AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Background

Hirsutism is defined as the excessive growth of thick dark hair in locations where hair growth in women usually is minimal or absent. 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.

Pathophysiology

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 3 stages:

1. Production of androgens by the adrenals and ovaries
2. Androgen transport in the blood on carrier proteins (principally sex-hormone–binding globulin [SHBG])
3. 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.

The severity of hirsutism does not correlate with the level of increased circulating androgens because of individual differences in 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 Media File 1.
• Congenital or delayed-onset adrenal hyperplasia
• Cushing syndrome
• Obesity
• Hyperinsulinemia
• Hyperprolactinemia
• Excess growth hormone
• Hypothyroidism

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.

Frequency

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.

Mortality/Morbidity

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.

Race

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.

Age

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.

CLINICAL

Section 3 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

History

In women, hirsutism exceeding culturally normal levels can be as distressing an emotional problem as the loss of scalp hair. The onset of hirsutism can take one of several forms. For example, in women with familial hirsutism, it often appears during puberty. Hirsutism usually develops gradually in patients with PCOS and CAH. Hirsutism appears abruptly when an androgen-secreting tumor arises.

Physical

A woman with hirsutism has excess terminal hair in a masculine pattern, but note that hirsutism may be difficult to evaluate in women who have blond hair.

A quantitative method of measuring hair growth, the Ferriman-Gallwey model, allows for the determination of the severity of hirsutism by assessing the extent of hair growth in 9 key anatomic sites, as follows:  

• Face (particularly, moustache, beard, and temple areas; see Media File 2)
• Chest
• Areolae 
• Linea alba 
• Upper back 
• Lower back 
• Buttocks 
• Inner thighs 
• External genitalia

Other accompanying signs and symptoms may include some of the following:  

• Acanthosis nigricans
• Obesity 
• Pelvic mass 
• Signs or symptoms of virility 
• Signs or symptoms of Cushing syndrome 
• Acne 
• Alopecia

Causes

Ovarian causes of hirsutism

PCOS is a disorder that affects androgen levels. The most common cause of androgen excess and hirsutism is PCOS. 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  

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.

Drug-induced hirsutism  

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.

Adrenal causes of hirsutism  

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.

Other causes

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.

DIFFERENTIALS

Section 4 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Other Problems to be Considered

Hypertrichosis
Hurler syndrome and other mucopolysaccharidoses
Trisomy 18
Malnutrition
Anorexia nervosa
Hair growth (in sites of trauma and scarring)
Hyperinsulinemia

WORKUP

Section 5 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Lab Studies

After familial and drug-induced causes for hirsutism have been excluded, hirsutism resulting from androgen excess should be considered. Initial screening for total or free testosterone and DHEA-S often determines whether further testing is necessary. Testosterone and DHEA-S levels may provide clues to the source of excessive androgen production.

Serum testosterone

Whether total testosterone is a better screening test than free testosterone is controversial. The evaluation of total testosterone is less expensive and probably easier to interpret. However, free testosterone may be a more sensitive indicator of hormonal level abnormality.

Early morning testing is advised to measure testosterone levels. The upper limit of the reference range for total plasma testosterone levels varies by laboratory, but it is generally in the range of 70-90 ng/dL. Also note that testosterone levels vary during the different phases of the menstrual cycle by approximately 25%.

No direct correlation exists between the levels of testosterone and the degree of hirsutism, because hirsutism is caused by the action of dihydrotestosterone, which is the more potent testosterone metabolite. Elevated free serum testosterone levels (>80 ng/dL) are found in most women with anovulation and hirsutism. In most patients in whom the total testosterone level is greater than 200 ng/dL (>100 ng/dL in postmenopausal women), a tumor workup is indicated. This workup includes a pelvic examination and ultrasound imaging, which usually are adequate to diagnose PCOS. If the test results are negative, an adrenal computed tomography scan is performed.

In some patients who are hirsute, the DHEA-S level is elevated. Moderate elevations suggest an adrenal origin of the hirsutism. Normal levels of DHEA-S accompanied by high levels of testosterone indicate that the ovaries, and not the adrenals, are producing the excess androgen.

