Hirsutism is a common endocrinological disorder in clinical practice. The causes vary from simple idiopathic hirsutism to most complicated malignant ovarian and adrenal tumors. Most common cause of hirsutism in endocrine clinic is due to a disorder known as PCOS (polycystic ovarian syndrome). Hirsutism poses embarrassment to the women. The purpose of this short review is to identify the common diseases associated with hirsutism, an approach to working through the differential diagnosis, investigations helping in diagnosis and the commonly available treatment modalities for the various forms of hirsutism. The review will provide the physician about the most efficient, cost effective and safe clinical approach to management of hirsutism.

1. Evaluation and Treatment of Hirsutism.

2. Review Article
Evaluation and treatment of hirsutism
Kalpana Dash*
Professor, Senior Consultant, Department of Endocrinology, Apollo Hospitals Bilaspur, Seepat Road, Lingiadih, Bilaspur 495006, India
a r t i c l e i n f o
Article history:
Received 25 April 2013
Accepted 21 May 2013
Available online 14 June 2013
Keywords:
Hirsutism
Hyperandrogenism
PCOS
a b s t r a c t
Hirsutism is a common endocrinological disorder in clinical practice. The causes vary from
simple idiopathic hirsutism to most complicated malignant ovarian and adrenal tumors.
Most common cause of hirsutism in endocrine clinic is due to a disorder known as PCOS
(polycystic ovarian syndrome). Hirsutism poses embarrassment to the women. The pur-
pose of this short review is to identify the common diseases associated with hirsutism, an
approach to working through the differential diagnosis, investigations helping in diagnosis
and the commonly available treatment modalities for the various forms of hirsutism. The
review will provide the physician about the most efficient, cost effective and safe clinical
approach to management of hirsutism.
Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved.
1. Definition of hirsutism
Hirsutism is defined as excessive male pattern terminal hair
growth in women.1
It must be distinguished from hyper-
trichosis which is excessive growth of vellus hair in androgen
independent non-sexual areas, commonly found in familial
back ground, metabolic diseases (anorexia nervosa, thyroid
disorders) and certain medications (phenytoin, minoxidil &
cyclosporine). The amount and location of the hair is
commonly measured by FerrimaneGallwey2
scoring system
which should score at least 8 (Fig. 1).3
Hirsutism can be defined
by a total score of 8 or more by FerrimaneGallwey hirsutism
scoring system.
2. Etiology of hirsutism
Most common (80%) cause of hirsutism is polycystic ovary
syndrome (PCOS).1,4
PCOS is a complex disorder comprising
both hormonal and metabolic abnormalities. This diagnosis is
typically made when there is unexplained chronic hyper-
androgenism and oligo-anovulation. Other features associ-
ated with PCOS are menstrual irregularity, polycystic ovaries,
or central obesity, abnormal carbohydrate and lipid meta-
bolism, acanthosis nigricans, or family history of type 2 dia-
betes mellitus and infertility.5
Gonadotropin-dependent
functional ovarian hyperandrogenism is the major source of
the hyperandrogenemia in majority of PCOS cases.6
Insulin
resistance is common in PCOS. Non-classic adrenal hyper-
plasia is present in less than 5% of hyperandrogenic women in
the general population. Androgen secreting tumors are
present in about 0.2% of hyperandrogenic women, 50% of
them are malignant.7
Hyperprolactinemia, Cushing’s syn-
drome, acromegaly, and thyroid dysfunction must be
considered as uncommon causes of hirsutism. Use of andro-
gens or androgenic medications, such as anabolic steroids or
danazol, or valproic acid should be ruled out while evaluation.
Those women having hirsutism without hyperandrogenemia
and normal menstrual cycle are known as idiopathic
hirsutism.
* Tel.: þ91 9630013474.
E-mail address: drkdash@rediffmail.com.
