• Hyperandrogenism
• Hirsutism in the absence of hyperandrogenism
• Hyperandrogenism references

Hyperandrogenism

Androgen induced hirsutism is characterized by hair growth in androgen sensitive hair follicles - primarily the beard, mustache, and escutcheon (area between the belly button and the top of the pubic hair). There may also be hair growth in mildly androgen responsive follicles on the arms, legs, chest, and back. In some instances the cause of hirsutism can be defined as "hyperandrogenism". Hyperandrogenism is essentially the increased production of androgen (male type) hormones in women. However, sometimes hyperandrogenism can also involve a decrease in androgen hormone antagonists such as sex hormone binding globulin (SHBG). There are a variety of underlying conditions that can cause hyperandrogenism.

• Polycystic ovarian syndrome (PCOS) or chronic anovulation
• Late onset congenital adrenal hyperplasia - an inherited disorder of hormone metabolism that causes increased hair growth in women after puberty
• Ovarian tumors - a rare cause of hirsutism
• Adrenal tumors - an extremely rare cause of hirsutism
• Pregnancy complications - also rare, e.g. luteoma of pregnancy (a tumor derived from the corpus luteum cells of the ovary)

PCOS is the most common underlying cause of hyperandrogenism leading to hirsutism. About 95% of hyperandrogenic women will have PCOS. A more detailed page on PCOS is provided elsewhere at keratin.com. Women are often first aware of PCOS through a variety of symptoms including irregular menstrual cycles (anovulation), hirsutism often beginning in teens and early 20s, and a progressive increase in hair growth with age. Usually PCOS can be determined with the aid of a blood tests although rarely there are subtle forms of PCOS where blood tests appear normal, but ultrasound scans reveal evidence of PCOS.

Much more rare is an ovary or adrenal gland tumor induced hirsutism. This risk, while very remote, is worth pointing out. Unfortunately some women with rare tumor induced causes of hirsutism are not correctly diagnosed. Because the conditions are so rare, doctors may not be experienced in conducting the appropriate tests to make the diagnosis. Pages on ovarian and adrenal tumors are provided elsewhere at keratin.com.

Where hyperandrogenism is suspected, a simple blood test is a good place to start and usually reveals the underlying problem. However, sometimes much more detailed investigations are required involving ultrasounds scans, adrenal and ovarian computed tomography, magnetic resonance imaging (MRI), radio-labelled cholesterol scintigraphy and positron emission tomography.

With hyperandrogenism, oral contraceptives and drugs that block androgen production, such as spironolactone and cyproterone acetate, are the most common treatment approach. Increasingly popular is the use of finasteride which blocks conversion of testosterone to DHT, but does not block actual androgen hormone production. With tumors, surgery may also be required.

Hirsutism in the absence of hyperandrogenism

Where there is an increase in systemic hormone production a blood sample provides very clear evidence of hyperandrogenism and the underlying cause of hirsutism is obvious. However, many women, probably the majority of women with hirsutism, have normal blood test results. These women apparently have an "idiopathic" hirsutism. That is, excess hair growth with normal menstrual cycles and normal androgen hormone levels. So what is the cause of the idiopathic hirsutism? The answer is still androgens!

Even though a blood test may return a normal result with all hormones within normal limits, this does not rule out androgen induced hair growth. Sometimes conditions like PCOS can be subtle such that blood tests are normal but polycystic ovaries are still present. In other cases where PCOS is confirmed to be absent androgens are still the cause of hirsutism. Hair follicles themselves have a variety enzymes capable of turning DHEAS into more potent testosterone and dihydrotestosterone (DHT). Some hair follicles may be more sensitive than others to androgen stimulation if the follicle express more androgen receptors. Other factors in hair follicles come into play such as the production levels of androgen antagonists like aromatase. These and other local skin activities may lead to androgen induced hirsutism in the absence of any systemic increase in androgen production. Blood tests primarily show the systemic levels of hormones, but the local levels within the hair follicles can be quite different. So hirsutism may be the result of an excess of androgens, but it may also be idiopathic, secondary to increased responsiveness of hair follicles to normal circulating levels of androgens.

