. Ibáñez L, Potau N, Zampolli M, Prat N, Gussinyé M, Saenger P, et al. Source localization of androgen excess in adolescent girls. J Clin Endocrinol Metab. Dec 1994;79(6):1778-84. [Medline].

  66. Arowojolu AO, Gallo MF, Lopez LM, Grimes DA, Garner SE. Combined oral contraceptive pills for treatment of acne. Cochrane Database Syst Rev. Jul 8 2009;CD004425. [Medline].

  67. Hundal RS, Krssak M, Dufour S, Laurent D, Lebon V, Chandramouli V, et al. Mechanism by which metformin reduces glucose production in type 2 diabetes. Diabetes. Dec 2000;49(12):2063-9. [Medline].

  68. Florez H, Luo J, Castillo-Florez S, Mitsi G, Hanna J, Tamariz L. Impact of metformin-induced gastrointestinal symptoms on quality of life and adherence in patients with type 2 diabetes. Postgrad Med. Mar 2010;122(2):112-20. [Medline].

  69. Tan S, Hahn S, Benson S, Dietz T, Lahner H, Moeller LC. Metformin improves polycystic ovary syndrome symptoms irrespective of pre-treatment insulin resistance. Eur J Endocrinol. Nov 2007;157(5):669-76. [Medline].

  70. Palomba S, Pasquali R, Orio F Jr, Nestler JE. Clomiphene citrate, metformin or both as first-step approach in treating anovulatory infertility in patients with polycystic ovary syndrome (PCOS): a systematic review of head-to-head randomized controlled studies and meta-analysis. Clin Endocrinol (Oxf). Feb 2009;70(2):311-21. [Medline].

  71. Brown J, Farquhar C, Lee O, Toomath R, Jepson RG. Spironolactone versus placebo or in combination with steroids for hirsutism and/or acne. Cochrane Database Syst Rev. Apr 15 2009;CD000194. [Medline].

  72. Hickman JG, Huber F, Palmisano M. Human dermal safety studies with eflornithine HCl 13.9% cream (Vaniqa), a novel treatment for excessive facial hair. Curr Med Res Opin. 2001;16(4):235-44. [Medline].

  73. Abroms L, Maibach E, Lyon-Daniel K, Feldman SR. What is the best approach to reducing birth defects associated with isotretinoin?. PLoS Med. Nov 2006;3(11):e483. [Medline].

  74. Consensus on infertility treatment related to polycystic ovary syndrome. Hum Reprod. Mar 2008;23(3):462-77. [Medline].

  75. Shenenberger DW, Utecht LM. Removal of unwanted facial hair. Am Fam Physician. Nov 15 2002;66(10):1907-11. [Medline].

  76. Pasquali R, Antenucci D, Casimirri F, Venturoli S, Paradisi R, Fabbri R, et al. Clinical and hormonal characteristics of obese amenorrheic hyperandrogenic women before and after weight loss. J Clin Endocrinol Metab. Jan 1989;68(1):173-9. [Medline].

  77. Pate RR, Pratt M, Blair SN, Haskell WL, Macera CA, Bouchard C, et al. Physical activity and public health. A recommendation from the Centers for Disease Control and Prevention and the American College of Sports Medicine. JAMA. Feb 1 1995;273(5):402-7. [Medline].

  78. Clark AM, Thornley B, Tomlinson L, Galletley C, Norman RJ. Weight loss in obese infertile women results in improvement in reproductive outcome for all forms of fertility treatment. Hum Reprod. Jun 1998;13(6):1502-5. [Medline].

  79. Cumming DC, Yang JC, Rebar RW, Yen SS. Treatment of hirsutism with spironolactone. JAMA. Mar 5 1982;247(9):1295-8. [Medline].

  80. Board JA, Rosenberg SM, Smeltzer JS. Spironolactone and estrogen-progestin therapy for hirsutism. South Med J. Apr 1987;80(4):483-6. [Medline].

  81. Cusan L, Dupont A, Gomez JL, Tremblay RR, Labrie F. Comparison of flutamide and spironolactone in the treatment of hirsutism: a randomized controlled trial. Fertil Steril. Feb 1994;61(2):281-7. [Medline].

