Hyperandrogenism is a medical condition characterized by high levels of androgens in women, and less commonly in men.[4] The presentation of hyperandrogenism may include acne, seborrhea (inflamed skin), hair loss on the scalp, increased body or facial hair, and infrequent or absent menstruation.[1][2] Complications may include high blood cholesterol and diabetes.[4] It occurs in about 5% of women of reproductive age.[2]

Other namesAndrogen excess
Testosterone is a type of androgen that is important in the development of hyperandrogenism since high levels of it can cause this condition.
SymptomsAcne, hair loss on scalp, increased body or facial hair, infrequent or absent menstruation[1][2]
CausesPolycystic ovary syndrome (PCOS), adrenal hyperplasia, Cushing's disease, cancer[1][3]
Diagnostic methodBlood tests, ultrasound[1][4]
TreatmentBirth control pills, cyproterone acetate[1]
Frequency5% (reproductive age women)[2]

Polycystic ovary syndrome (PCOS) accounts for about 70% of hyperandrogenism cases.[1] Other causes include adrenal hyperplasia, hirsutism, insulin resistance, hyperprolactinemia, Cushing's disease, certain types of cancers, and certain medications.[1][3][4] Diagnosis often involves blood tests for testosterone, 17-hydroxyprogesterone, and prolactin as well as a pelvic ultrasound.[1][4]

Treatment depends on the underlying cause.[4] Symptoms of hyperandrogenism can be improved with birth control pills or antiandrogens such as cyproterone acetate or spironolactone.[1][4] Other measures may include hair removal techniques.[3]

The earliest known descriptions of the condition are by Hippocrates in the 5th century BCE.[5][6]

In 2011 the International Association of Athletics Federations (now World Athletics), and IOC [7] released statements restricting the eligibility of female athletes with high testosterone, whether through hyperandrogenism or as a result of a disorder of sex development (DSD). These regulations were referred to by both bodies as hyperandrogenism regulations, and have led to athletes with (DSD) being described as having hyperandrogenism.[8][9]

Signs and symptomsEdit

A woman with hirsutism from increased androgen exposure

Hyperandrogenism affects 5-10% of women of reproductive age.[10] Hyperandrogenism can affect both men and women, but is more noticeable in women since elevated levels of androgens in women often facilitates virilization. Because hyperandrogenism is characterized by the elevation of male sex hormone levels, symptoms of hyperandrogenism in men are often negligible. Hyperandrogenism in women is typically diagnosed in late adolescence with a medical evaluation. The medical evaluation tends to consist of a pelvic exam, observation of external symptoms, and a blood test measuring androgen levels.[11]


Hyperandrogenism, especially high levels of testosterone, can cause serious adverse effects on women's bodies if left untreated. High testosterone levels have been seen to be associated with other health conditions such as obesity, hypertension, amenorrhea (cessation of menstrual cycles), and ovulatory dysfunction, which can lead to infertility. The more prominent signs of hyperandrogenism are hirsutism (unwanted growth of hair especially in the abdominal region and places on the back), acne after adolescence, deepening of the voice, and alopecia (balding).[12]

Hyperandrogenism has also been seen to cause individuals to have a high tolerance to insulin, which can lead to type two diabetes, and dyslipidemia, such as high cholesterol. These effects have also been seen to have a large psychological impact on the individual, sometimes leading to social anxiety and depression, especially in adolescent girls and young women. Paired with obesity and hirsutism, it can cause the individual to have low self-esteem and a poor view of oneself.[11][13]


Even though hyperandrogenism is not common in men, there are studies that look into the effects of high levels of testosterone in males. A study showed that although many of the male participants did not have behavioral changes[clarification needed] due to the increased levels of testosterone, there were cases where the participants had instances of uncharacteristic aggression. High levels of testosterone in males have not been seen to have a direct impact on their personality, but within those studies, there have been cases of sudden aggression within the male participants.[14] A study has also shown that acute high-dose anabolic-androgenic steroid administration in males have been demonstrated to acutely attenuate reproductive hormonal secretions and significantly impact thyroid axis balance. The authors of the study concluded that effects on mood and aggression observed during high-dose anabolic-androgenic steroid administration may occur secondarily to hormonal changes.[15] Another study showed that the same signs and symptoms that are shown in women such as alopecia and acne were also found in men. The article also showed enlarged prostates with men with hyperandrogenism.[16]


While hyperandrogenism in women can be caused by external factors, it can also appear from natural causes.

Polycystic ovary syndromeEdit

Ultrasound of a polycystic ovary

Polycystic ovary syndrome (PCOS) is an endocrine disorder characterized by an excess of androgens produced by the ovaries. It is estimated that approximately 90 per cent of women with PCOS demonstrate hypersecretion of these hormones.[17] A concrete cause for this condition is currently unknown. Speculations include genetic predisposition, although the gene or genes, in particular, have yet to be identified.[18] Evidence suggests that the condition may have a hereditary basis. Other possible causes include the effects of an increase in insulin production. Most of the cases of PCOS involve insulin resistance.[19] It is thought that adipose tissue dysfunction plays a role in the insulin resistance seen within PCOS.[19] Insulin itself has been observed capable of inducing excess testosterone levels in the ovaries.[20] A complication associated with polycystic ovary syndrome is high cholesterol (discussed in the introduction) which is treated with statins. In a meta-analysis, atorvastatin has been shown to decrease various androgen concentrations in persons with hyperandrogenism.[21]