There are no routine tests that can be conducted on the skin to identify localized androgen activity. Tests can be done experimentally as in laboratory research, but the dermatology clinic has no test to offer a woman with idiopathic hirsutism. If blood tests are negative, but the hair growth is in an obvious hirsute pattern, then androgen activity can still be concluded as the underlying problem. Some inexperienced dermatologists and endocrinologists are reluctant to prescribe anti androgen treatments when blood tests are negative. However, experts in the field will still use such an approach despite normal blood tests so long as the hair growth clearly has a hirsute, androgen induced, pattern to it.

Hyperandrogenism references

• Laven JS, Imani B, Eijkemans MJ, Fauser BC. New approach to polycystic ovary syndrome and other forms of anovulatory infertility. Obstet Gynecol Surv. 2002 Nov;57(11):755-67.
• Claman P, Graves GR, Kredentser JV, Sagle MA, Tan S, Tummon I, Fluker M. Hirsutism: evaluation and treatment. J Obstet Gynaecol Can. 2002 Jan;24(1):62-73.
• Carmina E, Lobo RA.Polycystic ovaries in Hirsute women with normal menses. Am J Med. 2001 Dec 1;111(8):602-6.
• Kashar-Miller M, Azziz R. Heritability and the risk of developing androgen excess. J Steroid Biochem Mol Biol. 1999 Apr-Jun;69(1-6):261-8.
• Danilowicz K, Albiger N, Vanegas M, Gomez RM, Cross G, Bruno OD. Androgen-secreting adrenal adenomas. Obstet Gynecol. 2002 Nov;100(5 Pt 2):1099-102.
• Aberg LE, Tiitinen A, Autti TH, Kivisaari L, Santavouri P. Hyperandrogenism in girls with juvenile neuronal ceroid lipofuscinosis. Eur J Paediatr Neurol. 2002;6(4):199-205.
• Schroeder B. Early diagnosis, presenting complaints, and management of hyperandrogenism in adolescents. Curr Womens Health Rep. 2001 Oct;1(2):124-30.
• Mathew RP, Najjar JL, Lorenz RA, Mayes DE, Russell WE. Premature pubarche in girls is associated with functional adrenal but not ovarian hyperandrogenism. J Pediatr. 2002 Jul;141(1):91-8.
• Franks S. Adult polycystic ovary syndrome begins in childhood. Best Pract Res Clin Endocrinol Metab. 2002 Jun;16(2):263-72.
• Hogeveen KN, Cousin P, Pugeat M, Dewailly D, Soudan B, Hammond GL. Human sex hormone-binding globulin variants associated with hyperandrogenism and ovarian dysfunction. J Clin Invest. 2002 Apr;109(7):973-81.
• Franks S, Gilling-Smith C, Gharani N, McCarthy M. Pathogenesis of polycystic ovary syndrome: evidence for a genetically determined disorder of ovarian androgen production. Hum Fertil (Camb). 2000;3(2):77-79.
• Pugeat M, Ducluzeau PH, Mallion-Donadieu M. Association of insulin resistance with hyperandrogenia in women. Horm Res. 2000;54(5-6):322-6.
• Rossi R, Tauchmanova L, Luciano A, Valentino R, Savastano S, Battista C, Di Martino M, Lombardi G. Functional hyperandrogenism detected by corticotropin and GnRH-analogue stimulation tests in women affected by apparently idiopathic hirsutism. J Endocrinol Invest. 2001 Jul-Aug;24(7):491-8.
• Derman RJ. Androgen excess in women. Int J Fertil Menopausal Stud. 1996 Mar-Apr;41(2):172-6.
• Lucky AW. Hormonal correlates of acne and hirsutism. Am J Med. 1995 Jan 16;98(1A):89S-94S.
• Winter JS. Hyperandrogenism in female adolescents. Curr Opin Pediatr. 1993 Aug;5(4):488-93.
• Erkkola R, Ruutiainen K. Hirsutism: definitions and etiology. Ann Med. 1990 Apr;22(2):99-103.