Available online at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/apme
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 3 8 e1 4 5
0976-0016/$ e see front matter Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.apme.2013.05.021

3. 3. Causes of hirsutism
1. Ovarian:
B Polycystic ovarian syndrome (PCOS) e 80%
B Hyperthecosis (a severe PCOS variant)
B Ovarian tumor.
2. Adrenal:
B Nonclassical adrenal hyperplasia e 4.3%
B Cushing’s syndrome
B Glucocorticoid resistance
B Adrenal tumor e 0.2%.
3. Specific conditions associated with pregnancy:
B Luteoma pregnancy
B Hyperreactio luteinalis
B Aromatase deficiency in fetus.
4. Others:
B Idiopathic hirsutism (ovulatory cycle with normal plasma
testosterone) e 7.6%
B Idiopathic hyperandrogenism (patients who do not fall
into any category) e 15.5%
B Medications e danazol, testosterone, phenytoin, minox-
idil, anabolic steroids, diazoxide, valproate
B Hyperprolactinemia, hypothyroidism, growth hormone
excess, insulin resistance.
4. Clinical approach & diagnosis of hirsutism
Hirsutism is a clinical diagnosis. Therapeutic approach to
patient with hirsutism needs accurate diagnosis of underlying
abnormalities in androgen production and metabolism. The
diagnosis of hirsutism depends on clinical history and phys-
ical examination. The age of onset of hirsutism, area of dis-
tribution and the rate of progression should be determined.
Simple hirsutism should be differentiated from virilization
which is a more severe form of androgen excess signifying
higher rates of plasma testosterone production. This is iden-
tified by the presence of temporal balding, deepening of voice,
decreased breast size, increased muscularity, presence of
clitoromegaly and loss of female body contours. Before going
for a major work-up for hirsutism or virilization, never forget
to rule out use of exogenous androgen or other medications
causing androgen excess and hirsutism. All old papers should
be thoroughly checked to look for these medications.
Androgen excess at the time of puberty is most commonly due
to PCOS or nonclassical adrenal hyperplasia. Patients with
PCOS present with menstrual irregularity (amenorrhea, oli-
gomenorrhea and DUB), hirsutism, infertility. Oligomenor-
rhea is missing 3e4 cycles in a year or cycle lengths more than
35 days. It is the most common form of chronic anovulation
Fig. 1 e FerrimaneGallwey hirsutism scoring system: Each of the nine body areas most sensitive to androgen is assigned a
score from 0 (no hair) to 4 (frankly virile), and these separate scores are summed to provide a hormonal hirsutism score.
R. Hatch et al: Am J Obstet Gynecol 140:815e830, 1981.3
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 3 8 e1 4 5 139

4. with androgen excess. PCOS is also associated with increased
metabolic and cardiovascular risk factors.
Most important features that should never be overlooked
include onset, severity and rapidity with which hirsutism
progress. Rapidly progressive severe androgen excess implies
androgen secreting tumors until proved otherwise. DHEAS
needs to be done if adrenal cortical adenoma or carcinomas
are suspected. Plasma DHEAS levels more than 800e1000 ug/
dl suggests adrenal cortical adenoma or carcinoma. In such
situation, CT scan or magnetic resonance imaging (MRI) of the
adrenal glands is done. Ovarian tumors are rare and small.
Adrenal tumors are small, more indolent are very rare.8
Ad-
renal tumors secrete androgens alone in 16%, 64% androgens
and cortisol and 16% androgens, cortisol and estrogens. Ad-
enocarcinomas are large and secrete other hormones in
addition to testosterone, usually glucocorticoids and some-
times estrogens. The treatment is surgical. If adrenal and
ovarian tumors are excluded, medications causing hirsutism
should be ruled out. If plasma testosterone level remains
between 50 and 200 ng/dl, consider nonclassic adrenal hy-
perplasia in younger women and ovarian hyperthecosis (se-
vere variant of PCOS) having high hirsutism score presenting
during pubertal period. CAH rarely produce plasma testos-
terone levels greater than 200 ng/dl. In these patients, the
search should focus on adrenal tumors in the form of ade-
noma or adenocarcinoma.