Elevated insulin concentration in the body leads to lower production of sex hormone binding globulin (SHBG), a regulatory glycoprotein that suppresses the function of androgens.[22] High blood levels of insulin also work in conjunction with ovarian sensitivity to insulin to cause hyperandrogenemia, the primary symptom of PCOS. Obese individuals may be more biologically inclined to display PCOS due to markedly higher amounts of insulin in their bodies. This hormonal imbalance can lead to chronic anovulation, in which the ovaries experience difficulty releasing mature eggs. These cases of ovulatory dysfunction are linked to infertility and menstrual disturbances.[17][23] A post hoc analysis from a randomized, placebo-controlled, multi-centre study carried out at 11 secondary care centres and a longitudinal single-centre study on healthy pregnant women in Norway also determined that metformin had no effect on maternal androgens in PCOS pregnancies.[24]

In systemic review, although still debatable, suggests that vitamin D receptor polymorphisms are associated with the prognosis of polycystic ovary syndrome.[25][26] These studies contributed small sample sizes, so definitive causation could be concluded. However, studies have shown benefits for vitamin D supplementation in women with vitamin D deficiency and polycystic ovary syndrome.[27]

Hyperthecosis and hyperinsulinemiaEdit

Hyperthecosis occurs when the cells of the ovarian stroma transition from interstitial cells, which are cells located in between other cells, into luteinized theca cells. Theca cells are located in the ovarian follicles and become luteinized when the ovarian follicle breaks and a new corpus luteum is formed. The dispersal of luteinized theca cells throughout the ovarian stroma, in contrast to PCOS where the luteinized theca cells are only around cystic follicles, causes women with Hyperthecosis to have higher testosterone levels and male-attributed characteristics (virilization) than women with PCOS. Excess levels of insulin in the blood, known as hyperinsulinemia, is also a characteristic of Hyperthecosis.[28] Hyperthecosis is mostly seen in postmenopausal women and is linked to acne, hirsutism, growth of the clitoris, baldness, and voice deepening.[29]

Low levels of insulin can also lead to hyperandrogenism. When the body's insulin levels drop too low, it can force itself to produce too much in an effort to make up for the loss. The result of such an overproduction is a disorder called hyperinsulinemia. An effect of hyperinsulinemia is the body's increased production of androgens in the ovaries.[30] This is all part of HAIR-AN syndrome, a multisystem disorder that involves increased insulin levels that prompt increased androgen levels.[31][32]

Of note, obesity can play a role in insulin resistance.[33] For instance, obesity makes thecal cells more responsive to Luteinizing Hormone, LH.[33] Therefore, obesity increases ovarian androgen production.[33] Additionally, obesity elevates inflammatory adipokines which leads to not only adipogenesis, but also heightened insulin resistance.[33]

Cushing’s syndromeEdit

Cushing syndrome develops due to long-term exposure to the hormone cortisol.[34][35] Cushing's syndrome can either be exogenous or endogenous, depending on whether it is caused by an external or internal source, respectively.[36] The intake of glucocorticoids, which are a type of steroid hormone, is a common cause for the development of exogenous Cushing's syndrome. Endogenous Cushing's syndrome can occur when the body produces excessive amounts of cortisol. This occurs when the hypothalamus of the brain transmits corticotropin-releasing hormone (CRH) to the pituitary gland, which in turn secretes Adrenocorticotropin hormone (ACTH). ACTH then causes the adrenal glands to release cortisol into the blood. Signs of Cushing's syndrome include muscle weakness, easy bruising, weight gain, male-pattern hair growth (hirsutism), colored stretch marks, and an excessively reddish complexion in the face.[37] Cushing's syndrome has been shown to cause androgen excess, which directly links it to the signs and symptoms seen in hyperandrogenism.[29]

Congenital adrenal hyperplasiaEdit

Congenital adrenal hyperplasia describes a group of autosomal recessive disorders that cause a lack of an enzyme needed for producing cortisol and/or aldosterone, both of which are steroid hormones. Most cases of CAH are due to 21-hydroxylase deficiencies, an enzyme used by the body to produce cortisol and aldosterone. The heightened androgen levels seen within congenital adrenal hyperplasia impact the hypothalamic pituitary-gonadal axis.[38] They can also impact the ovaries which can lead to infertility as well as chronic anovulation.[38]

Since congenital adrenal hyperplasia consists of multiple disorders, the signs and symptoms of hyperandrogenism, as well as their severity, depend upon the mutations that particular disorders are related to.[39] Therefore, genotyping is crucial to help verify diagnoses and establish prognostic factors for individuals.[40] Genotyping is also crucial for people interested in genetic counseling to aid in family planning.[40]

In women, CAH causes uncertainty in the genitals at birth and later on in adolescence excessive pubic hair, enlargement of the clitoris, hirsutism and although it causes rapid growth in childhood adult women with CAH are shorter than average due to early puberty and closure of growth plates. Symptoms in males include early showings of pubic hair, enlargement of the penis, and rapid body and skeletal growth.[41]


Adrenocortical carcinoma and tumorsEdit

This is very rare disease with an average incidence rate of 1–2 per million annually. This disease causes cancerous cells to form within the cortex of one or both of the adrenal glands. . Although these tumors are identified in fewer than two percent of patients diagnosed with hyperandrogenism, the prevalence of adrenocortical carcinomas is relevant within this population. These tumors are associated with elevations of androgen levels in more than half of affected patients including, androstenedione, dehydroepiandrosterone sulfate, and testosterone.[42] The elevation of androgens caused by these adrenocortical carcinomas often lead patients with these steroid hormone-producing tumors to develop Cushing's syndrome, Conn syndrome and Hyperandrogenism.[43][42] There have been many recent advances on the pathology and pathogenesis of adrenocortical tumors, however the molecular basis of this human disease and has yet to be elucidated.[42]

