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The Obstetrician & Gynaecologist 10.1576/toag.11.2.101.27483 www.rcog.org.uk/togonline 2009;11:101–107 Review

Review Hirsutism in young

women
Authors Rebecca Swingler / Alero Awala / Uma Gordon

Key content:
• Hirsutism is a distressing condition affecting 5–15% of women.
• It is usually associated with an underlying endocrine disorder: in 70–80%
of women with hirsutism this is polycystic ovary syndrome.
• Management depends upon the cause but combines lifestyle changes and
cosmetic, physical and medical treatments.
• It takes 9–12 months for hormonal treatments to take their maximum effect.

Learning objectives:
• To learn how to assess women with hirsutism.
• To understand common and less common aetiologies.
• To be able to take a sensitive and sensible approach to management.

Ethical issues:
• To what extent should drugs not yet approved for use in women with hirsutism
be used as a treatment for this condition?
• What is the role of the gynaecologist in ensuring women on drugs such as
finasteride are using effective contraception?
Keywords endocrine disorders / hyperandrogenism / polycystic ovary syndrome /
virilisation
Please cite this article as: Swingler R, Awala A, Gordon U. Hirsutism in young women. The Obstetrician & Gynaecologist 2009;11:101–107.

Author details
Rebecca Swingler MRCOG Alero Awala MRCOG Uma Gordon MD FRCOG
Specialist Registrar in Obstetrics Consultant Consultant
and Gynaecology Department of Obstetrics and Gynaecology, Bristol Centre for Reproductive Medicine,
Department of Obstetrics and Gynaecology, Watford General Hospital, Vicarage Road, Southmead Hospital, Westbury-on-Trym,
St Michael's Hospital, Southwell Street, Watford WD18 0HB, UK Bristol BS10 5NB, UK
Bristol BS2 8EG, UK
Email: rebeccaswingler@hotmail.com
(corresponding author)

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Introduction
Hirsutism is the presence of terminal (coarse) hairs
in females in a male-like pattern, affecting 5–15%
of women surveyed.1 It is extremely distressing,
especially in young women undergoing the
upheaval, both psychosocial and emotional, of
adulthood. Hirsutism is usually associated with, or
a sign of, an underlying endocrine disorder. It can
also be an isolated condition, referred to as
idiopathic hirsutism.
Normal hair growth
Of the 50 million hair follicles present on the
human body, 100 000–150 000 are found on the
scalp.2 The only parts of the body lacking hair
follicles are the palms of the hands, the soles of the
feet and the lips. Few hair follicles form after birth
and after the age of 40 years hair follicles decrease in
number. There are three types of hair:
• lanugo, a soft hair densely covering the fetus,
which is shed in the first 4 months postpartum
• vellus hair, which is soft, longer than lanugo hair
(2 cm), nonpigmented and which covers the
body
• terminal hair, which is longer still, pigmented
and which makes up the hair of the eyebrows,
scalp and axillary and pubic areas.
The three phases of hair growth consist of
anagen, the active growing phase; catagen, the
involuting phase, when the hair stops growing;
and telogen, the resting phase, when the hair is
shed.
In humans, the reason why hair appears to grow
continuously is because of disharmony in the
phases of hair growth; thus while some hairs are in
anagen, others are resting (telogen).2 The overall
length of the hair is determined by the duration of
the anagen phase.
Regulation of hair growth
The regulation of hair growth is multifactorial. A
number of local and systemic factors act on the hair
directly and indirectly in combination with sex
hormones, generating dermal papillae to promote
hair growth. Deficiencies in thyroid hormones and
growth hormone can result in an alteration of the
anagen:telogen ratio in scalp and body hair.
Androgens are the most important hormones
regulating hair type, growth and distribution.
The main circulating androgen, testosterone, is
converted in the hair follicle by the enzyme
5-reductase to its more potent form,
dihydrotestosterone. Other, weaker androgens, such
as androstenedione and dehydroepiandrosterone,
are metabolised in the skin to testosterone and
dihydrotestosterone, stimulating hair growth.
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The sensitivity of hair follicles to androgens varies
over the body. Hair growth in the eyelashes,
eyebrows and the occipital and lateral aspects of
the scalp, for example, is mostly independent of
androgenic effects. Areas such as the pubic region
and the axillae are sensitive to low levels of androgens,
while others, like the chest, lower abdomen, face,
upper thighs and lower back, need high levels of
androgens to increase hair growth. When hairs are
found in these areas, they are described as ‘male
pattern’ and in women are considered pathological.