Patients with plasma testosterone between 50 and
200 ng/dl could be due to nonclassic adrenal hyperplasia or due
to insulin resistance. These patients can present as premature
pubarche or peripubertal hirsutism, acne or amenorrhea.
Such cases account for 2e3% of hirsutism in total population.
The diagnostic test is the standard cortrosyn stimulation test
using plasma 17-hydroxyprogesterone. Values greater than
1000 ng/dl are considered to be diagnostic. Once diagnosis of
nonclassic adrenal hyperplasia is done, an effective and se-
lective therapy is available with a good result. Patients having
insulin resistance, usually have a history of significant weight
gain and signs of insulin resistance such as acanthosis nig-
ricans and glucose intolerance. Biochemical abnormalities
include hypercholesterolemia and hypertriglyceridemia. Many
of these patients will have polycystic ovaries. The underlying
cause of this disorder is weight gain leading to insulin resis-
tance.9
Half of the isolated mild hirsutism (FerrimaneGallwey
hirsutism score 8e15) may be unrelated to hyper-
androgenemia. In the remainder of cases of mild hirsutism and
in most cases of more severe hirsutism, plasma total and
free testosterone levels are elevated.10e12
Women with idio-
pathic hirsutism have normal ovulatory cycles and normal
Evaluation of hirsutism
History taking & clinical examination of
Hirsutism
Drug Use PCOS: Menstrual
irregularity or
infertility, acne,
seborrhea, balding,
central obesity,
acanthosis
nigricans
Others:
Cortisol excess,
idiopathic hirsutism,
hyperprolactinemia,
growth hormone excess,
thyroid dysfunction
Neoplasm Risks:
Sudden onset, rapid
progression,
virilization,
abdominal or pelvic
mass
Hirsutism mild Score (8-15) Hirsutism > moderate (score > 15)
Discontinue
if possible
Trial of cosmetic,
dermatological, or
oral contraceptive
therapy
Imaging & Endocrine work-up
Testosterone blood level in early AM
Testosterone Normal Testosterone Elevated with
signs of virilization
Course
stable or
improving
Idiopathic hirsutism, PCOS
& endocrinopathies Hyperandrogenemia
Trial of cosmetic, dermatological, or oral contraceptive,
antiandrogens, metformin
History or
signs
suggestive of
non classic
adrenal
hyperplasia
Hyperthe
cosis:
severe
PCOS
variant
Step 1
Step 2
Intermediate
Testosterone Level
PCOS, CAH, Idiopathic,
drugs, other causes of
hirsutism
Surgery
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 3 8 e1 4 5140

5. plasmatestosterone levels. No furthertestingis required in this
group.
Flow chart given below provides an approach to the work-
up for hyperandrogenism on the basis of degree of hirsutism,
most common identifiable cause of hirsutism that is PCOS,
virilizing disorders, androgenic medications, and other
endocrinopathies.
Given below is a flow chart of clinical approach to
hirsutism.
Mild to moderate hirsutism (FerrimaneGallwey score 8e15)
without other evidence of virilization and menses are regular,
testing for hyperandrogenemia may be omitted. Moderate to
severe hirsutism (with a score of more than 15), assessment of
androgens are must. Rapid onset and progression of hirsutism
or progression despite therapy or evidence of virilization (clit-
oromegaly, muscularity, frontal balding, deepening of voice)
suggest the likelihood of androgen secreting tumor. Some-
times such type of patients presenting with hirsutism and
ambiguous genitalia, points to the virilizing forms of congen-
ital adrenal hyperplasia. There are three virilizing forms: 21-
hydroxylase deficiency, 11-hydroxylase deficiency, and 3-b
hydroxysteroid dehydrogenase deficiency. 21-hydroxylase
deficiency is by far the most common. It is easily diagnosed
by AM plasma 17-hydroxyprogesterone or ACTH challenge test
as earlier described.13
Serum 17-hydroxyprogesterone in
excess of 1000 ng/dl confirms the diagnosis. 11-Hydroxylase
deficiency, seen in less than 5e10% of cases, is usually associ-
ated with hypertension. However, the laboratory criteria for
the diagnosis of 11-hydroxylase deficiency and 3-b hydrox-
ysteroid dehydrogenase deficiency are not well established.