Adenoma of the adrenal glandEdit

Adrenal Adenomas are benign tumors on the adrenal gland. In most cases, the tumors display no symptoms and require no treatment. In rare cases, however, some Adrenal Adenomas may become activated, in that they begin to produce hormones in much larger quantities than what adrenal glands tend to produce leading to a number of health complications including primary Aldosteronism and hyperandrogenism.[44]


An Arrhenoblastoma is an uncommon tumor of the ovary. It is often composed of sterol cells, leydig cells or some combination of the two. The tumor can produce male or female hormones in the patient and may cause masculinization. In a prepubescent child, a tumor may cause precocious puberty. Malignant Arrhenoblastoma accounts for 30% of all cases of Arrhenoblastoma, the other 70% being largely benign and curable with surgery.[45]

Hilar cell tumorEdit

An ovarian, Androgen producing tumor afflicting older women in most cases and often leading to the development of virilization. This tumor tends to occur around the region of the ovary where the blood vessels enter the organ otherwise known as the hilum. This type of tumor tends to be rather small in size and in most cases could be entirely removed and its symptoms reversed through surgery.[46]

Krukenberg tumorEdit

Krukenberg tumors are quickly developing malignant tumor that are normally found in one of or both ovaries that primarily originate from tissues in the stomach, pancreas, gallbladder, colon or breast. The tumor is caused by the trans coelomic spread, or the spread of metastatic tumors through body cavities.[47] These tumors cause virilization in the people they affect. Increased androgen production secondary to elevations in human chorionic gonadotropin is hypothesized to the primary causative reason for hyperandrogenism in people with Krukenberg tumors.[48]


One such cause is the end of ovulation and the beginning of menopause. When the body transitions from ovulation to menopause, it stops releasing estrogen at a faster rate than it stops releasing androgens. In some cases, estrogen levels can drop enough that there are substantially higher androgen levels leading to hyperandrogenism. A decrease in sex hormone levels while the free androgen index increases help to aid this process, as well.[49]


Many drugs can stimulate symptoms of hyperandrogenism. These symptoms include but are not limited to hirsutism, acne, dermatitis, androgenic alopecia, irregularities in menstruation, clitoral hypertrophy, and the deepening of the voice. The most frequently implicated drugs in causing hyperandrogenism are anabolic steroids, synthetic progestins, and antiepileptics, however many other drugs may cause hyperandrogenism.[50] This can happen according to one of five major mechanisms, namely the direct introduction of androgens to the body, the binding of the drug to androgen receptors and subsequent participation in androgenic action (as is the case with anabolic-androgenic steroids), the reduction of sex hormone-binding globulin plasma concentration that leads to a resulting increase in free testosterone, the interference with and alteration of the hypothalamic–pituitary–ovarian (HPO) axis, or the increase in release of adrenal androgens.[51] However, certain drugs do exist where the mechanism by which they cause hyperandrogenism remains unclear. For example, the molecular basis in which valproate induces hyperandrogenism and polycystic ovary syndrome has yet to be elucidated.[50] However, there was a study that showed that women taking valproic acid had higher testosterone levels and hyperandrogenism compared to those women who were not taking valproic acid for bipolar disorder.[52]


Because hyperandrogenism can appear as a symptom of numerous different genetic and medical conditions, it is difficult to make a general statement on whether hyperandrogenic symptoms can be passed from parent to offspring. However, a collection of the conditions with hyperandrogenic symptoms, including polycystic ovary syndrome, have been observed as hereditary in certain cases. Additionally, it is thought that epigenetics may aid in the pathogenesis of polycystic ovary syndrome.[53]

One potential cause of polycystic ovary syndrome is maternal hyperandrogenism, where the hormonal irregularities of the mother can affect the development of the child during gestation, resulting in the passing of polycystic ovary syndrome from mother to child.[54] Other studies compared the difference between umbilical cords with mothers with polycystic ovary syndrome and mothers without. The umbilical cords included both male and female infants. The results showed no significant androgen elevations. The testosterone levels from the umbilical cords were not associated with the polycystic ovary syndrome and the androstenedione levels were lower in female infants.[55]


Diagnosing hyperandrogenism can be complex due to the wide variety and severity of signs and symptoms that may present in women.[56]

Women may show symptoms of hyperandrogenism in their early life, but physicians become more concerned when the patient is in her late teens or older.[11]

Hyperandrogenism is most often diagnosed by checking for signs of hirsutism according to a standardized method that scores the range of excess hair growth.[10][11]

Checking medical history and a physical examination of symptoms are used for an initial diagnosis.[11] Patient history assessed includes age at thelarche, adrenarche, and menarche; patterns of menstruation; obesity; reproductive history; and the start and advancement of hyperandrogenism symptoms.[11] Patterns of menstruation are examined since irregular patterns may appear with hirsutism.[10] Other conditions that may present alongside hirsutism that can be utilized for diagnosis include androgenic alopecia and acne.[56] If hyperandrogenism is severe enough, virilization may occur.[56]

Family history is also assessed for occurrences of hyperandrogenism symptoms or obesity in other family members.[11]

A laboratory test can also be done on the patient to evaluate levels of FSH, LH, DHEAS, prolactin, 17OHP, and total and free testosterone in the patient's blood.[11] Abnormally high levels of any of these hormones help in diagnosing hyperandrogenism.[11]