A tumor workup is indicated in most patients in whom the DHEA-S level is greater than 700 mcg/dL (400 mcg/dL in postmenopausal women). An increase of this magnitude usually results from adrenal hyperplasia rather than from the extremely rare adrenal carcinomas.

• Serum androstenedione
• • Androstenedione can originate in the adrenal glands or in the ovaries, and the level often is elevated in patients with hyperandrogenism.
  • A serum androstenedione level greater than 100 ng/dL suggests the presence of an ovarian or adrenal neoplasm.
• Luteinizing hormone and follicle-stimulating hormone: Often, in women with PCOS, luteinizing hormone (LH) levels are elevated and follicle-stimulating hormone (FSH) levels are depressed, which results in elevated LH/FSH ratios (>2 is common).
• 17-Hydroxyprogesterone 
• • The screening test for late-onset CAH is a measurement of morning 17-hydroxyprogesterone levels.
  • DHEA-S and 17-ketosteroids levels are normal or moderately elevated.
  • Testosterone and precursors of cortisol levels are elevated. Urinary 17-ketosteroid levels also are elevated slightly in patients with PCOS.
  • A 17-hydroxyprogesterone level greater than 800 ng/dL is diagnostic for 21-hydroxylase deficiency, the most common defect associated with CAH.
  • An intermediate 17-hydroxyprogesterone level (200-800 ng/dL per distribution of lesions) requires a dexamethasone suppression test, but  this level is normal in some women with adult 21-hydroxylase deficiency, and corticotropin stimulation may result in overdiagnosis of the syndrome. Also unclear is whether screening for adult-onset 21-hydroxylase deficiency improves patient outcome, because patients generally do well with empiric antiandrogen therapy, laser hair removal, or both.
  • If a patient is oligomenorrheic, PCOS is likely. LH, FSH, and prolactin testing suffer from problems with sensitivity and specificity. Testing seldom improves patient outcome.
• Urinary cortisol testing: A 24-hour urinary cortisol test should be performed if Cushing syndrome is suspected.

Imaging Studies

In patients with suspected PCOS or a possible adrenal or ovarian neoplasm, imaging studies of these organs may be required. Consult an endocrinologist or gynecologist for guidance.

Histologic Findings

If a biopsy is performed on a hirsute region, terminal hairs are found; however, a biopsy is not necessary to make the diagnosis.

TREATMENT

Section 6 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical Care

Most patients with medically significant hirsutism have PCOS, and the most important interventions are to address the risk of endometrial hyperplasia and cardiac risk factors. Treatment of the hirsutism itself is only necessary if the patient finds the excess hair cosmetically objectionable.

As an alternative to hair removal, simple bleaching of hair is an inexpensive method that works well when hirsutism is not too excessive. Bleaches lighten the color of the hair so that it is less noticeable.

Hair removal

Depilation

Depilatories remove hair from the surface of the skin. Depilatory methods include ordinary shaving and the use of chemicals, such as thioglycolic acid.

Shaving removes all hairs, but it is immediately followed by regrowth of hairs that were previously in anagen; as these hairs grow in, they produce rough stubble. No evidence suggests that shaving increases the rate or coarseness of subsequent hair growth. Most women, however, prefer not to shave their facial hair.

Chemical depilation may be best suited for treatment of large areas in patients who are unable to afford more expensive treatments, such as electrolysis and laser epilation. Chemical depilatories separate the hair from its follicle by reducing the sulfide bonds that are found in abundance in hairs. Irritant reactions and folliculitis may result.

Temporary epilation

Epilation involves the removal of the intact hair with its root. Plucking or tweezing is widely performed. This method may result in irritation, damage to the hair follicle, folliculitis, hyperpigmentation, and scarring.

Waxing entails applying melted wax to the skin. When the wax cools and sets, it is abruptly peeled off the skin, and embedded hair is removed with it. This method is painful and sometimes results in folliculitis. Repetitive waxing may produce miniaturization of hairs, and, over the long term, it may permanently reduce the number of hairs.

Certain natural sugars, long used in parts of the Middle East, are becoming popular in place of waxes. They appear to epilate as effectively as, but less traumatically than, waxes.

