Dermatologic Manifestations of Hirsutism
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Hirsutism is defined as the excessive growth of thick dark hair in locations where hair growth in women usually is minimal or absent (see the image below). Such male-pattern growth of terminal body hair usually occurs in androgen-stimulated locations, such as the face, chest, and areolae.
Although the terms hirsutism and hypertrichosis often are used interchangeably, hypertrichosis actually refers to excess hair (terminal or vellus) in areas that are not predominantly androgen dependent. Whether a patient is hirsute often is difficult to judge because hair growth varies among individual women and across ethnic groups. What is considered hirsutism in one culture may be considered typical in another. For example, women from the Mediterranean and the Indian subcontinent have more facial and body hair than do women from East Asia, sub-Saharan Africa, and northern Europe. Dark-haired, darkly pigmented individuals of either sex tend to be more hirsute than blond or fair-skinned persons.
In most cases, hirsutism is a benign condition and is primarily of cosmetic concern. However, when hirsutism is accompanied by masculinizing signs or symptoms, particularly when these arise well after puberty, hirsutism may be a manifestation of a more serious underlying disorder such as an ovarian or adrenal neoplasm. Fortunately, these disorders are rare.
Hirsutism can be caused by abnormally high androgen levels or by hair follicles that are more sensitive to normal androgen levels. Therefore, increased hair growth often is observed in patients with endocrine disorders characterized by hyperandrogenism, which may be caused by abnormalities of the ovaries or the adrenal glands.
The physiologic mechanism proposed for androgenic activity consists of the following three stages:
Production of androgens by the adrenals and ovaries [1]
Androgen transport in the blood on carrier proteins (principally sex-hormone–binding globulin [SHBG])
Intracellular modification and binding to the androgen receptor
In short, central overproduction of androgen, increased peripheral conversion of androgen, decreased metabolism, and enhanced receptor binding are each potential causes of hirsutism. For circulating testosterone to exert its stimulatory effects on the hair follicle, it first must be converted into its more potent follicle-active metabolite, dihydrotestosterone. The enzyme, 5-alpha-reductase, which is found in the hair follicle, performs this conversion.
Overproduction of androgens results in an increased hair follicle size, hair fiber diameter, and duration of time hair follicles spend in the anagen (growth) phase. In addition to a change in hair quality and volume, oilier skin and hair may result from excess androgen secretion. The distribution of hair in women with high androgen levels is also altered. Excessive hair growth occurs in androgen-sensitive regions, but hair loss occurs on the scalp. [2]
The severity of hirsutism does not correlate directly with the level of increased circulating androgens because of individual differences in conversion to 5-alpha-reductase and androgen sensitivity of hair follicles.
Testosterone stimulates hair growth, increasing the size and intensifying the pigmentation of hair. Estrogens act in opposition, slowing growth and producing finer, lighter hairs. Progesterone has minimal effect on hair growth.
The amount of free testosterone—the biologically active androgen that, after conversion to dihydrotestosterone, causes hair growth—is regulated by SHBG. Lower levels of SHBG increase the availability of free testosterone. SHBG levels decrease in response to the following:
Exogenous androgens
Certain disorders that affect androgen levels, such as polycystic ovarian syndrome (PCOS) (see the image below)
Congenital or delayed-onset adrenal hyperplasia (see the image below)
Excess growth hormone
Conversely, SHBG levels increase with higher estrogen levels, such as the levels that occur during oral contraceptive therapy. The resultant increased SHBG levels lower the activity of circulating testosterone.
PCOS is a disorder that affects androgen levels. The most common cause of androgen excess and hirsutism is PCOS. [3] Virilization is minimal, and hirsutism is often prominent. Characteristic features include menstrual irregularities, dysmenorrhea, occasional glucose intolerance and hyperinsulinemia, and, often, obesity. The hyperinsulinemia is believed to hyperstimulate the ovaries into producing excess androgens. Women with PCOS may show other cutaneous manifestations of androgen excess in addition to hirsutism, such as recalcitrant acne, acanthosis nigricans, and alopecia on the crown area of the scalp (a pattern that contrasts with the bitemporal and vertex androgenic alopecia seen in men). See Polycystic Ovarian Syndrome for more information.
Hirsutism may also be seen in women with the following ovarian conditions, most of which are associated with virilization:
Luteoma of pregnancy
Arrhenoblastomas
Leydig cell tumors
Hilar cell tumors
Thecal cell tumors
Familial hirsutism is not associated with androgen excess. Familial hirsutism is both typical and natural in certain populations, such as in some women of Mediterranean or Middle Eastern ancestry. See the image below.
Drugs that can induce hirsutism by their inherent androgenic effects include dehydroepiandrosterone sulfate (DHEA-S), testosterone, danazol, and anabolic steroids. Currently used low-dose oral contraceptives are less likely to cause hirsutism than were previous formulations.
Drugs such as phenytoin, minoxidil, diazoxide, cyclosporine, streptomycin, psoralen, penicillamine, high-dose corticosteroids, metyrapone, phenothiazines, acetazolamide, and hexachlorobenzene presumably exert their effects independently of androgens. The exact mode of action of these drugs on hair follicles is not known, but the same mechanisms do not appear to be involved in all patients.
Drug-induced hirsutism can be distinguished from drug-induced hypertrichosis, in which a uniform growth of fine hair appears over extensive areas of the trunk, hands, and face and is unrelated to androgen-dependent hair growth.
CAH in children (ie, the classic form of adrenal hyperplasia) may cause hirsutism. These children may be born with ambiguous genitalia, symptoms of salt wasting, and failure to thrive. Additionally, they may develop masculine features. See Congenital Adrenal Hyperplasia for more information.