Since risk factors are not known and vary among individuals with hyperandrogenism, there is no sure method to prevent this medical condition.[57] Therefore, more long-term studies are needed first to find a cause for the condition before being able to find a sufficient method of prevention.[57]

However, there are a few things that can help avoid long-term medical issues related to hyperandrogenism like PCOS. Getting checked by a medical professional for hyperandrogenism; especially if one has a family history of the condition, irregular periods, or diabetes; can be beneficial.[58] Watching your weight and diet is also important in decreasing your chances, especially in obese women, since continued exercise and maintaining a healthy diet leads to an improved menstrual cycle as well as to decreased insulin levels and androgen concentrations.[57]


Currently, there is no definitive treatment for hyperandrogenism as it varies with the underlying condition that causes it. As a hormonal symptom of polycystic ovary syndrome, menopause, and other endocrine disorders, it is primarily treated as a symptom of these disorders. Drugs may be considered only in women who do not plan on becoming pregnant in the near future.[59] Some effective drugs for treating facial hirsutism includes eflornithine, which may cause birth defects in pregnant women,[60] retinoids and antibiotics for acne and minoxidil for alopecia.[60] Systemically, it is treated with antiandrogens such as cyproterone acetate, flutamide and spironolactone to control the androgen levels in the patient's body. For hyperandrogenism caused by late onset congenital adrenal hyperplasia (LOCAH), treatment is primarily focused on providing the patient with glucocorticoids to combat the low cortisol production and the corresponding increase in androgens caused by the swelling of the adrenal glands.[61][62] Oestrogen-based oral contraceptives are used to treat both CAH and PCOS caused hyperandrogenism. These hormonal treatments have been found to reduce the androgen excess and suppress adrenal androgen production and cause a significant decrease in hirsutism.[63][64]

Hyperandrogenism is often managed symptomatically. Hirsutism and acne both respond well to the hormonal treatments described above, with 60-100% reporting an improvement in hirsutism.[63] Androgenic alopecia however, does not show a significant improvement with hormonal treatments and requires other treatments, such as hair transplantation.[65]

Supplementation can also contribute to the managing treatment of symptomatic effects of hyperandrogenism. In a meta-analysis, multiple studies showed when high levels of vitamin D supplements were given to women with vitamin D deficiency due to polycystic ovary syndrome, there were improvements in glucose levels, insulin sensitivity, cholesterol levels, and lowering of certain hormones such as testosterone, sex hormone binding globulin, and free androgen index which are all associated with hyperandrogenism.[66] The supplementation of vitamin D with non-polycystic ovary syndrome women with vitamin D deficiency did not show the same results.[27]

Targeting Insulin Resistance and ObesityEdit

In every woman with polycystic ovary syndrome (PCOS), lifestyle modifications are recommended to help with controlling symptoms of hyperandrogenism. Of note, lifestyle modification is regarded as the first-line treatment for PCOS.[67] Lifestyle modifications have proven to help with improving overall body composition, insulin resistance, and hyperandrogenism. However, there is unclear results in overall improvement of mood, quality of life, and reproductive outcomes.[68] Additionally, lifestyle modifications and anti-obesity medications have not shown a proven benefit in the long run and some people turn to bariatric surgery.[69] A meta-analysis study in 2017 showed that bariatric surgery in women with severe obesity and PCOS had decreased levels of total and free testosterone in their body, and helped correct issues of hirsutism and menstrual dysfunction.[70]

One of the most common strategies in targeting insulin resistance in women with PCOS is through the use of insulin-sensitizer drugs, like metformin. Metformin can help to decrease weight and to decrease androgen levels in the body.[71] When combined with lifestyle modifications (changes in diet and exercise), it has been linked with lower BMI and helped with menstrual problems.[71] However, the use of metformin in women with PCOS should only be considered in patients with a known issue with glucose tolerance.a[citation needed]

Society and cultureEdit

Because androgen excess is manifested in noticeable physical features (ex. hirsutism), a certain social stigma is associated with it.


Theoretical and evidence-based claims currently exist that state that very high levels of circulating testosterone is associated with increased athletic performance in women with androgen sensitivity. However, there is much disagreement on whether or not testosterone is unlike any other physical parameter with reference to bestowing advantages or disadvantages in female athletes. Existing regulations throughout competitive sports are currently being refined to specifically address this, and many have stated the importance of guaranteeing fairness and respect for all female athletes during these proceedings.[72]

Caster Semenya, a genetically XY female athlete with 5-alpha reductase deficiency.

Following the case of South African athlete Caster Semenya, the International Association of Athletics Federations (IAAF) introduced its hyperandrogenism regulations, which restricted women with high testosterone levels, whether through hyperandrogenism or having testes and a DSD. These regulations replaced the earlier sex verification rules.[citation needed]

Eventually, following a series of legal challenges, the current set of regulations were released on 1 May 2019, now called the Eligibility Regulations for the Female Classification (Athletes with Differences of Sexual Development, or DSD).[73] These regulations only apply to athletes with XY DSDs and testes,[74] and no longer include hyperandrogenism from causes such as PCOS.