Threading, a method used in some Arab countries, is a technique in which cotton threads are used to pull out hairs by their roots. Home epilating devices that remove hair by a rotary or frictional method are available. Both methods may produce traumatic folliculitis.

Radiation therapy was a popular method of hair removal in the past. However, it has fallen out of favor and is no longer acceptable.

Permanent epilation 

Hair destruction by electrolysis, thermolysis, or a combination of both is performed with a fine, flexible electrical wire that produces an electrical current after it is introduced down the hair shaft. Thermolysis (diathermy) uses a high-frequency alternating current and is much faster than the traditional electrolysis method, which uses a direct galvanic current. Electrolysis and thermolysis are slow processes that can be used on all skin and hair colors, but multiple treatments are required. Electrolysis and thermolysis can be uncomfortable and may produce folliculitis, pseudofolliculitis, and postinflammatory pigmentary changes in the skin.

Lasers can treat larger areas and can do so faster than electrolysis and thermolysis. They have skin-cooling mechanisms that minimize epidermal destruction during the procedure. Skin and hair color often determine whether a laser should be used. Lasers are most effective on dark hairs on fair-skinned people. In such patients, lighter skin does not compete with darker hairs for the laser, which selectively targets the pigment, melanin. In dark-skinned people, a newer approach that delivers more energy to the hairs over a longer period may prove safe and effective.

As with electrolysis and thermolysis, multiple treatments are necessary for long-term hair destruction. Folliculitis, pseudofolliculitis, discomfort, and pigmentary changes may result from laser therapy. It remains to be proved whether lasers are more effective in permanent hair removal than the more traditional methods. They are certainly more costly.

Pharmacologic treatment

In general, pharmacologic treatments for hirsutism are selected based on the underlying cause. Medications (antiandrogens) are often administered while cosmetic hair removal techniques are being used. All these drugs must be given continuously because when they are stopped, androgens revert to their former levels. The following medications are all absolutely contraindicated for use during pregnancy because of the risk of feminization of a male fetus:

• Oral contraceptives - Ovarian suppression
• Spironolactone, flutamide, and cyproterone acetate - Androgen receptor blockade and inhibition
• Oral corticosteroids - Adrenal suppression
• Finasteride - 5-Alpha-reductase inhibition

These agents can be used singly or in combination.

New treatments

Eflornithine hydrochloride cream 13.9% (Vaniqa) is a prescription topical cream that acts as a growth inhibitor, not a depilatory. The agent inhibits ornithine decarboxylase, an enzyme required for hair growth. It is indicated for the reduction of unwanted facial hair in women. Continued twice-daily use for at least 4-8 weeks is necessary before effectiveness is noted.

Metformin (Glucophage) reduces insulin levels, and this change, in turn, reduces the ovarian testosterone levels by competitive inhibition of the ovarian insulin receptors. This drug is effective in treating hirsutism in women with PCOS.

Management depends on the underlying cause. For example, non–androgen-dependent excess hair, such as hypertrichosis, is treated primarily with physical hair removal methods. In contrast, patients with androgen-dependent hirsutism require a combination of physical hair removal and medical antiandrogen therapy.

Hormonal treatment of hirsutism resulting from androgen excess is long term, because the sources of excessive androgen rarely can be eliminated permanently. Consequently, the patient must understand that discontinuation of antiandrogen therapy usually results in the recurrence of hirsutism.

Surgical Care

If virilizing adrenal or ovarian tumors are found to be responsible for excess body hair, removal of the tumor often alleviates the condition. Unfortunately, many tumors are malignant and fatal.

Diet

Although many women with hirsutism are obese, the relationship of adipose tissue and hair growth is undefined. Clinically, it is recognized although undocumented that weight loss in women with hirsutism who are obese and have menstrual irregularities (eg, women with PCOS) may result in the regulation of menses and diminution of hirsutism.

