Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Androgen Excess

  • Author: Mohamed Yahya Abdel-Rahman, MD, MSc; Chief Editor: Richard Scott Lucidi, MD, FACOG  more...
 
Updated: Jul 27, 2015
 

Background

Androgen excess is the most common endocrine disorder in women of reproductive age. Androgens are produced primarily from the adrenal glands and the ovaries. However, peripheral tissues such as fat and skin also play roles in converting weak androgens to more potent ones. Androgen excess can affect different tissues and organs, causing variable clinical features such as acne, hirsutism, virilization and reproductive dysfunction.

Sources and types of androgens in women

The endocrine glands secrete 5 androgens through a similar pathway: testosterone, dehydroepiandrosterone sulfate (DHEAS), dehydroepiandrosterone (DHEA), androstenedione, and androstenediol, the latter of which has both androgenic and estrogenic activity. Testosterone and its biologically active metabolite dihydrotestosterone (DHT) are the only androgens with direct androgenic activity. DHEAS, DHEA, and androstenedione are all precursors of testosterone.

Androgen secretion pathway in adrenal glands and o Androgen secretion pathway in adrenal glands and ovaries.

Ovarian androgens

The ovaries produce 25% of circulating testosterone, which is dependent on luteinizing hormone (LH) secreted by the anterior pituitary. The ovaries also secrete 50% of the androstenedione and 20% of DHEA. Testosterone is used as a marker of ovarian androgen secretion. However, the adrenals also contribute to circulating testosterone via peripheral conversion of androstenedione to testosterone.

Adrenal androgens

The adrenal glands produce all the DHEAS and 80% of the DHEA. The adrenals also secrete 50% of androstenedione and 25% of circulating testosterone. DHEAS and 11-androstenedione are not secreted by the ovaries and, therefore, are used as markers of adrenal androgen secretion. Adrenal androgen secretion is dependent on adrenocorticotropic hormone (ACTH) secreted by the anterior pituitary. Both prolactin and estrogen can affect adrenal androgen production.

Peripheral conversion

Skin, fat, liver, and urogenital systems are important peripheral sites of androgen production. Androstenedione, and to some degree DHEA, are converted to testosterone in the skin.

Androgen metabolism

Of the circulating androgens, only testosterone and DHT are able to activate androgen receptors. In reproductive-aged women, 25% of the circulating testosterone comes from the adrenals; the ovaries contribute with another 25%. The rest of the testosterone is produced by the peripheral conversion of androstenedione in adipose tissue.[1] In healthy women, 80% of testosterone is bound to sex hormone binding globulin (SHBG), 19% is bound to albumin, and 1% circulates freely in the blood stream. The androgenicity depends mainly on the unbound fraction due to the high affinity of SHBG to the bound androgens. The levels of SHBG increase and decrease based on conditions and medications.

  • SHGB levels are increased by the following:
    • Estrogens
    • Thyroid hormone
    • Pregnancy
    • Estrogen-containing preparations
  • SHGB levels are decreased by the following:
    • Androgens
    • Synthetic progestins (norethindrone, norgestrel, desogestrel, norgestimate)
    • Glucocorticoids
    • Growth hormone
    • Insulin
    • Obesity
    • Acromegaly
    • Hypothyroidism
    • Hyperinsulinemia

The remaining androgens, DHEAS, DHEA, and androstenedione are almost entirely bound to albumin. Unlike SHBG; albumin has a low affinity for sex hormones, so the albumin-bound androgens are readily available to tissues.

Adrenal androgens increase in response to ACTH stimulation, while androgens do not influence the ACTH secretion. Also, LH stimulates theca cells of the ovaries to secrete androgens; however, there is no feedback regulatory loop that controls androgen secretion in women.

Most of the circulating testosterone is metabolized in the liver into androsterone and etiocholanolone, which are conjugated with glucuronic acid or sulfuric acid and execrated in the urine as 17-ketosteroids. Only 20-30% of urinary 17-ketosteroids are derived from testosterone metabolism; the rest originates from the metabolism of adrenal steroids.[2]

Androgen effects

Androgens induce virilization and are responsible for forming the male external genitalia in the fetus. Their absence or the absence of androgen receptors results in a female phenotype, despite the presence of a 46 XY karyotype (eg, androgen insensitivity syndrome). Androgens are also responsible for the development of the secondary sexual organs and ducts, the seminal vesicles, and the prostate.

Postnatal females are not as sensitive as the fetus to androgens, which induce the growth of sexual hair, temporal balding, acne, clitoral growth, sebum production, and a deepening of the voice.