Social definitionEdit

Cultural variation can define hyperandrogenism socially—aside from clinical and chemical definitions—to make some hair growth unacceptable even if it is considered clinically normal based on metrics like the Ferriman-Gallwey score. For example, only pubic and axillary hair in North American women is tolerated, while other androgen-dependent hair such as growth on the upper lip, over the linea alba, over the thighs, and any periareolar hair is not.[75]


Professional organizations like the Androgen Excess and PCOS Society exist to promote the research, treatment, diagnosis, and prevention of such disorders along with educating the public and scientific community about them.[76]

See alsoEdit


  1. ^ a b c d e f g h i Peigné M, Villers-Capelle A, Robin G, Dewailly D (2013). "[Hyperandrogenism in women]". Presse Médicale. 42 (11): 1487–99. doi:10.1016/j.lpm.2013.07.016. PMID 24184282.
  2. ^ a b c d Curtis M, Antoniewicz L, Linares ST (2014). Glass' Office Gynecology. Lippincott Williams & Wilkins. p. 39. ISBN 978-1-60831-820-9.
  3. ^ a b c Catteau-Jonard S, Cortet-Rudelli C, Richard-Proust C, Dewailly D (2012). "Hyperandrogenism in adolescent girls". Endocrine Development. 22: 181–193. doi:10.1159/000326688. ISBN 978-3-8055-9336-6. PMID 22846529.
  4. ^ a b c d e f g Carlson KJ, Eisenstat SA (2004). The New Harvard Guide to Women's Health. Harvard University Press. p. 286. ISBN 978-0-674-01282-0.
  5. ^ Banker M (2019). Nova IVI Textbook of Infertility & Assisted Reproductive Technology. JP Medical Ltd. p. 237. ISBN 978-9-3889-5884-4.
  6. ^ Pathobiology of Human Disease: A Dynamic Encyclopedia of Disease Mechanisms. Elsevier. 2014. p. 1385. ISBN 978-0-12-386457-4.
  7. ^ "IOC addresses eligibility of female athletes with hyperandrogenism". International Olympic Committee. 2011.
  8. ^ Washington Post Staff (2019). "What are the issues behind the Court of Arbitration for Sport ruling in Caster Semenya case?". The Washington Post.
  9. ^ Abraham R (2019). "What's with the gender inequality? Dutee Chand talks about the tests female athletes face before competing". The Economic Times. Bennett, Coleman & Co. Ltd.
  10. ^ a b c Yildiz BO (2006). "Diagnosis of hyperandrogenism: clinical criteria". Best Practice & Research. Clinical Endocrinology & Metabolism. 20 (2): 167–76. doi:10.1016/j.beem.2006.02.004. PMID 16772149.
  11. ^ a b c d e f g h i Goodman NF, Bledsoe MB, Cobin RH, Futterweit W, Goldzieher JW, Petak SM, et al. (2001). "American Association of Clinical Endocrinologists medical guidelines for the clinical practice for the diagnosis and treatment of hyperandrogenic disorders". Endocrine Practice. 7 (2): 120–34. doi:10.4158/EP.7.2.120. PMID 12940239.
  12. ^ Simon J (2015). "Androgen". Health Women. National Women's Health Resource Center. Retrieved 14 November 2016.
  13. ^ Brettenthaler N, De Geyter C, Huber PR, Keller U (2004). "Effect of the insulin sensitizer pioglitazone on insulin resistance, hyperandrogenism, and ovulatory dysfunction in women with polycystic ovary syndrome". The Journal of Clinical Endocrinology and Metabolism (published 28 April 2011). 89 (8): 3835–40. doi:10.1210/jc.2003-031737. PMID 15292314.
  14. ^ Pope HG, Kouri EM, Hudson JI (2000). "Effects of supraphysiologic doses of testosterone on mood and aggression in normal men: a randomized controlled trial". Archives of General Psychiatry. 57 (2): 133–40, discussion 155–6. doi:10.1001/archpsyc.57.2.133. PMID 10665615.
  15. ^ Daly, R.C.; Su, T.-P.; Schmidt, P.J.; Pagliaro, M.; Pickar, D.; Rubinow, D.R. (2003). "Neuroendocrine and behavioral effects of high-dose anabolic steroid administration in male normal volunteers". Psychoneuroendocrinology. 28 (3): 317–331. doi:10.1016/S0306-4530(02)00025-2. ISSN 0306-4530. PMID 12573299. S2CID 7170203.
  16. ^ See Table 1 in Singh, Garima; Magani, Sri Krishna Jayadev; Sharma, Rinku; Bhat, Basharat; Shrivastava, Ashish; Chinthakindi, Madhusudhan; Singh, Ashutosh (3 October 2019). "Structural, functional and molecular dynamics analysis of cathepsin B gene SNPs associated with tropical calcific pancreatitis, a rare disease of tropics". PeerJ. 7: e7425. doi:10.7717/peerj.7425. PMC 6778667. PMID 31592339. Retrieved 27 July 2021.
  17. ^ a b Franks S (1995). "Polycystic ovary syndrome". The New England Journal of Medicine. 333 (13): 853–61. doi:10.1056/NEJM199509283331307. PMID 7651477.
  18. ^ "Polycystic Ovary Syndrome (PCOS)." Causes. Mayo Clinic, n.d. Web. 9 November 2016.
