Background: Although hirsutism
is broadly defined as excessive hairiness, the common clinical use of the term
is in reference to women with excess growth of terminal hair in a male pattern.
In this sense, hirsutism is one of the most common endocrine disorders,
affecting approximately 10% of women in the US. In these women, the hairiness
implies the presence of abnormal androgen action, which may represent a serious
or, more likely, a nonserious medical problem. Regardless of the etiology,
hirsutism can produce mental trauma and emotional anguish. Even mild cases of
hirsutism may be viewed by the patient and others as a presumptive loss of
femininity. In more severe cases, it can be a cosmetic catastrophe. The major
objectives in the management of hirsutism are to rule out a serious underlying
medical condition and to devise a plan of treatment.
Pathophysiology: Both hormones and the intrinsic
characteristics of the hair follicle determine the quality of hair growth.
Vellus hairs are fine, unpigmented hairs that cover most of the body before
puberty. Pubertal androgens promote the conversion of these vellus hairs to
coarser pigmented terminal hairs. The level and duration of exposure to
androgens, the local 5 alpha-reductase activity, and the intrinsic sensitivity
of the hair follicle to androgen action determine the extent of conversion from
vellus to terminal hair. Some terminal-hair growth, however, is
androgen-independent, eg, scalp, eye brows, and lashes.
The development of terminal hair or reversion back to a vellus pattern may
not immediately be evident because of the characteristics of the hair cycle.
This cycle has 2 phases that include active hair growth (anagen phase) and a
resting period (telogen phase), which follows the anagen phase. During the
resting period, the hair shaft separates from the dermal papillae at the
follicle base and no further growth takes place. Eventually, growth restarts and
the old hair is pushed out by the new hair shaft formed by the reactivated
papillae. The cycle may take months to complete, and this causes a delay in
hair-growth response to changes in the androgen milieu.
Dihydrotestosterone is the androgen that acts on the hair follicle to produce
terminal hair. This hormone is derived from both the blood stream and local
conversion of a precursor, testosterone. The local production of
dihydrotestosterone is determined by 5 alpha-reductase activity in the skin.
Differences in the activity of this enzyme may explain why women with the same
plasma levels of testosterone can have different degrees of hirsutism.
- In the US: Hirsutism affects approximately 10% of women
in the US.
- Internationally: The prevalence rates of hirsutism in
northern Europe are similar to those in the US; in other places they are not
known with certainty.
Mortality/Morbidity: The mortality and morbidity of
hirsutism are determined by the underlying cause. The majority of women with
idiopathic hirsutism have no associated mortality or morbidity. On the other
extreme, a small number of women may have malignant disease with a grave
Race: Ethnic origin has a large effect on terminal hair
growth in normal women. Northern, fair-skinned Europeans have the least terminal
hair, whereas southern, dark-skinned Mediterranean women have the greatest
amount of terminal hair. The difference in the racial patterns of normal
terminal hair growth may be related to genetic differences of 5 alpha-reductase
activity in the skin. With the exception of congenital adrenal hyperplasia (CAH),
the prevalence of diseases causing hyperandrogenism and hirsutism has not been
shown to be different among races.
Sex: As a medical problem, hirsutism predominates in women.
While hirsutism can occur in men, it is more difficult to recognize because of
the wide variability of healthy male terminal-hair growth. Hirsutism in
prepubertal children occurs equally in both sexes, usually is a sign of
precocious puberty, and may signify a serious underlying disease. This
discussion, however, focuses on adult women.
Age: The age of onset of hirsutism depends on the etiology.
- Most forms of nonneoplastic hirsutism become evident around puberty. This
includes polycystic ovary syndrome (PCOS), CAH, and idiopathic hirsutism.
- Hirsutism also may develop after weight gain and cessation of the use of
oral contraceptives in young women.
- Normally, terminal-hair growth becomes apparent after adrenarche and
accelerates after puberty. Terminal hair continues to develop gradually in
healthy women, until after menopause when loss of ovarian androgen leads to a
loss of hair.
- Rapidly worsening hirsutism, especially in older women, should raise the
suspicion of an androgen-secreting tumor.