Aetiology
The causes of hirsutism can be divided broadly
into androgen excess, nonandrogen factors and
idiopathic causes.
Androgen excess
Polycystic ovary syndrome
Polycystic ovary syndrome (PCOS) is the most
common cause, accounting for 70–80% of women
with hirsutism.1 No single biochemical marker or
characteristic is definitive and, as such, the diagnosis
should be based upon the revised criteria adopted
by the ESHRE/ASRM-sponsored PCOS Consensus
Workshop (Rotterdam, 2004).3 Thus, the presence
of two out of three of the following criteria is said to
be diagnostic after the exclusion of other causes:
• oligo- or anovulation
• clinical or biochemical hyperandrogenism
• morphological features of polycystic ovaries on
ultrasound scans.
Insulin resistance is acknowledged as one of the
possible aetiological factors.4 Insulin increases
androgen levels directly by increasing androgen
production by the ovarian theca cells and indirectly
by reducing hepatic synthesis of sex hormone-
binding globulin. Between 30–75% of women with
PCOS are overweight,4 which increases their insulin
resistance and exacerbates hyperandrogenaemia.
It is now recognised that young girls who present
with premature growth of pubic hair, elevated
dehydroepiandrosterone and hyperinsulinaemia
are at high risk of developing PCOS in the future.5
Androgen-secreting tumours
These can be tumours of the ovary or the adrenal
glands. They are rare, accounting for between 1 in
300 and 1 in 1000 hirsute women,6 and are
suspected if the onset of symptoms is rapid, or if
they lead to virilisation or they are associated with
cushingoid features. The best way to diagnose an
androgen-secreting tumour is by clinical
presentation rather than through analysis of
biochemical markers, as suppression and
stimulation tests can be misleading.1 Examples of
ovarian tumours associated with androgen excess
are: arrhenoblastomas; Leydig, hilar and thecal cell
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tumours; and luteomas of pregnancy. More than
half of adrenal tumours associated with
hyperandrogenism are malignant.7
Nonclassic congenital adrenal hyperplasia
This autosomal recessive condition is found in
1.5–2.5% of hyperandrogenic women. The
underlying enzyme defect, 21-hydroxylase
deficiency, results in elevated levels of
17-hydroxyprogesterone, which is androgenic.
Other causes
Conditions such as thyroid dysfunction, acromegaly,
Cushing syndrome and hyperprolactinaemia are
causes of androgen excess, although women with
these conditions tend to present with symptoms
other than hirsutism.
Hyperandrogenic insulin-resistant acanthosis
nigricans syndrome is an inherited condition that
occurs in around 3% of women with androgen
excess.1 It is characterised by extremely high levels
of insulin, resulting from severe insulin resistance.
Women with this condition may be severely
hyperandrogenic, very difficult to treat and they
can even present with signs of virilisation.
Drugs such as testosterone, danazol and anabolic
steroids all induce hirsutism via their inherent
androgenic properties.
Nonandrogen factors
Factors with unknown mechanisms of action on
the hair follicle include drugs that can induce excess
hair growth independently of androgens, such as
phenytoin, minoxidil, diazoxide, streptomycin,
high-dose corticosteroids, psoralen and
penicillamine.
Idiopathic causes
A small group of women have what is termed
idiopathic hirsutism, where all other causes of
hirsutism have been ruled out.2 These women have
no detectable hormonal abnormalities, normal
menses, normal ovarian appearance and no
evidence of adrenal or ovarian tumours. Earlier
studies have reported prevalences of 50–55%;6,8
however, as diagnostic techniques continue to
improve, this subgroup of women is shrinking and
more recent studies quote a prevalence of 6–7%.9
Evaluation
This must include an in-depth history, with care
taken to note any drugs used, changes in weight
and facial contours, the presence of acne, hair
loss/balding, menstrual and reproductive history
and relevant family history, such as premature male
balding and diabetes in the context of PCOS.
The extent, type and pattern of the hair growth can
be established by physical examination. The
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presence of abnormalities, such as signs of
virilisation, thyroid enlargement, galactorrhoea,
pelvic/abdominal masses, cushingoid features,
obesity and signs of systemic illness should also be
established. This will help in determining the
presence and extent of hirsutism and whether or
not it is related to an underlying endocrine
problem.