  19. ^ a b Goodarzi, Mark O.; Dumesic, Daniel A.; Chazenbalk, Gregorio; Azziz, Ricardo (2011). "Polycystic ovary syndrome: etiology, pathogenesis and diagnosis". Nature Reviews. Endocrinology. 7 (4): 219–231. doi:10.1038/nrendo.2010.217. ISSN 1759-5037. PMID 21263450. S2CID 205479927.
  20. ^ "Defining PCOS". The University of Chicago Medical Center.
  21. ^ Sathyapalan, Thozhukat; Smith, Karen A.; Coady, Anne-Marie; Kilpatrick, Eric S.; Atkin, Stephen L. (2012). "Atorvastatin therapy decreases androstenedione and dehydroepiandrosterone sulphate concentrations in patients with polycystic ovary syndrome: randomized controlled study". Annals of Clinical Biochemistry. 49 (Pt 1): 80–85. doi:10.1258/acb.2011.011071. ISSN 1758-1001. PMID 21972424.
  22. ^ Hammond GL, Bocchinfuso WP (1996). "Sex hormone-binding globulin: gene organization and structure/function analyses". Hormone Research. 45 (3–5): 197–201. doi:10.1159/000184787. PMID 8964583.
  23. ^ Burd I, Zieve D, Ogilvie I (27 January 2020). "Polycystic Ovary Syndrome". MedlinePlus Medical Encyclopedia.
  24. ^ Andræ F, Abbott D, Stridsklev S, Schmedes AV, Odsæter IH, Vanky E, Salvesen Ø (2020). "Sustained Maternal Hyperandrogenism During PCOS Pregnancy Reduced by Metformin in Non-obese Women Carrying a Male Fetus". The Journal of Clinical Endocrinology and Metabolism. 105 (12): 3762–3770. doi:10.1210/clinem/dgaa605. PMC 7538101. PMID 32866967.
  25. ^ Reis, Guilherme Victor Oliveira Pimenta Dos; Gontijo, Natália Alves; Rodrigues, Kathryna Fontana; Alves, Michelle Teodoro; Ferreira, Cláudia Natália; Gomes, Karina Braga (2017). "Vitamin D receptor polymorphisms and the polycystic ovary syndrome: A systematic review". The Journal of Obstetrics and Gynaecology Research. 43 (3): 436–446. doi:10.1111/jog.13250. ISSN 1447-0756. PMID 28127831. S2CID 11152805.
  26. ^ El-Shal, Amal S.; Shalaby, Sally M.; Aly, Nader M.; Rashad, Nearmeen M.; Abdelaziz, Ahmed M. (2013). "Genetic variation in the vitamin D receptor gene and vitamin D serum levels in Egyptian women with polycystic ovary syndrome". Molecular Biology Reports. 40 (11): 6063–6073. doi:10.1007/s11033-013-2716-y. ISSN 1573-4978. PMID 24078159. S2CID 18113257.
  27. ^ a b Karadağ, Cihan; Yoldemir, Tevfik; Yavuz, Dilek Gogas (2018). "Effects of vitamin D supplementation on insulin sensitivity and androgen levels in vitamin-D-deficient polycystic ovary syndrome patients". The Journal of Obstetrics and Gynaecology Research. 44 (2): 270–277. doi:10.1111/jog.13516. ISSN 1447-0756. PMID 29094433. S2CID 46784152.
  28. ^ Pasquali R (2011). "Research in Polycystic Ovary Syndrome Today and Tomorrow". Medscape. Blackwell Publishing. Retrieved 14 November 2016.
  29. ^ a b Atmaca M, Seven İ, Üçler R, Alay M, Barut V, Dirik Y, Sezgin Y (16 December 2014). "An interesting cause of hyperandrogenemic hirsutism". Case Reports in Endocrinology. 2014: 987272. doi:10.1155/2014/987272. PMC 4280803. PMID 25580312.
  30. ^ Barbieri RL, Hornstein MD (December 1988). "Hyperinsulinemia and ovarian hyperandrogenism. Cause and effect". Endocrinology and Metabolism Clinics of North America. 17 (4): 685–703. doi:10.1016/S0889-8529(18)30405-5. PMID 3058472.
  31. ^ James W, Berger T, Elston D (2005). Andrews' Diseases of the Skin: Clinical Dermatology (10th ed.). Saunders. ISBN 978-0-8089-2351-0.
  32. ^ Somani N, Harrison S, Bergfeld WF (2008). "The clinical evaluation of hirsutism". Dermatologic Therapy. 21 (5): 376–91. doi:10.1111/j.1529-8019.2008.00219.x. PMID 18844715. S2CID 34029116.
  33. ^ a b c d Glueck, Charles J.; Goldenberg, Naila (2019). "Characteristics of obesity in polycystic ovary syndrome: Etiology, treatment, and genetics". Metabolism: Clinical and Experimental. 92: 108–120. doi:10.1016/j.metabol.2018.11.002. ISSN 1532-8600. PMID 30445140.
  34. ^ "Cushing's Syndrome". National Endocrine and Metabolic Diseases Information Service (NEMDIS). July 2008. Archived from the original on 10 February 2015. Retrieved 16 March 2015. These benign, or noncancerous, tumors of the pituitary gland secrete extra ACTH. Most people with the disorder have a single adenoma. This form of the syndrome, known as Cushing's disease
  35. ^ Forbis P (2005). Stedman's medical eponyms (2nd ed.). Baltimore, Md.: Lippincott Williams & Wilkins. p. 167. ISBN 978-0-7817-5443-9.
  36. ^ "Cushing's Syndrome". The Lecturio Medical Concept Library. Retrieved 11 July 2021.
  37. ^ "Cushing's Syndrome". National Institute of Diabetes and Digestive and Kidney Diseases. April 2012. Retrieved 14 November 2016.