History: An accurate history of the
patient’s onset of hirsutism and developmental milestones can be helpful in the
- Idiopathic hirsutism and the other less-serious causes of hirsutism
usually begin at puberty.
- Conversely, hirsutism occurring in middle-aged or older women should
suggest an adrenal or ovarian tumor.
- A patient with a family history of hirsutism is consistent with CAH;
however, idiopathic hirsutism and PCOS can also be familial.
- Severity and rapidity of progression of the hirsutism
- The history of a benign form of hirsutism usually is characterized by
pubertal onset with slow progression over many years.
- When a history of rapid severe hirsutism or other signs of virilization
is obtained, an androgen-secreting tumor is a possibility.
- Because the development of pubic hair depends on adrenal androgens,
early development points toward CAH. In contrast, ovarian hyperandrogenism
is associated with normal adrenarche and delayed menarche or irregular
Physical: The most important goal in
the clinical evaluation of a patient with hirsutism is to rule out significant
underlying disease. To do this, seek to understand the cause of hyperandrogenism,
if this is present.
- Excess androgens either can be from an exogenous or endogenous source.
- Exogenous androgens usually can be elicited by history; however,
surreptitious androgen use has been reported in women athletes, especially
those at a high level of competition.
- Endogenous androgens originate from 1 of 2 sources, either the adrenal
cortex or the ovary. Therefore, the evaluation of androgen excess can focus
on disorders of these 2 glands. The principal possibilities are tumors of
the ovary or the adrenal cortex, Cushing syndrome, CAH, and PCOS. Idiopathic
hirsutism is the most common etiology, but it is a diagnosis of exclusion,
so seek other causes first.
- The initial task in evaluating hirsutism on physical examination is to
quantitate the disorder. The task requires that terminal hair, which is
dependent on androgen, be differentiated from vellus hair, which is androgen
- As mentioned above, vellus hair is fine, soft, and nonpigmented. An
excess of vellus hair, called hypertrichosis, is associated with metabolic
disorders, such as hyperthyroidism, anorexia nervosa, and porphyria, and
with some medications (eg, phenytoin, diazoxide, minoxidil, glucocorticoids,
- By contrast, terminal hair is coarse, curly, and pigmented. Because
small amounts of terminal hair are normal in women, quantitation is
- The best method of quantitation employs the Ferriman and Gallway scale. In
this approach, hair growth is judged in each of 11 androgen-sensitive areas
(see Picture 1).
- The grade for each area ranges from 0 (no terminal hair) to 4 (frankly
- Areas such as the axilla and pubis are not included because
terminal-hair growth occurs in these places at normal androgen levels in
- The total score correlates roughly with the elevation of androgen
levels. A woman with a score of 8 or more is considered to have hirsutism.
The majority of women seeking medical attention for the disorder have scores
of 15 or more.
- In women with moderate to severe hirsutism (score >15), seek additional
signs of hyperandrogenism including temporal hair recession, oily skin,
masculine voice, well-developed musculature, enlargement of the clitoris (>35
mm2 in surface area), irregular menses, and psychological changes
(see Picture 2).
- The degree to which these clinical factors are present suggests the level
of androgen overproduction and, thus, determines the degree of suspicion of an
- The extent of evaluation for the cause of hirsutism is greater in women
with more severe clinical evidence of masculinization.
- A good abdominal and pelvic examination is important in patients with
hirsutism because more than one half of androgen-secreting adrenal and ovarian
tumors are palpable.
- Examine the skin for acanthosis nigricans, a manifestation of insulin
- These patients usually are obese and are thought to be at increased risk
for atherosclerosis and coronary heart disease.
Causes: Multiple diseases can cause hyperandrogenism and
hirsutism (see Picture 3).
- Adrenal and ovarian tumors: Adrenocortical tumors in patients presenting
with hirsutism almost always are malignant. They usually are large and are
associated with a very poor prognosis. Ovarian tumors may also be malignant
and the threat can be serious.
- Androgen-secreting ovarian tumors are a less-serious threat. The most
common among them, accounting for fewer than 1% of all ovarian tumors, is
arrhenoblastoma. In this neoplasm, serum testosterone always is elevated,
and most patients have amenorrhea and a palpable ovarian mass.