The clinical diagnosis of hirsutism tends to be
subjective and is based upon determining, by visual
assessment of the hair type and growth, whether the
hair is vellus (which may be due to familial/ethnic
origins) or terminal and whether or not it follows a
male-like pattern. In 1961, Ferriman and Gallwey10
described a method for assessing the degree of
hirsutism (see Figure 1). Using a score of 0 in the
absence of terminal hair and 4 for extensive
terminal hair growth, they scored the density of
hair at 11 different body sites. Scores of 6 were
deemed significant. A modified scheme was
introduced by Hatch et al. in 1981,11 which uses only
nine areas (excluding lower legs and forearms, as
these are less sensitive to androgens). Although
these scoring systems are an attempt to provide an
objective assessment of hirsutism, the perception of
the extent of excess hair growth in two women with
the same Ferriman–Gallwey score, and the impact
on their lives, may be very different. The scoring
schemes are typically used for research rather than
in a clinical setting.
Mild hirsutism (Ferriman–Gallwey score 8–15),
without any other features such as menstrual
irregularity, can be treated cosmetically and
investigated further if treatment is not effective or
hirsutism worsens. When hirsutism is moderate–
severe (Ferriman–Gallwey score 15), it is likely
that androgen excess is present; the possible causes
should be investigated. History and examination
will determine which investigations are appropriate.
Although free testosterone levels are the most
sensitive measure of hyperandrogenism, there is no
uniform laboratory standard and assay-specific
results vary.12 If a reliable free testosterone level is
not available, then it should be calculated from a
total testosterone and sex hormone-binding
globulin. A very high (1.5–2 ng/ml) testosterone
level increases the likelihood of an underlying
neoplasm and an elevated dehydroepiandrosterone
sulphate level would indicate an adrenal source, as
ovaries do not produce it. In nonclassic congenital
adrenal hyperplasia, testosterone levels are elevated,
as is 17-hydroxyprogesterone, which should be
measured as an early morning sample. In PCOS
17-hydroxyprogesterone can be slightly elevated
but levels 200 ng/dl are suggestive of nonclassic
congenital adrenal hyperplasia. Pelvic ultrasound
can help in the diagnosis of PCOS or ovarian
tumours, although normal findings may be seen in
both of these conditions.
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Figure 1
The Ferriman–Gallwey scoring
system for hirsutism (using 9 out
of the original 11 areas initially
described by Ferriman and
Gallwey in 1961).7 Copyright ©
2005 Massachusetts Medical
Society. All rights reserved.
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2009;11:101–107
Management
Figure 2 illustrates a pragmatic approach to the
evaluation of hirsutism.
In young women with mild hirsutism, a detailed
consultation, with reassurance that their
appearance is not as bad as they perceive and an
explanation of the possible causes, can be helpful
and all that is needed. Local PCOS groups can
also be a valuable source of support. Further
management options include lifestyle changes
and cosmetic, physical and hormonal therapies.
Whilst cosmetic and hormonal therapies are
effective for as long as they are in place, more
permanent reductions can be achieved using
physical methods.
Weight loss and lifestyle changes
Weight reduction has been shown to reduce
hyperandrogenism and insulin resistance, particularly
in overweight women with PCOS.13,14 Weight
reduction of 5–10% can induce an improvement in
hirsutism by 40–55% within 6 months of weight
loss.15 In obese women with PCOS, weight loss
programmes should be the first line of intervention,
to include a low calorie diet and an exercise
schedule over a period of at least 6 months.14,16 This
requires a multidisciplinary team approach, which
may be difficult to put in place in an NHS setting
because of resource and financial constraints.
Cosmetic methods
These include plucking, waxing, bleaching and the
use of depilatory creams. Shaving should be
avoided as it leads to blunt hairs that may feel like
The Obstetrician & Gynaecologist
stubble—although it does not lead to an increase in
hair growth, which is a common misconception.
Using depilatory creams and bleaching are useful
for minimising local hair growth but chronic use
can lead to skin irritation. Meanwhile, plucking
and waxing in androgenised areas should be
discouraged, as it can result in folliculitis and
ingrown hairs, which lead to skin damage.
Physical methods
These can be used alone or in combination with
cosmetic measures.
Electrolysis
This involves the destruction of individual hair
follicles via an electrode. It needs to be
administered by an expert and it results in
permanent hair reduction. It is, however, expensive,
time-consuming (taking from 18 months to 4 years,
depending on the extent of hirsutism), painful and
really only practical for a limited area of affected
skin. It can also cause burns, depigmentation and
scarring of skin, so it is not without adverse effects.
