Dermatologic Manifestations of Hirsutism

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:

1. Production of androgens by the adrenals and ovaries[1]

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.

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)

  The photograph depicts hirsutism in a young woman with polycystic ovarian syndrome. Note the acne lesions and excessive hair on her face and neck.

• Congenital or delayed-onset adrenal hyperplasia (see the image below)

  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.

• 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.

Ovarian causes of hirsutism

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

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.

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. A 2009 study found significant insulin resistance in nonobese patients with idiopathic hirsutism.[4]

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.

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.

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.

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.

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 the image below)

  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.

• 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

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

A 2008 cohort study found a high prevalence of eating disorders such as bulimia nervosa in women with hirsutism caused by polycystic ovarian syndrome (PCOS). Furthermore, women with hirsutism had high levels of depression, anxiety, low self-esteem, and poor social adjustment. Although a causal association remains unclear, hirsutism appears to be associated with eating disorders and other severe social and psychological conditions. Therefore, physicians treating women with hirsutism should consider screening these patients for psychiatric comorbidities during the management of their care.[5]

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 dehydroepiandrosterone sulfate (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 polycystic ovarian syndrome (PCOS). If the test results are negative, an adrenal computed tomography scan is performed.

Serum DHEA-S

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.

Other laboratory tests

If a woman shows severe or rapidly progressive hirsutism or she shows signs or symptoms of virilism (eg, infrequent or absent menses, acne, deepening of the voice, male-pattern balding, increased muscle mass, increased libido, clitoral hypertrophy), consider performing the following additional tests:

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.

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.

Quantification of hirsutism

The definition of hirsutism suggests that the amount of terminal hair needs to be determined before confirming the diagnosis. In 1981, Hatch and coworkers established the current criterion standard for quantification of hirsutism, the modified Ferriman-Gallwey (mFG) score, which is a revised method of the original standard developed by S.M. Garn, D. Ferriman, J.D. Gallwey, and E. Moncada-Lorenzo.[6] The mFG score approximates the amount of terminal hair in 9 regions of the female body: upper lip, chin, chest, abdominal region above and below the navel, upper and lower back, arms, and thighs, and then it provides a score from 0 (absent) to 4 (complete coverage) to each of these areas, for a total score ranging from 0 to 36. Hirsutism is characterized as mild within scores up to 15, moderate from 16-25, and severe above 25.[6]

The scoring system allows for clinicians and researchers to share a common language in defining the degree of hirsutism. However, a significant limitation of this method lies in the fact that it relies on a subjective nature of assessment.

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

Most patients with medically significant hirsutism have polycystic ovarian syndrome (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.[7]

Pharmacologic treatment

In general, pharmacologic treatments[8] 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:

• Estrogen-progestin oral contraceptives - Ovarian suppression

• Antiandrogens (eg, spironolactone, flutamide) - Androgen receptor blockade and inhibition[9, 10]

• Oral corticosteroids - Adrenal suppression

• Finasteride - 5-Alpha-reductase inhibition

These agents can be used singly or in combination.[11]

Newer 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. It can be combined with laser treatments for enhanced effects.[12]

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.

See Laser-Assisted Hair Removal and Nonlaser Hair Removal.

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.

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.

A 2008 study found that women with PCOS experienced a significant decrease in hirsutism after undergoing 16 weeks of therapy with oral essential amino acids. This therapy also resulted in a significant decrease in the levels of fasting insulin, luteinizing hormone, follicle-stimulating hormone, and total testosterone. This research suggests that a diet supplemented with essential amino acids may reduce hirsutism in patients with PCOS.[13]

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.

The Endocrine Society has released new guidelines on evaluation and treatment of hirsutism in premenopausal women.[14, 15]

Test for elevated androgen levels is recommended in all women with an abnormal hirsutism score. Guidelines suggest against testing for elevated androgen levels in eumenorrheic women with unwanted local hair growth (ie, in the absence of an abnormal hirsutism score).

For most women with patient-important hirsutism despite cosmetic measures (shaving, plucking, waxing), start with pharmacologic therapy and add direct hair removal methods (electrolysis, photoepilation) for those who desire additional cosmetic benefit. For women with mild hirsutism and no evidence of an endocrine disorder, either pharmacologic therapy or direct hair removal methods are suggested.

For pharmacologic therapy, oral combined estrogen–progestin contraceptives are suggested for the majority of women, with the addition of an antiandrogen agent after 6 months if the response is suboptimal. Guidelines recommend against antiandrogen monotherapy unless adequate contraception is used. They suggest against using insulin-lowering drugs.

For most women who choose hair removal therapy, laser epilation/photoepilation is suggested.

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.

Class Summary

May have properties that improve symptoms of hirsutism.

Spironolactone (Aldactone)

Spironolactone is effective for hormonal acne and hirsutism. It may cause menstrual irregularities (usually metrorrhagia). Normal menses may resume with a reduction of dosage. Do not administer in patients already receiving antihypertensive medications, cardiac drugs, or diuretics. Spironolactone is not recommended in patients with renal insufficiency.

Class Summary

Block active androgen production.

Flutamide (Eulexin)

Flutamide is a nonsteroidal antiandrogen that inhibits androgen uptake or binding of androgen to target tissues. It is approved for the treatment of prostate cancer.

Class Summary

May inhibit cell growth and proliferation.

Eflornithine cream (Vaniqa)

Eflornithine cream is a prescription topical cream that acts as a growth inhibitor, not a depilatory. It inhibits ornithine decarboxylase, an enzyme required for hair growth. It reportedly takes up to 2 months to work in approximately 30% of patients.

Class Summary

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.

Dexamethasone (Decadron, Dexasone)

Dexamethasone decreases immune reactions by suppressing the migration of PMN leukocytes and reducing capillary permeability.

Prednisone (Deltasone, Sterapred, Orasone)

Prednisone may decrease immune reactions by reversing increased capillary permeability and suppressing PMN activity.

Class Summary

Insulin-sensitizing agents appear to improve symptoms of hirsutism.

Metformin (Glucophage)

Patients with a clinical diagnosis of persistent anovulation who wish to become pregnant may benefit from metformin. It is effective in treating hirsutism in women with PCOS. Women with PCOS also often receive oral contraceptives and/or spironolactone. If PCOS primarily is considered to be a metabolic syndrome of insulin resistance, perhaps first-line treatment should be with an insulin-sensitizing agent such as metformin.