Oral androgens decrease high-density lipoprotein (HDL) cholesterol and increase low-density lipoprotein (LDL) cholesterol. With androgen excess, the extent of these changes is dependent on the level of androgens in the blood.

Androgen effects on various tissues and systems

Androgens have direct effects on different body systems and also act as precursor hormones for ovarian and extragonadal estrogen synthesis. Androgen receptors are present in a variety of tissues like skeletal muscles, skin, gastrointestinal tract, genitourinary tract, bone, brain, cardiovascular system, placenta, and adipose tissues. Androgen actions are not completely understood in all of these tissues.[3]

Brain

Androgen receptors are distributed throughout the brain in close proximity to estrogen receptors. The highest concentrations are present in the preoptic area of the hypothalamus. Some areas contain 5α-reductase and aromatase and are able to convert testosterone to DHT or estradiol.[4] Androgen can have activational behavior on women and may have some negative effects on the cognitive functions of older women.[5]

Growing evidence supports the role of androgens in physiologic levels and sexual desire. Decreased sexual function has been reported in hyperandrogenic women receiving antiandrogens; on the other hand, administration of testosterone in women with hypoactive sexual desire disorder results in improvements in libido and sexual function.[6, 7]

Bone

Androgens have important roles in bone mineralization either directly or through aromatization to estrogen. Lower androgen concentrations have been associated with bone loss in various age groups.[8]

Breast

Androgen receptors are present in mammary epithelial cells in addition to estrogen and progesterone receptors. The proposed mechanisms include either direct stimulation of the androgen receptors or conversion to estradiol by the aromatase enzyme present in breast tissue. Androgens, particularly DHEA and testosterone, have been reported to protect against mammary epithelial proliferation in female monkeys. The reverse effect was reported when the antiandrogen flutamide was given to those animals.[9]

Few data are available regarding the effects of androgens on human breasts. Hyperandrogenemia in women with polycystic ovary syndrome (PCOS)[link] doesn’t appear to have significant risk of breast cancer.[10] In a prospective randomized controlled study in postmenopausal women evaluating breast cell proliferation and testosterone, the authors found no significant difference when testosterone was added to estrogen and progesterone, while they found a 5-fold increase in breast cell proliferation in women taking the placebo.[11]

Endometrium

Unopposed estrogen stimulation of the endometrium increases the risk of endometrial hyperplasia and eventually cancer. The proposed mechanism of androgen aromatization to estradiol may not be applicable because the aromatase expression has not been detected in normal endometrium and stromal cells.[12] In vitro studies have shown that androgens have an inhibitory effect on endometrial proliferation.[13]

Cardiovascular system

There is a great concern about the relation between sex hormones and cardiovascular events. Women with PCOS have hyperandrogenemia and are at higher risk of cardiovascular events.[14, 15, 16] However, the insulin resistance associated with PCOS is likely more relevant to the pathogenesis of cardiovascular disease. Moreover, the exogenous administration of testosterone for female to male transsexual has not been associated with the increased risk of cardiovascular disease.[17]

Mechanism of androgen action

In the target tissues, androgens enter the cell cytoplasm by simple diffusion across the cell membrane. Once inside the cell, the androgens bind and activate the androgen receptors. The androgen-receptor complex attaches to a specific DNA site and stimulates the production of messenger RNA, which, in turn, stimulates the production of the enzymes and proteins necessary to affect androgen action.

Next

Pathophysiology

Androgen excess affects mainly the pilosebaceous unit (PSU) and the reproductive system. The PSU secretes sebum and is the unit from which hair grows. Three types of hair, lanugo, vellus, and terminal hairs, exist. The fine hairs of the fetus are lanugo and the peach fuzz hair of adults is vellus hair. These hairs are fine, short, and nonpigmented. Thick and pigmented hair is referred to as terminal hair. Those hairs of the pubic, axillary, sternal, and facial areas are responsive to androgens and those in scalp, eyelashes, and eyebrows are androgen-independent. Their prevalence depends largely on genetics. As androgen levels rise, more vellus hairs in the androgen-sensitive areas are converted into terminal hairs, resulting in hirsutism.

Androgens prolong the growth phase of hair and promote their conversion from vellus to terminal type. Hirsutism affects 70-80% of women with androgen excess. Sebum production from the PSU is also increased by androgens.[18]

 Acne vulgaris can be aggravated or initiated by increased androgen levels as the excess sebum production and the shedding of hyperkeratinized epithelium may occlude the hair follicle. Propionibacterium acnes proliferate and triglycerides of sebum are then hydrolyzed by the bacterial lipases to form glycerol and free fatty acids, which, together with other bacterial metabolites, cause inflammation. It is also commonly proposed that hypersensitivity of PSU to androgens is the cause of acne.[19] Sebum production increases markedly during the prepubertal period, a time when serum levels of DHEAS, a precursor to testosterone, are also elevated. Individuals who are insensitive to androgen  have less active sebaceous glands and do not develop acne.