MEDICATION

Section 7 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Usually, pharmacologic treatments for hirsutism are selected based on the underlying cause. Medications (antiandrogens) often are administered simultaneously while cosmetic hair removal techniques are performed. All of these drugs must be administered continuously, because when they are discontinued, androgens revert to their former levels. These medications are absolutely contraindicated for use during pregnancy, because a risk exists of feminization of a male fetus.

Oral contraceptives are often the initial treatment for hirsutism caused by ovarian hyperandrogenism and idiopathic hirsutism. Oral contraceptives also help enhance antihirsutism effects and prevent adverse effects of menstrual irregularity caused by spironolactone and other antiandrogen therapy. Finasteride, a 5-alpha reductase inhibitor approved for use in benign prostatic hypertrophy and in male-pattern alopecia, blocks conversion of testosterone to its more active metabolite, dihydrotestosterone. Currently, finasteride is being evaluated for use in hormonal treatment of acne accompanied by hirsutism. For androgen-excess syndromes, such as PCOS, the following medications are used, often in combination with oral contraceptives.

Drug Category: Antihypertensives

May have properties that improve symptoms of hirsutism.

Drug Category: Antiandrogens

Block active androgen production.

Drug Name	Cyproterone (Diane-35)
Description	Steroidal androgen-receptor blocker and potent progestin available in the United States only for compassionate use. Acts as competitive inhibitor of testosterone and DHEA-S at level of androgen receptors. Powerful antiandrogen usually administered with estrogens to maintain regular menstruation and to prevent conception. Contains a combination of cyproterone acetate and ethinyl estradiol.
Adult Dose	50-100 mg/d PO, administered with 0.05 mg/d of ethinyl estradiol
Pediatric Dose	Not established
Contraindications	Documented hypersensitivity
Interactions	None reported
Pregnancy	X - Contraindicated; benefit does not outweigh risk
Precautions	Adverse effects include weight gain, fatigue, loss of libido, mastodynia, nausea, headaches, and depression

Drug Category: Dermatologic agents

May inhibit cell growth and proliferation.

Drug Category: Glucocorticoids

For classic CAH, systemic corticosteroids are used. Corticosteroids are effective in reducing serum androgen levels, but contradictory reports exist regarding their therapeutic effect on hair growth.

For late-onset CAH and PCOS, oral contraceptives and spironolactone are used. In addition, small doses of dexamethasone may be helpful in reducing androgen production in late-onset CAH; however, changes suggesting Cushing disease may develop in patients receiving long-term corticosteroids.

Drug Name	Prednisone (Deltasone, Sterapred, Orasone)
Description	May decrease immune reactions by reversing increased capillary permeability and suppressing PMN activity.
Adult Dose	5-7 mg PO qd
Pediatric Dose	4-5 mg/m2/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2 wk as symptoms resolve
Contraindications	Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective-tissue infections; fungal or tubercular skin infections
Interactions	Coadministration with estrogens may decrease clearance; when used with digoxin, digitalis toxicity secondary to hypokalemia may increase; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Abrupt discontinuation may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur

Drug Category: Antidiabetic agents

Insulin-sensitizing agents appear to improve symptoms of hirsutism.

FOLLOW-UP

Section 8 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Further Outpatient Care

Outpatient follow-up care depends on the cause of hirsutism. Idiopathic or familial hirsutism can be monitored and treated, if desired, by a dermatologist or dermatologic surgeon. Women with hormonal or gynecologic causes of hirsutism should be monitored closely by an endocrinologist, gynecologist, or both.

Complications

Complications vary depending on the etiology of the hirsutism. Complications may result from the adverse effects of hormonal or surgical treatment.

Prognosis

Prognosis of hirsutism depends on the underlying cause and the type of therapeutic intervention, if any.

Patient Education

If determined, explain to the patient the specific reason why she has hirsutism. In addition, explain the various therapeutic options available to her.

MISCELLANEOUS

Section 9 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Medical/Legal Pitfalls

Failure to recognize the association of hirsutism with a major medical disorder or the possibility of missing an ovarian or adrenal neoplasm are the primary medicolegal pitfalls.