  38. ^ a b Pignatelli, Duarte; Pereira, Sofia S.; Pasquali, Renato (2019). "Androgens in Congenital Adrenal Hyperplasia". Frontiers of Hormone Research. 53: 65–76. doi:10.1159/000494903. ISBN 978-3-318-06470-4. ISSN 1662-3762. PMID 31499506.
  39. ^ Witchel, Selma Feldman (2017). "Congenital Adrenal Hyperplasia". Journal of Pediatric and Adolescent Gynecology. 30 (5): 520–534. doi:10.1016/j.jpag.2017.04.001. ISSN 1873-4332. PMC 5624825. PMID 28450075.
  40. ^ a b Török, Dóra (2019). "Congenital Adrenal Hyperplasia". Experientia Supplementum. 111: 245–260. doi:10.1007/978-3-030-25905-1_12. ISBN 978-3-030-25904-4. ISSN 1664-431X. PMID 31588535.
  41. ^ Wilson T (23 June 2016). "Congenital Adrenal Hyperplasia". Medscape. Retrieved 14 November 2016.
  42. ^ a b c Di Dalmazi, Guido (2019). "Hyperandrogenism and Adrenocortical Tumors". Frontiers of Hormone Research. 53: 92–99. doi:10.1159/000494905. ISBN 978-3-318-06470-4. ISSN 1662-3762. PMID 31499503.
  43. ^ "Adrenocortical Carcinoma". National Cancer Institute. 27 February 2019.
  44. ^ "Adenoma of the Adrenal Gland". Genetic and Rare Diseases Information Center(GARD) – an NCATS Program. U.S National Library of Medicine. U.S. National Library of Medicine. 26 November 2014.
  45. ^ Martin E, ed. (2015). "Arrhenoblastoma". Concise medical dictionary. Oxford University Press. p. 11. ISBN 978-0-19-968799-2.
  46. ^ Martin E, ed. (2015). "Hilar cell tumour". Concise medical dictionary. Oxford University Press. p. 353. ISBN 978-0-19-968799-2.
  47. ^ Concise medical dictionary. E. A. Martin (8th ed.). [Oxford]: Oxford University Press. 2010. ISBN 978-0-19-172701-6. OCLC 894628585.CS1 maint: others (link)
  48. ^ Bustamante, Carmen; Hoyos-Martínez, Alfonso; Pirela, Daniela; Díaz, Alejandro (2017). "In utero virilization secondary to a maternal Krukenberg tumor: case report and review of literature". Journal of Pediatric Endocrinology and Metabolism. 30 (7): 785–790. doi:10.1515/jpem-2016-0433. ISSN 2191-0251. PMID 28682787. S2CID 13760498.
  49. ^ Fogle RH, Stanczyk FZ, Zhang X, Paulson RJ (August 2007). "Ovarian androgen production in postmenopausal women". The Journal of Clinical Endocrinology & Metabolism. 92 (8): 3040–3. doi:10.1210/jc.2007-0581. PMID 17519304.
  50. ^ a b Neraud, Barbara; Dewailly, Didier (2007), Azziz, Ricardo; Nestler, John E.; Dewailly, Didier (eds.), "Drug-Induced Hyperandrogenism", Androgen Excess Disorders in Women, Totowa, NJ: Humana Press, pp. 121–127, doi:10.1007/978-1-59745-179-6_10, ISBN 978-1-58829-663-4, retrieved 29 July 2021
  51. ^ Neraud B, Dewailly D (8 November 2007). Azziz R, Nestler JE, Dewailly D (eds.). Contemporary Endocrinology: Androgen Excess Disorders in Women: Polycystic Ovary Syndrome and Other Disorders (Second ed.). Totowa, NJ: Humana Press Inc. ISBN 978-1-59745-179-6.
  52. ^ Zhang, Lin; Li, Hua; Li, Shaoping; Zou, Xiaoyi (2016). "Reproductive and metabolic abnormalities in women taking valproate for bipolar disorder: a meta-analysis". European Journal of Obstetrics, Gynecology, and Reproductive Biology. 202: 26–31. doi:10.1016/j.ejogrb.2016.04.038. ISSN 1872-7654. PMID 27160812.
  53. ^ Spinedi, Eduardo; Cardinali, Daniel P. (2018). "The Polycystic Ovary Syndrome and the Metabolic Syndrome: A Possible Chronobiotic-Cytoprotective Adjuvant Therapy". International Journal of Endocrinology. 2018: 1349868. doi:10.1155/2018/1349868. ISSN 1687-8337. PMC 6083563. PMID 30147722.
  54. ^ Puttabyatappa M, Cardoso RC, Padmanabhan V (November 2016). "Effect of maternal PCOS and PCOS-like phenotype on the offspring's health". Molecular and Cellular Endocrinology. 435: 29–39. doi:10.1016/j.mce.2015.11.030. PMC 4884168. PMID 26639019.
  55. ^ Duan, Changling; Pei, Tianjiao; Li, Yujing; Cao, Qi; Chen, Hanxiao; Fu, Jing (2020). "Androgen levels in the fetal cord blood of children born to women with polycystic ovary syndrome: a meta-analysis". Reproductive Biology and Endocrinology. 18 (1): 81. doi:10.1186/s12958-020-00634-8. ISSN 1477-7827. PMC 7418394. PMID 32782029.
  56. ^ a b c Yildiz, Bulent O. (2006). "Diagnosis of hyperandrogenism: clinical criteria". Best Practice & Research Clinical Endocrinology & Metabolism. 20 (2): 167–176. doi:10.1016/j.beem.2006.02.004. ISSN 1521-690X. PMID 16772149.
  57. ^ a b c Apter D (October 1998). "How possible is the prevention of polycystic ovary syndrome development in adolescent patients with early onset of hyperandrogenism". Journal of Endocrinological Investigation. 21 (9): 613–7. doi:10.1007/bf03350786. PMID 9856415. S2CID 24263988.