Androgen excess is a common feature of PCOS, which is also the most common cause of anovulatory infertility. The ovarian theca cells increase their ovarian androgen production under the stimulatory activity of the raised LH levels, and in many cases, raised insulin levels.

Hyperinsulinemia due to peripheral insulin resistance is often present in women with PCOS and it promotes hyperandrogenemia through the binding of insulin to the insulin-like growth factor–1 (IGF-1) receptor. Insulin mimics the action of insulin growth factor 1 (IGF-1), which augments androgen production by the theca cell in response to LH. Since insulin decreases levels of SHBG, the circulating levels of free testosterone are also increased.

Previous
Next

Epidemiology

Frequency

United States

The prevalence of androgen excess is 8%.

International

The international incidence rate is dependent on the particular culture, but, essentially, it is similar to that of the United States.

Mortality/Morbidity

Androgen excess per se does not cause mortality or morbidity, but it is associated with insulin resistance, dyslipidemia, hypertension, and vascular diseases; therefore, it is a forerunner of cardiovascular disease.

  • In premenopausal African-American women, relative androgen excess is associated with insulin resistance and increased risk for development of type 2 diabetes. [20]
  • Impaired glucose tolerance and type 2 diabetes affect about 40% of women with PCOS.
  • The presence of PCOS is an independent cardiovascular risk factor. Women who have anovulatory PCOS have greater cardiovascular risk compared with women who have ovulatory PCOS and idiopathic hyperandrogenism.
  • Androgen-secreting tumors are rare and about 30% of them are malignant.

Race

Androgen excess occurs equally in all races. Congenital adrenal hyperplasia prevalence due to 21-hydroxylase deficiency is greater among those of Ashkenazi Jewish descent.

Sex

Congenital adrenal hyperplasia occurs equally in both sexes; however, this article focuses on females.

Age

The most common causes of hyperandrogenism begin in early adolescence or in childbearing age. Androgen-producing tumors may rarely affect postmenopausal women.

Previous
 
 
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 School of Medicine; Assistant Lecturer, Sohag University School of Medicine, Egypt

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

Disclosure: Nothing to disclose.

Coauthor(s)

William W Hurd, MD, MSc, MPH Professor and Director, Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Duke University Medical Center

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

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: Received salary from Medscape for employment. for: Medscape.

Steven R Feldman, MD, PhD Professor, Departments of Dermatology, Pathology and Public Health Sciences, and Molecular Medicine and Translational Science, Wake Forest Baptist Health; Director, Center for Dermatology Research, Director of Industry Relations, Department of Dermatology, Wake Forest University School of Medicine

Steven R Feldman, MD, PhD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, North Carolina Medical Society, Society for Investigative Dermatology

Disclosure: Received honoraria from Amgen for consulting; Received honoraria from Abbvie for consulting; Received honoraria from Galderma for speaking and teaching; Received consulting fee from Lilly for consulting; Received ownership interest from www.DrScore.com for management position; Received ownership interest from Causa Reseasrch for management position; Received grant/research funds from Janssen for consulting; Received honoraria from Pfizer for speaking and teaching; Received consulting fee from No.

Chief Editor

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

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

Disclosure: Nothing to disclose.

Additional Contributors

Arash Taheri, MD Research Fellow, Center for Dermatology Research, Department of Dermatology, Wake Forest University School of Medicine

Disclosure: Nothing to disclose.

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

  2. Gupta M, Chia SY. Ovarian Hormones: Structure, Biosynthesis, Function, Mechanism of Action, and Laboratory Diagnosis. 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. 2006 Apr. 24(2):71-7. [Medline]. [Full Text].

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

  5. Hogervorst E, Matthews FE, Brayne C. Are optimal levels of testosterone associated with better cognitive function in healthy older women and men?. Biochim Biophys Acta. 2010 Oct. 1800(10):1145-52. [Medline].

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

  7. 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. 2005 May. 105(5 Pt 1):944-52. [Medline].

  8. 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. 1996 Jan 1. 97(1):14-21. [Medline]. [Full Text].

  9. 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. 2003 Jul-Aug. 10(4):292-8. [Medline].