- Gonadoblastomas usually occur in younger persons (aged 10-30 y) who are
genetic males with female external genitalia. Nearly one half of these
tumors are malignant, and many are bilateral. Pelvic examination is abnormal
because internal female genitalia are absent.
- Lipoid cell tumors are of 2 histologic types, with adrenal-like cells in
patients who are younger and hilar or Leydiglike cells in patients who are
older. These tumors usually are palpable, but they seldom are malignant.
Ovarian tumors, even less often encountered, include dysgerminomas, Brenner
tumors, and cystic granulose-theca tumors.
- Polycystic ovary syndrome: This syndrome is the most common ovarian
disorder associated with hirsutism. Although the cause of PCOS is not known,
the etiology is speculated to be multifactorial. By definition, polycystic
ovaries have 20 or more subcapsular follicles, ranging from about 1-15 mm in
diameter. The follicles are at various states of atresia, and hyperplasia of
the theca interna, the anatomic source of ovarian androgens, is present. The
basic abnormalities in PCOS, however, are functional rather than anatomic in
nature. In particular, levels of luteinizing hormone (LH) are tonically
elevated (with LH levels higher than those of follicle-stimulating hormone [FSH]).
- Many women with PCOS have insulin resistance manifest by acanthosis
nigricans and elevated plasma insulin levels. Increased insulin levels have
been speculated to possibly stimulate androgen production from the ovarian
theca interna cells. The importance of insulin resistance is emphasized by
the therapeutic effect of insulin-sensitizing medications (eg, metformin,
thiazolidinediones), which restore normal ovarian androgen production and
- PCOS usually begins at puberty. The incidence has been estimated to be
about 5% among adolescent girls and adult women in the US. As noted, the
characteristic endocrine abnormality is an elevation in plasma free
testosterone that is not suppressed by dexamethasone; however, as many as
50% of patients also show abnormal adrenal androgen secretion.
- Cushing syndrome: In most instances, Cushing syndrome is caused by
glucocorticoid therapy. Because pure glucocorticoids have no androgenic
activity, the treatment rarely produces hirsutism. Instead, glucocorticoid
therapy is one of the causes of hypertrichosis (see
resulting in vellus hair growth, especially on the face. Thus, excess growth
of terminal hair in a patient with the clinical stigmata of Cushing syndrome
suggests that the syndrome has an endogenous origin—a pituitary tumor secreting
adrenocorticotrophin (ACTH), an adrenal tumor secreting both cortisol and
androgens, or an ectopic ACTH-secreting tumor. The most likely one of these
possibilities is the pituitary tumor. As noted, Cushing syndrome as a cause of
hirsutism is diagnosed by demonstrating that dexamethasone fails to suppress
both androgens and cortisol.
- Congenital adrenal hyperplasia: CAH actually is a family of defects in 1
of 5 enzymes responsible for the biosynthesis of cortisol. (The resulting
cortisol deficiency heightens the secretion of ACTH and thereby leads to
adrenal-cell proliferation.) Only 3 of these defects, however, can produce
hirsutism?1-hydroxylase (most frequent), 3 beta-hydroxysteroid dehydrogenase
(less frequent), and 11 beta-hydroxylase deficiency (least frequent).
- If CAH is suspected, an ACTH-stimulation test is indicated, which
constitutes a search for exaggerated quantities of the precursors of
cortisol. The stimulation test is required because baseline elevation of
these steroids may not be out of the normal range. Hyperandrogenism in CAH
can cause infertility, but dexamethasone therapy in this setting may induce
ovulation. Two important reasons for diagnosing CAH are that specific
therapy is available and that genetic counseling may be necessary.
- Idiopathic hirsutism: In this diagnosis, made by exclusion, the patient's
hirsutism is not caused by well-defined abnormalities such as an
androgen-secreting tumor or CAH. The spectrum of clinical presentations ranges
from normal menses and mild hirsutism to amenorrhea and signs of virilization,
and testosterone levels range from normal to frankly elevated. The hirsutism
usually begins at puberty. The disorder often is familial and may be
associated with obesity and insulin resistance.