  58. ^ Nader S (July 2013). "Hyperandrogenism during puberty in the development of polycystic ovary syndrome". Fertility and Sterility (Review). 100 (1): 39–42. doi:10.1016/j.fertnstert.2013.03.013. PMID 23642453.
  59. ^ Escobar-Morreale, H.F.; Carmina, E.; Dewailly, D.; Gambineri, A.; Kelestimur, F.; Moghetti, P.; Pugeat, M.; Qiao, J.; Wijeyaratne, C.N.; Witchel, S.F.; Norman, R.J. (2012). "Epidemiology, diagnosis and management of hirsutism: a consensus statement by the Androgen Excess and Polycystic Ovary Syndrome Society". Human Reproduction Update. 18 (2): 146–170. doi:10.1093/humupd/dmr042. ISSN 1460-2369. PMID 22064667.
  60. ^ a b Escobar-Morreale, Héctor F. (2018). "Polycystic ovary syndrome: definition, aetiology, diagnosis and treatment". Nature Reviews Endocrinology. 14 (5): 270–284. doi:10.1038/nrendo.2018.24. ISSN 1759-5029. PMID 29569621. S2CID 4698059.
  61. ^ Hughes IA (November 1988). "Management of congenital adrenal hyperplasia". Archives of Disease in Childhood. 63 (11): 1399–404. doi:10.1136/adc.63.11.1399. PMC 1779155. PMID 3060026.
  62. ^ Merke DP, Bornstein SR (2005). "Congenital adrenal hyperplasia". Lancet. 365 (9477): 2125–36. doi:10.1016/S0140-6736(05)66736-0. PMID 15964450. S2CID 40860427.
  63. ^ a b Burkman RT (January 1995). "The role of oral contraceptives in the treatment of hyperandrogenic disorders". The American Journal of Medicine. 98 (1A): 130S–136S. doi:10.1016/s0002-9343(99)80071-0. PMID 7825633.
  64. ^ Mastorakos G, Koliopoulos C, Creatsas G (May 2002). "Androgen and lipid profiles in adolescents with polycystic ovary syndrome who were treated with two forms of combined oral contraceptives". Fertility and Sterility. 77 (5): 919–27. doi:10.1016/s0015-0282(02)02993-x. PMID 12009344.
  65. ^ Sinclair R, Wewerinke M, Jolley D (March 2005). "Treatment of female pattern hair loss with oral antiandrogens". The British Journal of Dermatology. 152 (3): 466–73. doi:10.1111/j.1365-2133.2005.06218.x. PMID 15787815. S2CID 26089277.
  66. ^ Menichini, Daniela; Facchinetti, Fabio (2020). "Effects of vitamin D supplementation in women with polycystic ovary syndrome: a review". Gynecological Endocrinology. 36 (1): 1–5. doi:10.1080/09513590.2019.1625881. ISSN 1473-0766. PMID 31187648. S2CID 186205997.
  67. ^ Jin, Peipei; Xie, Yongyong (2018). "Treatment strategies for women with polycystic ovary syndrome". Gynecological Endocrinology. 34 (4): 272–277. doi:10.1080/09513590.2017.1395841. ISSN 1473-0766. PMID 29084464. S2CID 4443092.
  68. ^ Opiyo, Newton (2019). "In women with polycystic ovary syndrome, how do lifestyle changes affect outcomes?". Cochrane Clinical Answers. doi:10.1002/cca.2649. ISSN 2050-4217.
  69. ^ SCHAUER, P (2007), "Weight Loss Surgery: State of the Art", Aesthetic Surgery After Massive Weight Loss, Elsevier, pp. 1–12, doi:10.1016/b978-1-4160-2952-6.50007-5, ISBN 978-1-4160-2952-6, retrieved 29 July 2021
  70. ^ Escobar-Morreale, Hector F.; Santacruz, Elisa; Luque-Ramírez, Manuel; Botella Carretero, José I. (2017). "Prevalence of 'obesity-associated gonadal dysfunction' in severely obese men and women and its resolution after bariatric surgery: a systematic review and meta-analysis". Human Reproduction Update. 23 (4): 390–408. doi:10.1093/humupd/dmx012. ISSN 1355-4786. PMID 28486593.
  71. ^ a b Naderpoor, Negar; Shorakae, Soulmaz; de Courten, Barbora; Misso, Marie L.; Moran, Lisa J; Teede, Helena J. (2015). "Metformin and lifestyle modification in polycystic ovary syndrome: systematic review and meta-analysis". Human Reproduction Update. 21 (5): 560–574. doi:10.1093/humupd/dmv025. ISSN 1355-4786. PMID 26060208.
  72. ^ Bermon, Stéphane; Vilain, Eric; Fénichel, Patrick; Ritzén, Martin (2015). "Women With Hyperandrogenism in Elite Sports: Scientific and Ethical Rationales for Regulating". The Journal of Clinical Endocrinology & Metabolism. 100 (3): 828–830. doi:10.1210/jc.2014-3603. ISSN 0021-972X. PMID 25587809.
  73. ^ "Eligibility Regulations for the Female Classification (Athletes with Differences of Sex Development)". International Association of Athletics Federations. 1 May 2019.
  74. ^ "IAAF publishes briefing notes and Q&A on Female Eligibility Regulations". World Athletics.
  75. ^ Krishna UR, Sheriar NK (1 January 2000). "9. Hyperandrogenism in Adolescence". Adolescent Gynecology (pb). Orient Blackswan. p. 119. ISBN 978-8-12-501793-6.
  76. ^ Wang SQ. "Androgen Excess and PCOS Society". www.ae-society.org. Retrieved 10 November 2016.

External linksEdit

External resources