Measurement of the 11-deoxycortisol/cortisol ratio and the 17-
hydroxypregnenolone/17-hydroxyprogesterone ratios are the
most commonly applied criteria.14
Patients with abnormal
external genitalia who do not have CAH should be referred to a
medical genetics clinic.
5. Laboratory test for differential diagnosis
of androgen excess
1. Initial testing:
B Pregnancy test, in case of amenorrhea
B Total testosterone, Prolactin, TSH, FSH.
2. Further testing depending on clinical presentation:
B 17-Hydroxyprogesterone (8AM)
B 17-Hydroxyprogesterone 60 min after IV ACTH (cortrosyn)
B Cortisol (8AM) after 1 mg dexamethasone at midnight
B DHEAS
B Androstenedione.
3. Imaging of ovaries & adrenal gland: trans-vaginal ultraso-
nography to detect an ovarian neoplasm or a polycystic
ovary. Adrenal imaging by abdominal USG, CT scan/MRI.
The most useful initial test to evaluate androgen excess is
serum total testosterone. Plasma testosterone should remain
normal in all ovulatory cycles and remain elevated in all
anovulatory cycles. If all the above tests turn out to be negative,
then the symptoms suggestive of an anovulatory cycle or other
symptoms like oligomenorrhea, infertility and hirsutism which
fulfills the criteria of PCOS along with raised testosterone level
makes a diagnosis of PCOS.15e17
If androgen levels are high,
further work-up required to determine the source of androgen
which includes assessment of serum androstenedione;
computed tomography of abdomen to exclude adrenal tumor;
dynamic testing of the response to ACTH to exclude nonclassic
adrenal hyperplasia and dexamethasone suppression test to
exclude Cushing’s syndrome. When testing for elevated
androgen levels, early morning plasma total testosterone level
should be considered as the initial test. If the plasma total
testosterone is normal in the presence of hyperandrogenism or
hirsutism, measure an early morning free testosterone.
In patients with high likelihood of congenital adrenal hy-
perplasia [positive family history, certain high-risk ethnic
group such as Ashkenazi Jews (prevalence 1 in 27)] and His-
panics (1 in 40), and Slavics (1 in 50), measurement of an early
morning follicular phase 17-hydroxyprogesterone is done, if
elevated confirms the diagnosis. If not elevated can go for
ACTH stimulated plasma 17-hydroxyprogesterone level.
6. Treatment of hirsutism
Women with hirsutism seek treatment for reduction of hair
growth, acne, regularizing menstrual cycle and infertility.
PCOS patients are prone to develop metabolic abnormalities
like diabetes, hypertension and hyperlipedemia. Hence, pa-
tients are increasingly seeking advice for the treatment of the
above metabolic abnormalities. Treatments include life style
modification, mechanical removal of hair in the form of
depilation, waxing, shaving, topical anti androgen, systemic
antiandrogens (spironolactone, flutamide), OCPs and GnRH
agonists. Experts have often made treatment recommenda-
tions based on the severity of hirsutism using Ferri-
maneGallwey scores (mild, score 8e15, or severe, score >15),
this approach has several limitations: 1) Majority of clinicians
are unfamiliar with calculating FerrimaneGallwey scores; 2)
Most women use cosmetic measures before their first medical
consultation and continue to use them during pharmaco-
therapy, making it impossible to accurately determine a Fer-
rimaneGallwey score. Therapeutic choice also depends on (a)
patient preferences for pregnancy or treating hirsutism or
menstrual irregularity (b) the extent of hirsutism (c) accessi-
bility and affordability. (d) Fertility status (e) age of patient.