Some classification schemes distinguish patients with elevated adrenal
androgens (DHEAS); in these cases, the disorder is called idiopathic adrenal
hyperandrogenism. Some patients with idiopathic hirsutism have normal plasma
androgen levels. As noted previously, the mechanism underlying the hirsutism
in these patients may be an increase in androgen sensitivity or in 5 alpha-reductase
activity in the skin. Increased activity of the enzyme has been demonstrated
by skin biopsy and by elevated urinary levels of dihydrotestosterone
metabolites; however, tests for 5 alpha-reductase activity presently have
found use only in research.
C-11 Hydroxylase Deficiency
C-17 Hydroxylase Deficiency
Malignant Lesions of the
Ovarian Polycystic Disease
Other Problems to be Considered:
Androgen-secreting adrenal tumors
Androgen-secreting ovarian tumors
Congenital adrenal hyperplasia
- Laboratory studies in hirsutism serve both to confirm the clinical
impression of hyperandrogenism and to identify the source of excess androgens,
either adrenal or ovarian. The work-up described in Picture 4 uses two visits,
a baseline evaluation followed by a two-week dexamethasone treatment period.
Specific discussion of the testing is below.
- Testosterone: The most important assay is of serum testosterone, the
major circulating androgen. If the results from testing the total serum
testosterone are normal, measure the free serum level because
hyperandrogenism (and insulin resistance, if present) decreases sex
steroid-binding globulin, so that the unbound, biologically active
testosterone moiety may be elevated, even if the total level is
unremarkable. Extremely high testosterone levels are likely to be associated
with adrenal or ovarian tumors, whereas very mild elevations are found in
idiopathic and benign etiologies. Indeed, in idiopathic hirsutism, the
results from testing androgen levels often are normal. In some of these
women, hirsutism is thought to be caused by increased skin sensitivity to
androgen or by increased skin 5 alpha-reductase activity. As mentioned
above, this enzyme is located in the skin near the hair follicle, and it
converts plasma testosterone into the androgen metabolite
- Dehydroepiandrosterone sulfate: Because testosterone can originate in
either the adrenal cortex or the ovary, an elevated testosterone level does
not reveal the gland of origin. Accordingly, measurement of elevated plasma
levels of DHEAS, an androgen synthesized almost exclusively by the adrenal
cortex, can indicate excess adrenal function. Elevations in both
testosterone and DHEAS suggest an adrenal origin, whereas an isolated
testosterone elevation indicates an ovarian source.
- Dexamethasone suppression (see
Laboratory testing of testosterone (free or total) and DHEAS can be
performed on the initial visit. At the same time, a diagnostic trial of
dexamethasone therapy for 7-14 days can be initiated to help exclude
ACTH-dependent hirsutism (see
When the patient returns, free testosterone, DHEAS, and plasma cortisol are
measured. Dexamethasone-mediated suppression of androgens is seen in healthy
women who do not have hirsutism and also in those with CAH and idiopathic
- Adrenocorticotrophin stimulation: An ACTH-stimulation test (250 mcg for
30 min) can differentiate between these diagnoses because CAH produces
abnormal findings (elevations in metabolic precursors of cortisol).
- CAH causing hirsutism is due to one of 3 cortisol biosynthetic defects,
ie, 21-hydroxylase deficiency, 3 beta-hydroxysteroid dehydrogenase, or 11
- Because 21-hydroxylase deficiency accounts for the vast majority of
cases of CAH (approximately 90%), the discussion is focused on this
diagnosis. Investigate possible 21-hydroxylase deficiency by measurement of
plasma 17-hydroxyprogesterone obtained between 0700 and 0900 hours. Values
less than 7 nmol/L exclude the diagnosis, and values greater than 45 nmol/L
(in women who are nongestational) confirm 21-hydroxylase deficiency. When
basal values of 17-hydroxyprogesterone are between 7 and 45 nmol/L, an
ACTH-stimulated concentration of greater than 45 nmol/L also is diagnostic.
- Although elevated basal plasma 17-hydroxyprogesterone levels (as high as
17 nmol/L) may be present during the luteal phase of the menstrual cycle and
in PCOS, ACTH-stimulated increments are blunted.