Laser photothermolysis
This type of laser is used to destroy hair follicles
without damaging nearby tissue. It is also known as
‘selective photothermolysis’ and it relies on the
selective absorption of a radiation pulse by darker
coloured hairs and the penetration of the dermis. It
appears that light-skinned women make the best
candidates, as they need lower radiation pulses
than darker-skinned women. Thus, to avoid skin
damage, women who are heavily tanned or
naturally dark-skinned should be treated with
lasers that have built-in cooling devices to offset the
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necessary increases in energy levels needed. An
advantage over electrolysis is that laser treatment
can cover a wider area; it is also less painful and has
fewer dermatological adverse effects. It reduces
hair density permanently by 30% after three to
four sessions.7 A randomised controlled trial17
comparing low-fluence (placebo) with high-
fluence laser treatment in women with PCOS
showed that it significantly reduced the severity
of hirsutism.
Hormonal therapy
The basis of action of hormonal therapy is either
suppression of androgen production or blocking
of the action of androgens on the skin. This results
in the hairs reverting back to vellus-type hair. It
takes 9–12 months for the maximum effects to be
noticed because of the cyclical nature of hair
growth. It requires patience, therefore, on the part
of both women and doctors, but it can be
combined with cosmetic measures.
The combined oral contraceptive pill
The combined oral contraceptive pill (COCP)
reduces free plasma testosterone levels: the
progestogen component suppresses luteinising
hormone and, thus, androgen production by the
ovaries. The estrogen component also increases
sex hormone-binding globulin production by the
liver. Although the COCP will not reverse
hirsutism, it can reduce the need for shaving by
50% and it may halt the progression of the
condition.7 The progestogen component in COCPs
is of variable androgenicity and newer pills
containing less androgenic progestogens, such as
norgestimate and desogestrel, are available.
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Figure 2
Algorithm for the management
of hirsutism
Drospirenone, the progestogen in the COCP
Yasmin® (Bayer Schering Pharma, Berks, UK) has
an antiandrogenic effect.
The advantage of the COCP in women with
PCOS is that, not only does it reduce hirsutism,
but it also gives cycle control, acts as a
contraceptive and reduces the risk of endometrial
hyperplasia. Theoretically, however, the effects
of the COCP on carbohydrate and lipid
metabolism could exacerbate the long-term
metabolic outcomes of PCOS (type II diabetes
and cardiovascular disease).18 The evidence for
this is limited and contradictory19 but it has
highlighted the potential of insulin-sensitising
agents as a safer alternative.
Cyproterone acetate
Cyproterone acetate is a strong progestogen which,
by decreasing plasma levels of luteinising hormone,
results in a lowering of testosterone and
androstenedione levels. It also acts peripherally as
an androgen antagonist and is, therefore, a
progestational antiandrogen. Although there is a
wide variation in response between women,
cyproterone acetate can be expected to lower the
Ferriman–Gallwey score by 15–40% within
6 months; again, maximum effects occur between
6–12 months.1,7 The COCP Dianette® (Bayer
Schering Pharma, Berks, UK) contains 35 g of
ethinylestradiol and 2 mg of cyproterone acetate. A
systematic review20 found cyproterone acetate to be
as effective as other antiandrogens at treating
hirsutism; however, it concluded that larger, more
carefully designed studies are needed to compare
the efficacy and safety profiles between drug
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therapies for hirsutism. Reported adverse effects
of cyproterone acetate are weight gain, depression,
fatigue and sexual dysfunction. It can also, rarely,
alter liver function; liver function tests should be
performed prior to commencing treatment
and after 6 months. It is thought to have a
thromboembolic risk similar or greater than second
generation COCPs. Although a contraceptive,
Dianette is not licensed for contraceptive purposes
but only for use in the treatment of acne and
hirsutism. For women who are resistant to long-
term treatment with Dianette, a higher dose of
cyproterone acetate (50 mg/day) combined with
ethinylestradiol can be effective in the short-term
management of hirsutism.21
Spironolactone
Commonly used in the USA, spironolactone is an
aldosterone antagonist and a mild diuretic; it is also
an androgen inhibitor and it is structurally similar to
progesterone. It competes with dihydrotestosterone
for sites on androgen receptors. It only has
one-twentieth of the binding potential of
dihydrotestosterone, therefore, high doses of this
drug are needed to suppress hair growth.1 When
used in conjunction with the combined oral
contraceptive pill, however, its overall effectiveness
can be improved and effects such as dysfunctional
bleeding or worsening oligomenorrhoea can be
minimised. Indeed, a Cochrane review22 found that
100 mg/day of spironolactone is superior to both
finasteride 5 mg/day and low-dose cyproterone
acetate 12.5 mg/day for up to 12 months after the
end of treatment.