  82. Van der Spuy ZM, le Roux PA. Cyproterone acetate for hirsutism. Cochrane Database Syst Rev. 2003;CD001125. [Medline].

  83. Wysowski DK, Freiman JP, Tourtelot JB, Horton ML 3rd. Fatal and nonfatal hepatotoxicity associated with flutamide. Ann Intern Med. Jun 1 1993;118(11):860-4. [Medline].

  84. Wong IL, Morris RS, Chang L, Spahn MA, Stanczyk FZ, Lobo RA. A prospective randomized trial comparing finasteride to spironolactone in the treatment of hirsute women. J Clin Endocrinol Metab. Jan 1995;80(1):233-8. [Medline].

  85. Erenus M, Yücelten D, Durmusoglu F, Gürbüz O. Comparison of finasteride versus spironolactone in the treatment of idiopathic hirsutism. Fertil Steril. Dec 1997;68(6):1000-3. [Medline].

  86. Erickson GF, Magoffin DA, Dyer CA, Hofeditz C. The ovarian androgen producing cells: a review of structure/function relationships. Endocr Rev. Summer 1985;6(3):371-99. [Medline].

  87. Nestler JE, Powers LP, Matt DW, Steingold KA, Plymate SR, Rittmaster RS, et al. A direct effect of hyperinsulinemia on serum sex hormone-binding globulin levels in obese women with the polycystic ovary syndrome. J Clin Endocrinol Metab. Jan 1991;72(1):83-9. [Medline].

  88. Ehrmann DA, Cavaghan MK, Imperial J, Sturis J, Rosenfield RL, Polonsky KS. Effects of metformin on insulin secretion, insulin action, and ovarian steroidogenesis in women with polycystic ovary syndrome. J Clin Endocrinol Metab. Feb 1997;82(2):524-30. [Medline].

  89. Ibáñez L, Valls C, Potau N, Marcos MV, de Zegher F. Sensitization to insulin in adolescent girls to normalize hirsutism, hyperandrogenism, oligomenorrhea, dyslipidemia, and hyperinsulinism after precocious pubarche. J Clin Endocrinol Metab. Oct 2000;85(10):3526-30. [Medline].

  90. Pasquali R, Gambineri A, Biscotti D, Vicennati V, Gagliardi L, Colitta D, et al. Effect of long-term treatment with metformin added to hypocaloric diet on body composition, fat distribution, and androgen and insulin levels in abdominally obese women with and without the polycystic ovary syndrome. J Clin Endocrinol Metab. Aug 2000;85(8):2767-74. [Medline].

  91. Sturrock ND, Lannon B, Fay TN. Metformin does not enhance ovulation induction in clomiphene resistant polycystic ovary syndrome in clinical practice. Br J Clin Pharmacol. May 2002;53(5):469-73. [Medline].

  92. Costello M, Shrestha B, Eden J, Sjoblom P, Johnson N. Insulin-sensitising drugs versus the combined oral contraceptive pill for hirsutism, acne and risk of diabetes, cardiovascular disease, and endometrial cancer in polycystic ovary syndrome. Cochrane Database Syst Rev. Jan 24 2007;CD005552. [Medline].

  93. Cosma M, Swiglo BA, Flynn DN, Kurtz DM, Labella ML, Mullan RJ, et al. Clinical review: Insulin sensitizers for the treatment of hirsutism: a systematic review and metaanalyses of randomized controlled trials. J Clin Endocrinol Metab. Apr 2008;93(4):1135-42. [Medline].

 
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Androgen secretion pathway in adrenal glands and ovaries.
Chemical structures of spironolactone and drospirenone. The testosterone core is in black.
Table. Ferriman-Gallwey Scoring System
Body Area EvaluatedScore



(Graded from 0-4*)



Upper lip
Chin
Upper abdomen
Lower abdomen
Upper arm
Thighs
Upper back
Lower back/buttocks
*0 = No hirsutism, 4 = Severe hirsutism
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