ACKNOWLEDGMENTS

Section 10 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous Editor-in-Chief, William James, MD, to the development and writing of this article.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Media file 1:  Idiopathic hirsutism in an elderly woman.
	View Full Size Image
Media type:  Photo

Media file 2:  The patient has late-onset congenital adrenal hyperplasia. She has clinical features similar to those found in polycystic ovarian syndrome, including hirsutism, acne, obesity, diabetes, and menstrual irregularities.
	View Full Size Image
Media type:  Photo

Media file 3:  The photograph depicts hirsutism in a young woman with polycystic ovarian syndrome. Note the acne lesions and excessive hair on her face and neck.
	View Full Size Image
Media type:  Photo

Media file 4:  The photograph depicts familial hirsutism in a Pakistani woman.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

• Berek JS, Hillard PA, Adashi EY. Novak's Gynecology. 12^th ed. Baltimore, Md: Williams & Wilkins; 1996:799-801; 833-52.
• Bergfeld WF. Hirsutism in women. Effective therapy that is safe for long-term use. Postgrad Med. Jun 2000;107(7):93-4, 99-104. [Medline].
• Clarke Secor, RM. Hirsutism in women. Clin Rev. 2000;10(2):61-72.
• Androgen excess. In: Scott JR, Disaia PJ, et al, eds. Danforth's Obstetrics and Gynecology. 7^th ed. Philadelphia, Pa: Lippincott-Raven; 1994:681-93.
• de Berker D. The diagnosis and treatment of hirsutism. Practitioner. Jun 1999;243(1599):493-8, 501. [Medline].
• Diamanti-Kandarakis E, Bartzis MI, Zapanti ED, Spina GG, Filandra FA, Tsianateli TC, et al. Polymorphism T-->C (-34 bp) of gene CYP17 promoter in Greek patients with polycystic ovary syndrome. Fertil Steril. Mar 1999;71(3):431-5. [Medline].
• Falsetti L, Gambera A, Legrenzi L, Iacobello C, Bugari G. Comparison of finasteride versus flutamide in the treatment of hirsutism. Eur J Endocrinol. Oct 1999;141(4):361-7. [Medline].
• Fauci AS, Braunwald E, Hauser SL, et al, eds. Harrison's Principles of Internal Medicine. 14^th ed. New York, NY: McGraw-Hill; 1998:292-4.
• Friedberg IM, Eisen AZ, Wolff K, eds. Fitzpatrick's Dermatology in General Medicine. Vol 1. 5^th ed. New York, NY: McGraw-Hill; 1999:746-9.
• 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. Jul 2007;57(1):54-9. [Medline].
• Marchell N, Alster T. Evaluation of hair removal methods. Aesthetic Surg Cosmet Surg. 1999;1(1):3-11.
• Moghetti P, Toscano V. Treatment of hirsutism and acne in hyperandrogenism. Best Pract Res Clin Endocrinol Metab. Jun 2006;20(2):221-34. [Medline].
• Moghetti P, Tosi F, Tosti A, Negri C, Misciali C, Perrone F, 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. Jan 2000;85(1):89-94. [Medline].
• Patel SR, Korytkowski M. Polycystic ovarian syndrome. Women Health Prim Care. 2000;3(1):55-69.
• Pugeat M, Ducluzeau PH. Insulin resistance, polycystic ovary syndrome and metformin. Drugs. 1999;58 Suppl 1:41-6; discussion 75-82. [Medline].
• Sperling LC, Heimer WL 2nd. Androgen biology as a basis for the diagnosis and treatment of androgenic disorders in women. I. J Am Acad Dermatol. May 1993;28(5 Pt 1):669-83. [Medline].
• Sperling LC, Heimer WL 2nd. Androgen biology as a basis for the diagnosis and treatment of androgenic disorders in women. II. J Am Acad Dermatol. Jun 1993;28(6):901-16. [Medline].
• Waggoner W, Boots LR, Azziz R. Total testosterone and DHEAS levels as predictors of androgen-secreting neoplasms: a populational study. Gynecol Endocrinol. Dec 1999;13(6):394-400. [Medline].
• Watts J. Understanding the causes and management of hirsutism. Nurs Times. Feb 21-27 2006;102(8):26-8. [Medline].

Article Last Updated: Jan 7, 2008