  10. 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. 1997 Feb 1. 79(3):494-9. [Medline].

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

  12. 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. 1993 Jun. 76(6):1458-63. [Medline].

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

  14. 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. 1995 Jul. 15(7):821-6. [Medline].

  15. 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. 1997 Jul. 82(7):2108-16. [Medline].

  16. 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. 1998 Apr. 83(4):1143-50. [Medline].

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

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

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

  20. 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. 2007 Fall. 2(4):254-9. [Medline].

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

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

  23. 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. 1992 Nov-Dec. 37(6):354-7. [Medline].

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

  25. 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. 1999 Jan. 84(1):38-43. [Medline].

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

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

  28. 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. 2003 Nov. 149(5):439-42. [Medline].

  29. 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].

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

  31. 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 Feb. 91(2):456-88. [Medline].

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

  33. 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. 2010 Feb. 162(2):213-20. [Medline].

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

  35. 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. 2009 Aug. 92(2):643-7. [Medline].

  36. 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. 1985 Feb. 34(2):101-7. [Medline].

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

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

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

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

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

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

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

  44. Reyss AC, Dewailly D. Cushing's Syndrome, Acromegaly, and Androgen Excess. 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.

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

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

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

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

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

  50. Kanova N, Bicíkova M. Hyperandrogenic states in pregnancy. Physiol Res. 2011. 60(2):243-52. [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. 2008 Apr. 93(4):1105-20. [Medline].

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

  53. Somani N, Harrison S, Bergfeld WF. The clinical evaluation of hirsutism. Dermatol Ther. 2008 Sep-Oct. 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. 2012 Mar. 18(2):146-70. [Medline].

  55. [Guideline] ACOG technical bulletin. Evaluation and treatment of hirsute. Int J Gynaecol Obstet. June. 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. 1984 Jul. 42(1):76-81. [Medline].

  57. Hunter MH, Carek PJ. Evaluation and treatment of women with hirsutism. Am Fam Physician. 2003 Jun 15. 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. 1999 Nov. 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. 1990 May. 35(5):491-5. [Medline].

  60. Blake MA, Holalkere NS, Boland GW. Imaging techniques for adrenal lesion characterization. Radiol Clin North Am. 2008 Jan. 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. 2005 Mar-Apr. 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. 2007 Dec. 92(12):4546-56. [Medline].

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

  64. Mortada R, Comerford K, Kallail KJ, Karakas SE. Utility of hemoglobin-A1C in nondiabetic women with polycystic ovary syndrome. Endocr Pract. 2013 Mar-Apr. 19(2):284-9. [Medline].

  65. Celik C, Abali R, Bastu E, Tasdemir N, Tasdemir UG, Gul A. Assessment of impaired glucose tolerance prevalence with hemoglobin A1c and oral glucose tolerance test in 252 Turkish women with polycystic ovary syndrome: a prospective, controlled study. Hum Reprod. 2013 Apr. 28(4):1062-8. [Medline].

  66. Kim JJ, Choi YM, Cho YM, Jung HS, Chae SJ, Hwang KR, et al. Prevalence of elevated glycated hemoglobin in women with polycystic ovary syndrome. Hum Reprod. 2012 May. 27(5):1439-44. [Medline].

  67. 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. 1988 Jan. 66(1):165-72. [Medline].

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

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

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

  71. 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. 1989 Jan. 68(1):173-9. [Medline].

  72. 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. 1995 Feb 1. 273(5):402-7. [Medline].

  73. 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. 1998 Jun. 13(6):1502-5. [Medline].

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

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

  76. 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. 1994 Feb. 61(2):281-7. [Medline].

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

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

  79. 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. 1995 Jan. 80(1):233-8. [Medline].

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

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

  82. 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. 1991 Jan. 72(1):83-9. [Medline].

  83. 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. 1997 Feb. 82(2):524-30. [Medline].

  84. Ibanez 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. 2000 Oct. 85(10):3526-30. [Medline].

  85. 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. 2000 Aug. 85(8):2767-74. [Medline].

  86. 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. 2002 May. 53(5):469-73. [Medline].

  87. 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. 2007 Jan 24. CD005552. [Medline].

  88. 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. 2008 Apr. 93(4):1135-42. [Medline].

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

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

  91. 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. 2009 Apr 15. CD000194. [Medline].

  92. 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. 2010 Mar. 122(2):112-20. [Medline].

  93. 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). 2009 Feb. 70(2):311-21. [Medline].

  94. 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. 2007 Nov. 157(5):669-76. [Medline].

 
Previous
Next
 
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 Evaluated Score



(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
Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.