- Cortisol suppression: Investigation of subnormal dexamethasone
suppression of androgens can be guided by the patient' s cortisol level,
without need for an ACTH-stimulation test. Polycystic ovary disease and
adrenal and ovarian tumors are associated with normal suppression of
cortisol by dexamethasone, whereas cortisol levels in patients with Cushing
syndrome are not suppressed.
- Women with hirsutism and amenorrhea of unknown cause should have a serum
prolactin or FSH test to evaluate for either a prolactinoma or ovarian
- Women with hirsutism, PCOS, obesity, or acanthosis nigricans may have
insulin resistance, and screening for diabetes and hyperlipidemia is
- If indicated by clinical evaluation and laboratory testing, perform
ovarian ultrasonography and adrenal computed tomography or magnetic resonance
imaging to evaluate for either ovarian or adrenal sources of androgen
Medical Care: The treatment of
hirsutism begins with a careful explanation to the patient about the cause of
her problem and with reassurance that she is not losing her femininity. Then,
direct intervention, if possible, at the underlying disorder. If hirsutism
persists (or the patient has idiopathic hirsutism), other cosmetic or systemic
treatment may be necessary. In some cases, cosmetic measures may be sufficient.
In others, the slow progress of systemic therapy may necessitate more immediate
cosmetic treatment. The most effective strategy is to combine systemic therapy,
which has a slow onset of effectiveness, with mechanical depilation (shaving,
plucking, waxing, and depilatory creams).
Hirsutism requires a careful and systematic clinical evaluation coupled with
a rational approach to treatment. Throughout this process, the patient must
understand that even though diagnostic testing can be time consuming (and even
inconclusive), it sometimes is essential for determining an effective
intervention. In other cases, counseling and education may be all that is
needed. For the patient who desires treatment, a wide variety of pharmacologic
strategies can be followed. Informing the patient that current systemic therapy
is imperfect is important. Furthermore, none of the drugs used to treat
hirsutism have Food and Drug Administration (FDA) approval for such use. Only
initiate therapy in patients who give informed consent after a complete
explanation of the potential benefits and risks of a particular treatment and
- Systemic therapies directed at hirsutism can be divided into those that
decrease ovarian or adrenal androgen production and those that inhibit
androgen action in the skin.
- Glucocorticoids: Glucocorticoids (dexamethasone or prednisone), which
suppress ACTH-dependent adrenal androgen synthesis, have been used with
variable success in women with adrenal hirsutism, as in CAH or idiopathic
adrenal hyperandrogenism. Usually, 0.5-1 mg of dexamethasone at bedtime is
sufficient to suppress ACTH and adrenal androgen production. Unfortunately,
some patients gain weight and cushingoid features develop, even on this
small of a dose. Further investigations may establish that lower doses
(perhaps 0.25 mg) can be effective without adverse effects.
- Oral contraceptives: The drugs most widely used to suppress ovarian
androgen production are oral contraceptives (OCs). They probably are the
first choice for young women with hirsutism who do not want to become
- OCs are inexpensive, and they promote regular uterine bleeding. In
addition, OCs can be used in combination with one of the antiandrogens or
other forms of therapy. On the other hand, do not use OCs in women with a
history of migraines, known or suspected thrombotic disease, or breast or
- Moreover, OCs have a significant failure rate in patients with
hirsutism for several reasons. Low-dose OCs and progestin-only minipills
fail to suppress ovulation in as many as 50% of women. Ovarian function
continues at a variable rate, and ovarian androgens continue to be
produced. Second, the progestins in OCs are attenuated derivatives of
testosterone and have variable degrees of androgenic activity in women.
The degree depends on the type of progestin and, more importantly, on
- Spironolactone: Spironolactone, in daily doses of 50-200 mg, blocks
androgen receptors. Spironolactone also decreases testosterone production,
making it additionally effective for hirsutism. Spironolactone especially is
useful in a patient with hypertension or edema because the drug is a mild
- Sexually active women taking spironolactone should ensure that
contraceptive measures are adequate. In some cases, spironolactone can be
combined with an OC for added effect on the hirsutism.
- With current systemic therapies for hirsutism, it usually takes 6
months to a year before results are noticeable. Even then, only about one
half to three quarters of patients show improvement. The problem partially
may lie in the nature of the hair follicle, which will persist for 6
months to a year even after androgen levels have been normalized.