Late-onset CAH usually occurs as an incomplete version of CAH and affects approximately 1-5% of women who are hyperandrogenic. In patients with late-onset CAH, hirsutism (without salt-wasting symptoms) may not develop until adulthood.
Signs of virilization and menstrual irregularities may not be observed until puberty or adulthood. Patients have clinical features that resemble PCOS.
Hirsutism and oligomenorrhea suggest 21-hydroxylase deficiency (elevated 17-alpha-hydroxyprogesterone). Another uncommon disorder is 3-beta-, 11-hydroxysteroid dehydrogenase deficiency (elevated 3-beta-, 11-hydroxysteroid levels), which may result in early- or late-onset CAH. See 3-Beta-Hydroxysteroid Dehydrogenase Deficiency for more information.
Cushing syndrome is a noncongenital form of adrenal hyperplasia characterized by an excess of adrenal cortisol production. The excessive growth is predominantly vellus (non–androgen dependent) hair.
Less common but potentially serious disorders that may be associated with hirsutism include anorexia nervosa, acromegaly, hypothyroidism, hyperprolactinemia, and porphyria.
Idiopathic hirsutism or end-organ hirsutism occurs in a small proportion of women with hirsutism. Neither a familial form nor any detectable hormonal abnormality usually is diagnosed. Such patients have normal menses, normal-sized ovaries, no evidence of adrenal or ovarian tumors or dysfunction, and no significant elevations of plasma testosterone or androstenedione. Antiandrogen therapy may improve hirsutism in some idiopathic cases, which suggests that this form may be androgen induced. One theory is that many of these women may have mild or early PCOS and androgen levels in the upper-normal ranges. Eventually, idiopathic hirsutism probably may be recognized as a more subtle form of hypersecretion of hormones from the ovary or, possibly, the adrenal gland. A 2009 study found significant insulin resistance in nonobese patients with idiopathic hirsutism. [4]
United States
Hirsutism is common and is estimated to occur in 1 in 20 women of reproductive age.
International
Familial hirsutism is found most commonly in southern European and South Asian countries, in which it is considered to be a normal trait. Hirsutism indicative of underlying endocrinopathy varies from culture to culture, depending on the incidence of the various endocrinopathies in a particular society.
Familial hirsutism is noted most frequently in dark-skinned white persons. It is uncommon in sub-Saharan and African American blacks and is observed least commonly in East Asians and Native Americans.
The onset of hirsutism depends on its cause. Familial or ethnic hirsutism typically begins during puberty. Hirsutism resulting from congenital adrenal hyperplasia (CAH) begins early in childhood, while late-onset CAH and PCOS often have onset after puberty. The growth of facial hair commonly observed in postmenopausal women may be caused by unopposed androgen.
Hirsutism is a symptom, rather than a disease. Primarily, hirsutism is of cosmetic and psychological concern; however, it may indicate the presence of more serious associations, such as adrenal hyperplasia and ovarian tumors, particularly if it develops well after puberty. Prognosis of hirsutism depends on the underlying cause and the type of therapeutic intervention, if any.
If determined, explain to the patient the specific reason why she has hirsutism. In addition, explain the various therapeutic options available to her.
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Falsetti L, Gambera A, Legrenzi L, Iacobello C, Bugari G. Comparison of finasteride versus flutamide in the treatment of hirsutism. Eur J Endocrinol. 1999 Oct. 141(4):361-7. [Medline].
Moghetti P, Tosi F, Tosti A, et al. Comparison of spironolactone, flutamide, and finasteride efficacy in the treatment of hirsutism: a randomized, double blind, placebo-controlled trial. J Clin Endocrinol Metab. 2000 Jan. 85(1):89-94. [Medline].
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Hamzavi I, Tan E, Shapiro J, Lui H. A randomized bilateral vehicle-controlled study of eflornithine cream combined with laser treatment versus laser treatment alone for facial hirsutism in women. J Am Acad Dermatol. 2007 Jul. 57(1):54-9. [Medline].
Unfer V, Zacche M, Serafini A, Redaelli A, Papaleo E. [Treatment of hyperandrogenism and hyperinsulinemia in PCOS patients with essential amino acids. A pilot clinical study]. Minerva Ginecol. 2008 Oct. 60(5):363-8. [Medline].
Brown T. Updated Guidelines on Hirsutism in Premenopausal Women. Medscape News & Perspective. Available at https://www.medscape.com/viewarticle/893904. March 14, 2018; Accessed: April 13, 2018.
[Guideline] Martin KA, Anderson RR, Chang RJ, Ehrmann DA, Lobo RA, Murad MH, et al. Evaluation and Treatment of Hirsutism in Premenopausal Women: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2018 Mar 7. [Medline].
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Basil M Hantash, MD, PhD, MBA Medical Director, Advanced Skin Institute
Basil M Hantash, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for Dermatologic Surgery, Sigma Xi, Society for Investigative Dermatology
Disclosure: Nothing to disclose.
Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society
Disclosure: Nothing to disclose.
Lester F Libow, MD Dermatopathologist, South Texas Dermatopathology Laboratory
Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, Texas Medical Association
Disclosure: Nothing to disclose.
William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
Leonard Sperling, MD Chair, Professor, Department of Dermatology, Uniformed Services University of the Health Sciences
Leonard Sperling, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.
Herbert P Goodheart, MD Assistant Clinical Professor, Department of Dermatology, Mount Sinai Hospital
Disclosure: Nothing to disclose.
Bobby Y Reddy, MS University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Disclosure: Nothing to disclose.
Hendrik I Uyttendaele, MD, PhD Instructor, Department of Dermatology, Columbia Presbyterian Medical Center
Disclosure: Nothing to disclose.
Dermatologic Manifestations of Hirsutism
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