General treatment of androgen excess is to prevent abnormal
hair growth and virilization. This approach is followed in
PCOS, idiopathic hirsutism and nonclassic adrenal hyperpla-
sia. PCOS is often treated with a combination therapy of OCPs
and antiandrogen (spironolactone) so as to suppress ovarian
and peripheral androgen respectively. Treatment of androgen
excess in nonclassic adrenal hyperplasia includes combina-
tion of OCPs, antiandrogen (spironolactone) and a glucocorti-
coid. GnRH analog has been used for treating ovarian
hyperthecosis. Apart from these basic treatments, specific
treatments like surgical intervention for ovarian and adrenal
tumors and Cushing’s disease are followed separately. There
are 3 types of therapeutic options for hirsutism:
Pharmacological therapy
Direct hair removal methods.
Cosmetic therapy.
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 3 8 e1 4 5 141

6. 7. Pharmacological treatments
7.1. Monotherapy
7.1.1. Oral contraceptives (OCP)
OCP are the first line drug to be used in hirsutism. Oral con-
traceptive agents contain either 30 or 35 mcg of ethinyl
estradiol in combination with a progestin or cyproterone
acetate (CPA) or drospirenone. Later two molecules are
structurally unrelated to testosterone and function as
androgen receptor antagonists. Most of these progestins are
derived from testosterone and exhibit mild degrees of
androgenicity.18
OCPS decrease circulating androgens19
in
PCOS and synergize the effect of anti androgens. This also
stimulates hepatic production of SHGB, reduction in adrenal
androgen secretion, and also blocks the binding of androgens
to their receptors. OCPs also provide the additional benefits
control of bleeding and contraception. OCPs are given 21 days
(d 5e25) in a month starting from day 5 of menstrual cycle.
Women, who do not want to conceive, can use either oral
contraceptives (OCPs) or antiandrogens in combination with
OCP.
7.1.2. Antiandrogens
Antiandrogen drugs have teratogenic potential. Hence it is
recommended not to use antiandrogen as first line mono-
therapy unless adequate contraception is used. Commonly
used antiandrogens are spironolactone, cyproterone acetate
(CPA), drospirenone, finasteride and flutamide.
Spironolactone is the most commonly used aldosterone
antagonist having dose-dependent competitive inhibition of
androgen receptor as well as inhibition of 5a-reductase activ-
ity.20
It is most effective for androgen excess in PCOS and idio-
pathichirsutism.Inmostclinicalstudiesdoseofspironolactone
varies from 50 to 400 mg/day.21
However most effective dose is
generally accepted as 100 mg/day in divided doses. Because of
the dangers of antiandrogens for fetal genital development, it is
recommended that spironolactone be given only in combina-
tion with an oral contraceptive agent.22
Spironolactone is
generally well tolerated but sometimes associated with men-
strual irregularity unless an OCP is used concomitantly. It rarely
can cause hyperkalemia, increased diuresis, postural hypo-
tension and dizziness early in treatment.
CPA (Cyproterone acetate) is used worldwide for the
treatment of hirsutism and acne but is not available in the
United States. CPA is a progestogenic compound with anti-
androgen activity and acts by inhibiting the androgen receptor
and 5a-reductase activity.23
It also suppresses serum gonad-
otropin and androgen levels. There are evidence that CPA in
combination with ethinyl estradiol can inhibit 5a-reductase
activity in skin. In one systematic review, CPA (2 mg) with
ethinyl estradiol was more effective than placebo but not
better than any other antiandrogen.24
Because of its long half-
life, CPA is usually administered in a reverse sequential way.
Doses of ethinyl estradiol (20e50 mg/d) are given for 3 weeks (d
5e25) to assure normal menstrual cycle, and CPA is adminis-
tered for the first 10 d (d 5e15) of the cycle. Doses of CPA are
50e100 mg/d, often prescribed until the maximal effect is
obtained, and then lower doses (such as 5 mg/d) are prescribed
for maintenance. CPA is also available as an oral contraceptive
at lower daily doses of 2 mg CPA with 35 mg ethinyl estradiol.