Ineffectiveness also may be due to the inability of treatment to
completely normalize elevated tissue dihydrotestosterone levels. Newer
therapies directed at inhibition of 5 alpha-reductase or blockade of the
androgen receptor may improve the ability to treat patients.
- Flutamide: Flutamide, for example, is a potent, nonsteroidal selective
antiandrogen without progestational, estrogenic, corticoid, or
antigonadotropin activity. Preliminary data indicate that it is effective as
therapy for hirsutism (and also acne); however, flutamide is expensive and
has caused fatal hepatitis.
Finasteride: Finasteride is a 5 alpha-reductase inhibitor approved for
the treatment of benign prostatic hyperplasia. No adverse effects have been
reported in women, and the efficacy is similar to spironolactone; however,
the main concern is the risk of ambiguous genitalia in the male fetus
exposed to the enzyme inhibitor during the first trimester. Therefore, use
this drug only in women who are postmenopausal with no chance of becoming
Cyproterone acetate has been effective in the treatment of hirsutism but
is not available in the United States.
- Cosmetic measures for hirsutism (and their disadvantages)
- Hydrogen peroxide bleaching - Not suitable for severe hirsutism
- Plucking - Can cause skin irritation, folliculitis, and scarring
- Low-melting point wax - Can cause skin irritation, folliculitis, and
- Shaving - May be psychologically unacceptable
- Chemical depilatories - Can cause skin irritation
- Electrolysis (This can be painful, and short-wave diathermy can cause
The most effective strategy in treating hirsutism
is to combine systemic therapy, which has a slow onset of effectiveness, with
mechanical depilation (shaving, plucking, waxing, depilatory creams).
Systemic therapies directed at hirsutism can be divided into those that
decrease ovarian or adrenal androgen production and those that inhibit androgen
action in the skin.
Drug Category: Oral contraceptives -- Inhibit
ovarian androgen production. They probably are the first choice for young women
with hirsutism who do not want to become pregnant. OCs are inexpensive, and they
promote regular uterine bleeding. OCs can be used in combination with
antiandrogens or other agents. They have a significant failure rate in hirsutism
for several reasons. Low-dose oral contraceptives and progestin-only minipills
fail to suppress ovulation in as many as 50% of women. Ovarian function
continues at a variable rate, and ovarian androgens continue to be produced.
Second, the progestins in OCs are attenuated derivatives of testosterone and
have variable degrees of androgenic activity in women. The degree depends on the
type of progestin and, more importantly, on individual susceptibility.
|Estrogen-progestin combinations (Ortho-Novum,
Ortho-Tri-Cyclen, Triphasil) -- Reduces secretion of LH and FSH from the
pituitary by decreasing amount of gonadotropin-releasing hormones.
||1 tab qd
thrombophlebitis, undiagnosed vaginal bleeding, cerebral apoplexy
||May reduce hypoprothrombinemic effects
of anticoagulants; estrogen levels may be reduced with coadministration of
barbiturates, rifampin, and other agents that induce hepatic microsomal
enzymes; an increase in corticosteroid levels may occur when administered
concurrently with ethinyl estradiol; use of ethinyl estradiol with
hydantoins may cause spotting, breakthrough bleeding, and decreased
contraception; increase in fluid retention caused by estrogen intake may
reduce seizure control
||X - Contraindicated in pregnancy
||Caution in patients with hepatic
impairment, migraine, seizure disorders, cerebrovascular disorders, breast
cancer, thromboembolic disease, asthma, depression, and renal or cardiac
Drug Category: Glucocorticoids -- Used to
inhibit adrenal androgens. These agents have anti-inflammatory properties and
cause profound and varied metabolic effects. Suppress ACTH-dependent adrenal
androgen synthesis. Used with variable success in women with adrenal hirsutism,
CAH, and idiopathic adrenal hyperandrogenism.
|Prednisone (Deltasone, Orasone,
Meticorten) -- May inhibit ACTH-dependent androgen synthesis through
||5 mg PO qhs
||Documented hypersensitivity, viral
infection, peptic ulcer disease, hepatic dysfunction, connective tissue
infections, fungal or tubercular skin infections, GI disease
||Coadministration with estrogens may
decrease clearance; concurrent use with digoxin may cause digitalis toxicity
secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may
increase metabolism of glucocorticoids (consider increasing maintenance
dose); monitor for hypokalemia with coadministration of diuretics
||B - Usually safe but benefits must
outweigh the risks.