Finasteride
Finasteride is an inhibitor of the enzyme
5-reductase and it is also used for the treatment
of benign prostatic hyperplasia. It was thought to
be less effective in treating hirsutism than
antiandrogens,7 although a recent Cochrane
review20 suggests that it has similar effectiveness to
cyproterone acetate. It has very few adverse effects
or drug interactions, although feminisation of a
male fetus is a particular concern. Women taking
this drug should be advised of this and offered
effective contraception as well.
Flutamide
Flutamide is a nonsteroidal antiandrogen. It blocks
androgen receptors and at high doses may decrease
the production of androgens. It is also used in the
treatment of prostate cancer. It has been found to be
just as effective, if not more so, than spironolactone20
but adverse effects include a greenish tinge to the
urine; dry scalp and skin; and liver enzyme
abnormalities. It is advisable to check liver function
whilst on this medication as, rarely, fatal hepatic
toxicity has been reported. Doses range from
250–500 mg/day, usually as a single dose. Concerns
about the effects on the liver have limited its use.
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Insulin sensitisers
Metformin hydrochloride is an oral biguanide,
which reduces insulin levels by inhibiting hepatic
production of glucose and increasing the number
of insulin receptors. High insulin levels in women
with PCOS stimulate androgen secretion by the
ovaries and adrenal glands and reduce sex
hormone-binding globulin production by the liver.
By lowering insulin levels, metformin reduces
androgen levels by around 20% in women with
PCOS.7 The theoretical advantages of metformin
over the COCP for treatment of hirsutism in women
with PCOS are that, as well as improving hirsutism
and acne via a reduction in hyperandrogenism, it
may also have long-term benefits for the prevention
of type II diabetes and cardiovascular disease. A
recent Cochrane review23 comparing metformin
with the COCP found no difference in their effects
on hirsutism and acne but there was either
insufficient or no data on their relative efficacy at
preventing type II diabetes and cardiovascular
disease. The results of three studies on the effect of
metformin on hirsutism used in the meta-analysis
were contradictory, although this may be due to
differences in selection criteria. There are several
studies,24 however, that have shown improvements
in hirsutism in young adults and teenagers using
metformin. It may be useful not only in obese
women with PCOS but also in women of normal
weight,25 as it is possible that all women with PCOS,
whether lean or obese, have reduced insulin
sensitivity.26 Theoretically, metformin appears to be
a treatment for hirsutism that also provides long-
term benefits for all women with PCOS; however,
further studies are needed to confirm this.
Cell cycle inhibitors
Eflornithine acts to inhibit irreversibly the enzyme
ornithine decarboxylase in the skin, thereby
decreasing and/or arresting hair growth for as long
as it is used. It is licensed for use on the face and is
thought to act on the hair follicle to reduce the rate
of growth by inhibiting keratin protein synthesis. It
is recommended for topical use twice a day and
women can apply moisturisers or cosmetics on top
of the cream, which is rapidly absorbed by the skin,
after 5 minutes. It can also be used in combination
with laser treatment.27 The main adverse effect is a
rash, although there is a potential for systemic
toxicity if applied over a wide area.1,7 Acne is
another common adverse effect, which can be a
particular problem in some women. In one study1
eflornithine was found to reduce hair growth
significantly in around 60% of women with facial
hirsutism. The authors wished to note that if no
benefit is seen after 4 months of treatment, it
should be stopped.
Gonadotrophin-releasing hormone agonists
Studies28 have shown the use of gonadotrophin-
releasing hormone agonists to be an effective way of
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treating hirsutism in hyperandrogenic women,
although in clinical practice they are rarely used.
They act by suppressing testosterone levels,
resulting in a decrease in hair diameter and
Ferriman–Gallwey scores and their use can lead to
long-term remission. The main risks include
osteopenia and osteoporosis. Studies29 have shown
a largely reversible loss of bone mineral density,
amounting to 2–8% after 6 months, which can be
ameliorated by additionally using estrogen or
tibolone.
Follow-up
Women with hirsutism require a sympathetic
approach to their management, including
emotional support, as many find this condition
very distressing. It can affect their self-esteem,
especially when it occurs in adolescents and young
women, who may already have body image issues.
Conclusion
Treatment for hirsutism is lengthy, it can be
expensive and painful, it can have adverse effects
and it may not be instantly satisfactory. It is
important to ensure that women on antiandrogens
also use effective contraception. Efficacy may be
improved by combining therapies, such as cosmetic
therapy with hormonal manipulation and, in the
presence of obesity, weight loss.
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