CPA is generally well tolerated, should be discontinued 6
months before planning for pregnancy to avoid its teratogenic
effect.
Drospirenone, a progestin used in several OCPs having
weak antiandrogen effect. 3 mg of drospirenone (the dose
used in OCPs) is roughly equivalent to 25 mg spironolactone
and 1 mg CPA.25
A 12-month trial comparing oral contracep-
tives containing either 3 mg drospirenone or 2 mg CPA showed
similar reductions in hirsutism scores.26
Finasteride is 5a-reductase inhibitor it reduces hirsutism
scores by 30e60% and also reduces hair shaft diameter.27
It
has been seen that 5 mg finasteride and 100 mg spi-
ronolactone have equal efficacy.28
Most commonly used dose
of finasteride is 5 mg/day, some data suggest that 7.5 mg is
more effective.29
At a dose of 5 mg/day for 6 months period
shows very good response without side effects.
Flutamide is a pure antiandrogen that works by competi-
tively inhibiting androgen receptors.30
Several studies show
that flutamide is as effective as spironolactone (100 mg/d) and
finasteride (5 mg/d) in the treatment of androgen-mediated
hirsutism.31e37
Most frequently used dose is 500 mg/d. The
major concern is, it causes hepatic toxicity in a dose-depen-
dent manner and which is not trivial. Death and liver failure
are reported.38e40
Hence lowest effective dose should be used
and the patient should be monitored closely.
7.1.3. Glucocorticoids
Glucocorticoids are used for women with hirsutism due to
nonclassic adrenal hyperplasia who have a suboptimal
response to OCPs and/or antiandrogens or cannot tolerate
them, or are seeking ovulation induction. Women with hirsut-
ism who do not have classic or nonclassic adrenal hyperplasia
due to 21-hydroxylase deficiency (CYP21A2), glucocorticoid
therapy should not be used.
Women with severe forms of hyperandrogenemia, such as
ovarian hyperthecosis or who have a suboptimal response to
OCPs and antiandrogens, GnRH agonists is recommended.
7.1.4. GnRH agonists
Consideration of GnRH agonist therapy is based on the
assumption that hirsutism is at least in part gonadotropin-
dependent. The action of chronic GnRH agonist therapy is to
inhibit LH and to a lesser extent FSH secretion, thereby leading
to a decline in ovarian function and consequently decreased
ovarian androgen production. Data on the effect of GnRH ag-
onists on hirsutism come almost exclusively from non-
placebo-controlled trials, with only one RCT published.41
7.1.5. Combination therapy
If hirsutism remains despite 6 or more months of mono-
therapy with an oral contraceptive, antiandrogens are added
to the therapy.
7.1.6. Treatment of insulin resistance
Basic pathophysiology of PCOS is hyperinsulinemia and
hyperandrogenemia. Reducing insulin levels pharmacologi-
cally attenuates both hyperinsulinemia and hyper-
androgenemia. Role of insulin sensitizers in treating
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 3 8 e1 4 5142

7. hirsutism, in the absence of the menstrual or metabolic dis-
turbances is controversial. Both metformin (a biguanide) and
the thiazolidinediones (troglitazone and pioglitazone) have
been used to reduce insulin levels. Metformin inhibits hepatic
glucose production and thereby reduces plasma insulin con-
centrations over time. The usual dose is 500 mg three times a
day. Most studies show reduced levels of insulin in response
to a glucose challenge, reduced weight, and reduced plasma
testosterone levels.
For all pharmacological therapies for hirsutism, at least 6
months of trial is taken before making any changes in dose,
medication, or adding medication.