||Abrupt discontinuation of
glucocorticoids may cause adrenal crisis; hyperglycemia, edema,
osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis,
euphoria, psychosis, myasthenia gravis, growth suppression, and infections
may occur with glucocorticoid use
|Dexamethasone (Decadron, AK-Dex, Alba-Dex)
-- May inhibit ACTH-dependent androgen synthesis through negative feedback.
Lower doses (eg, 0.25 mg) may prove to be effective with fewer adverse
||0.5-1 mg/d PO hs
||Documented hypersensitivity, active
bacterial or fungal infection
||Effects decrease with coadministration
of barbiturates, phenytoin, and rifampin; decreases effect of salicylates
and vaccines used for immunization
||C - Safety for use during pregnancy has
not been established.
||Increases risk of multiple
complications, including severe infections; monitor adrenal insufficiency
when tapering drug; abrupt discontinuation of glucocorticoids may cause
adrenal crisis; hyperglycemia, edema, weight gain, osteonecrosis, myopathy,
peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis,
myasthenia gravis, and growth suppression may occur
Drug Category: Antiandrogen -- Used to block
|Spironolactone (Aldactone) -- Decreases
testosterone production. Can be combined with OCs for added effects.
||50-200 mg/d PO
||Documented hypersensitivity, anuria,
renal failure, hyperkalemia
||May decrease effect of anticoagulants;
potassium and potassium-sparing diuretics may increase toxicity
||D - Unsafe in pregnancy
||Caution in renal and hepatic
impairment; contraception is imperative in sexually-active women
Drug Category: 5 alpha-reductase inhibitor --
Indicated for treatment of benign prostatic hyperplasia and male pattern
baldness. Unlabeled use for treatment of female hirsutism.
|Finasteride (Proscar, Propecia) --
Specific inhibitor the intracellular enzyme that converts testosterone into
the androgen 5a-dihydrotestosterone (DHT). Efficacy in hirsutism is similar
Only to be used in women who are postmenopausal with no chance of becoming
||5 mg/d PO
||Do not administer
||Documented hypersensitivity; not to be
used in children, pregnancy, or women who may potentially become pregnant
||X - Contraindicated in pregnancy
||Caution in hepatic impairment; may
cause ambiguous genitalia development in the male fetus during first
trimester of pregnancy
- Prognosis depends on etiology of the hirsutism, eg, benign or malignant.
- Hirsutism requires a careful and systematic clinical evaluation coupled
with a rational approach to treatment. Throughout this process, the patient
must understand that even though diagnostic testing can be time consuming (and
even inconclusive), it sometimes is essential for determining an effective
intervention. In other cases, counseling and education may be all that is
- For the patient who desires treatment, a wide variety of pharmacologic
strategies can be followed. Informing the patient that current systemic
therapy is imperfect is important. Furthermore, none of the drugs used to
treat hirsutism has FDA approval for such use. Only initiate therapy in
patients who give informed consent after a complete explanation of the
potential benefits and risks of a particular treatment and alternative
- None of the drugs used to treat hirsutism has FDA approval for such use.
- Therapy should be initiated only in patients who give informed consent
after a complete explanation of the potential benefits and risks of a
particular treatment and alternative approaches.
|Caption: Picture 1.
|Picture Type: Graph
|Caption: Picture 2.
|Picture Type: Graph
|Caption: Picture 3.
|Picture Type: CT
|Caption: Picture 5.
|Picture Type: Graph
- Azziz R, Hincapie LA, Knochenhauer ES: Screening for
21-hydroxylase-deficient nonclassic adrenal hyperplasia among hyperandrogenic
women: a prospective study. Fertil Steril 1999 Nov; 72(5): 915-25[Medline].
- Azziz R, Black VY, Knochenhauer ES: Ovulation after glucocorticoid
suppression of adrenal androgens in the polycystic ovary syndrome is not
predicted by the basal dehydroepiandrosterone sulfate level. J Clin Endocrinol
Metab 1999 Mar; 84(3): 946-50[Medline].
- Chang RJ, Katz SE: Diagnosis of polycystic ovary syndrome. Endocrinol
Metab Clin North Am 1999 Jun; 28(2): 397-408, vii[Medline].
- Ehrmann DA, Schneider DJ, Sobel BE: Troglitazone improves defects in
insulin action, insulin secretion, ovarian steroidogenesis, and fibrinolysis
in women with polycystic ovary syndrome. J Clin Endocrinol Metab 1997 Jul;
- Franks S, Gilling-Smith C, Watson H: Insulin action in the normal and
polycystic ovary. Endocrinol Metab Clin North Am 1999 Jun; 28(2): 361-78[Medline].
- Goudas VT, Dumesic DA: Polycystic ovary syndrome. Endocrinol Metab Clin
North Am 1997 Dec; 26(4): 893-912[Medline].
- Guzick D: Polycystic ovary syndrome: symptomatology, pathophysiology, and
epidemiology. Am J Obstet Gynecol 1998 Dec; 179(6 Pt 2): S89-S93[Medline].
- Ibanez L, Potau N, Marcos MV: Treatment of hirsutism, hyperandrogenism,
oligomenorrhea, dyslipidemia, and hyperinsulinism in nonobese, adolescent
girls: effect of flutamide. J Clin Endocrinol Metab 2000 Sep; 85(9): 3251-5[Medline].
- Knochenhauer ES, Key TJ, Kahsar-Miller M: Prevalence of the polycystic
ovary syndrome in unselected black and white women of the southeastern United
States: a prospective study. J Clin Endocrinol Metab 1998 Sep; 83(9): 3078-82[Medline].
- Mestayer C, Berthaut I, Portois MC: Predominant expression of 5 alpha-reductase
type 1 in pubic skin from normal subjects and hirsute patients. J Clin
Endocrinol Metab 1996 May; 81(5): 1989-93[Medline].
- Moghetti P, Tosi F, Tosti A: 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):
- Morin-Papunen LC, Vauhkonen I, Koivunen RM: Endocrine and metabolic
effects of metformin versus ethinyl estradiol- cyproterone acetate in obese
women with polycystic ovary syndrome: a randomized study. J Clin Endocrinol
Metab 2000 Sep; 85(9): 3161-8[Medline].
- Negri C, Tosi F, Dorizzi R: Antiandrogen drugs lower serum
prostate-specific antigen (PSA) levels in hirsute subjects: evidence that
serum PSA is a marker of androgen action in women. J Clin Endocrinol Metab
2000 Jan; 85(1): 81-4[Medline].
- Olsen EA: Methods of hair removal. J Am Acad Dermatol 1999 Feb; 40(2 Pt
1): 143-55; quiz 156-7[Medline].
- Pasquali R, Gambineri A, Biscotti D: Effect of long-term treatment with
metformin added to hypocaloric diet on body composition, fat distribution, and
androgen and insulin levels in abdominally obese women with and without the
polycystic ovary syndrome. J Clin Endocrinol Metab 2000 Aug; 85(8): 2767-74[Medline].
- Rittmaster RS: Antiandrogen treatment of polycystic ovary syndrome.
Endocrinol Metab Clin North Am 1999 Jun; 28(2): 409-21[Medline].
- Shaw JC: Antiandrogen and hormonal treatment of acne. Dermatol Clin 1996
Oct; 14(4): 803-11[Medline].
- Sherif K: Benefits and risks of oral contraceptives. Am J Obstet Gynecol
1999 Jun; 180(6 Pt 2): S343-8[Medline].
- Venturoli S, Marescalchi O, Colombo FM: A prospective randomized trial
comparing low dose flutamide, finasteride, ketoconazole, and cyproterone
acetate-estrogen regimens in the treatment of hirsutism. J Clin Endocrinol
Metab 1999 Apr; 84(4): 1304-10[Medline].
- Yucelten D, Erenus M, Gurbuz O: Recurrence rate of hirsutism after 3
different antiandrogen therapies. J Am Acad Dermatol 1999 Jul; 41(1): 64-8[Medline].