8. Direct hair removal methods
Permanent methods of hair removal therapy are laser/pho-
toepilation and electrolysis. Hair removal with laser devices
and IPL sources is based on the principle of selective photo-
thermolysis.42
The most commonly used lasers include alex-
andrite, neodymiumeyttriumealuminumegarnet (Nd: YAG),
and ruby lasers. Women undergoing photoepilation therapy
requiring more rapid initial response, eflornithine cream
during treatment may be added. Before undergoing hair
removal therapy, pharmacologic therapy is done first to
minimize hair regrowth. Electrolysis can be painful and time-
consuming because it treats each hair individually.
9. Cosmetic measures
(a) Depilation, removing hair shafts from the skin surface and
epilation extracting hairs to above the bulb. Shaving
sometimes can be used as a depilation method and
chemical depilatory agents are also commonly used to
dissolve the hair. However, most depilatories can cause
dermatitis.
(b) Epilation methods are plucking and waxing, are relatively
safe and inexpensive, but cause some discomfort. This can
cause scarring, folliculitis, and hyperpigmentation.
(c) Bleaching can be used with products containing hydrogen
peroxide and sulfates are a method for masking the pres-
ence of undesired hair, particularly facial hair. Side effects
include irritation, pruritus, and possible skin discoloration.
(d) Topical treatment.
Eflornithine is an irreversible inhibitor of ornithine decar-
boxylase, an enzyme that catalyzes the rate-limiting step for
follicular polyamine synthesis, which is necessary for hair
growth. Eflornithine hydrochloride cream 13.9% (Vaniqa) is a
topical preparation is approved in many countries for the
treatment of unwanted facial hair in women. Eflornithine
does not remove hair but acts to reduce the rate of hair
growth. Open-label43e47
and randomized48
trials have shown
that eflornithine reduces the growth and appearance of facial
hair and helps to improve quality of life. Noticeable results
take about 6e8 weeks, and once the cream is discontinued,
hair returns to pretreatment levels after about 8 weeks. Side
effects are itching and dry skin.
10. Conclusion
Hirsutism is a common disorder in endocrine clinic during
reproductive period. It requires proper investigation and
diagnosis. Treatment plan depends on the etiology and
severity of the disease. For all practical purposes physical
removal of the hair by depilation or epilation and imple-
menting life style modification in losing weight, are the
mainstay of treatment for all forms of hirsutism. OCPs are the
most common medical therapy used for hirsutism and are
most effective when hyperandrogenism is of ovarian origin.
Most common cause of hirsutism that is PCOS is often treated
with combination of antiandrogens and OCPs. Antiandrogens
(spironolactone) suppress extra ovarian action of androgens
and OCPs suppresses ovarian sources of androgens. Which-
ever drug is used, improvement in hirsutism scoring takes at
least 6 months period because one hair cycle growth takes at
least 3e6 month period. Cosmetic therapies for the terminal
hairs should be done by mechanical/physical methods like
epilation, depilation or electrolysis, diathermy, or laser treat-
ment. All of them should be done at least 3 months after
androgen suppression is achieved. Eflornithine is currently
thought of as a replacement for shaving. However, the clinical
effects of eflornithine require 8e12 weeks reaching maximum
effect. The best approach is physical removal of hair and use
of OCPs for at least 6e8 months before the decision to use an
antiandrogen is made. However, if pregnancy is not a concern
combining OCPs with spironolactone for treating androgen
excess in PCOS has been seen to be very effective.
Because of the danger of antiandrogen-induced abnor-
malities of fetal genital development, antiandrogen treatment
should only be given to women known to be infertile or use of
OCPs must always precede antiandrogen treatment. Finally, if
a patient does not respond to monotherapy, a combination of
birth control pills with or without the addition of physical
removal of hair, eflornithine, or antiandrogens should be
used. In severe form of disease, addition of cyproterone ace-
tate or finasteride helps. Weight loss programs have to be
implemented because of many associated health benefits.
Every effort should be made to treat these patients with an
aggressive weight loss regimen because most common cause
of hirsutism is PCOS and this is associated with many meta-
bolic abnormalities in future.
Conflicts of interest
The author has none to declare.
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