16
Disorders of the PA RT
Hair and Nails
Chapter 85 :: Androgenetic Alopecia
:: Ulrike Blume-Peytavi & Varvara Kanti
AT-A-GLANCE
■ Androgenetic alopecia (AGA) is a nonscarring
progressive miniaturization of the hair follicle in
genetically predisposed men and women, usually
in a specific pattern distribution.
■ AGA onset may be at any age following puberty,
showing an increasing frequency with age.
■ The etiology of AGA is multifactorial and
polygenic with, as of this writing, 12 genetic
regions recognized to associate with AGA in men.
In men, AGA is an androgen-dependent trait. Even
though the role of androgens in female AGA is less
certain than in men, there is a subset of women
with AGA and associated hormonal dysregulation.
■ Generally, diagnosis of AGA is based on history
and clinical examination. Depending on patient
history and clinical evaluation, however, additional
diagnostics may become necessary to exclude
differential diagnoses; for example, ferritin level or
thyroid-stimulating hormone in diffuse effluvium
or endocrinologic workup in women with signs of
hyperandrogenism.
■ Biopsy is very rarely indicated in AGA. Biopsy
is indicated only if, for example, the differential
diagnoses cicatricial alopecia or diffuse alopecia
areata are suspected.
■ AGA has a naturally progressive course, meaning that
the main therapeutic aim is the prevention of disease
progression or enhancement of hair growth during
the early, mild to moderate stages of the disease.
■ The best clinical evidence according to current
study data exists for topical application of
minoxidil in both genders and for the oral intake
of finasteride in men. Alternatively, cosmetically
satisfactory results can be achieved using hair
transplantation in nonprogressive stable AGA with
sufficient available donor area.
Kang_CH085_p1495-1506.indd 1495
DEFINITION
Androgenetic alopecia (AGA) is the most common
type of hair loss, a nonscarring progressive minia-
turization of the hair follicle with shortening of the
anagen phase in genetically predisposed men and
women, usually in a specific pattern distribution.1
Life quality may be significantly impaired in
affected individuals, independent of severity, age,
or gender.
EPIDEMIOLOGY
Although AGA onset may be at any age follow-
ing puberty, there is an increasing frequency with
age. Reportedly, approximately 50% to 60% of
men are affected by the age of 50 years increasing
to approximately 80% by the age of 70 years and
beyond. 2,3 The prevalence of AGA is reportedly
lower and its severity less among Asians, Native
Americans, and African Americans compared to
the European population. 4,5 Approximately 10% to
20% of Chinese men are affected by the age of 40 to
49 years, rising to 40% to 60% by the age of 70 years
and beyond. 6,7
The frequency and severity of AGA is lower in
women than in men, but it still affects a sizeable
proportion of the population. Reported prevalence
rates in white women in the United Kingdom and
United States range between 3% and 6% in women
younger than 30 years of age, increasing to 29% to
42% in women 70 years of age and older.8,9 AGA
is less common and appears to start later in life in
Asian women with a reported prevalence of 25%
in Korean10 and of 12% to 15% in Chinese women
70 years of age and older.6,7
03/12/18 10:24 am
16 CLINICAL FEATURES FEMALE PATTERN
MALE PATTERN HAIR LOSS HAIR LOSS

MALE PATTERN, HAMILTON- FEMALE PATTERN,

NORWOOD TYPE
This is the most frequent clinical pattern in men with
AGA, and only occasionally observed in women.
Recession of the frontal hairline, mainly in a triangular
pattern is the characteristic finding, later followed by
a vertex thinning with progression until the top of the
scalp is completely bald (Figs. 85-1 and 85-2). Occipi-
Part 16
LUDWIG TYPE
The so-called female pattern hair loss is charac-
terized by a diffuse thinning of the centroparietal
region with maintenance of the frontal hair line
(Fig. 85-3). It is the most common type of AGA in
women; it is occasionally observed in men. There
are 2 scales describing this pattern, the 3-point

tal area and sides of the scalp are spared even in long- Ludwig scale (Fig. 85-4) and the 5-point Sinclair
standing male pattern hair loss. scale (Fig. 85-5).
::
Disorders of the Hair and Nails

Hamilton-Norwood classification of male pattern hair loss

I II IIa

III III vertex IIIa

IV V IVa

VI VII Va

1496 Figure 85-1 Hamilton-Norwood classification. (Redrawn from Blume-Peytavi U, Blumeyer A, Tosti A, et al. S1 guideline for
diagnostic evaluation in androgenetic alopecia in men, women and adolescents. Br J Dermatol. 2011;164[1]:5-15.)

Kang_CH085_p1495-1506.indd 1496 03/12/18 10:24 am

 16

Chapter 85 :: Androgenetic Alopecia

Figure 85-2 Male-pattern androgenetic alopecia, grade III vertex according to the Hamilton-Norwood classification.
Standardized global photography overview (Canfield system).

CHRISTMAS TREE PATTERN ETIOLOGY AND

Frequently observed in women, the Christmas tree
pattern shows diffuse centroparietal thinning similar
PATHOGENESIS
to the Ludwig pattern with an additional breaching of
the frontal hair line (Fig. 85-6). RISK FACTORS
The etiology of AGA is multifactorial and polygenic.1

MEN
Male AGA is largely determined by genetic factors.11,12
There is a strong paternal influence on the risk of
balding.3 Although once thought to be an autosomal
dominant trait, it is now clear that AGA has a complex
polygenic basis. As of this writing, molecular studies

Ludwig classification of female pattern hair loss

I II III

Figure 85-4 Ludwig pattern of hair loss (3-point scale).

(Redrawn from Blume-Peytavi U, Blumeyer A, Tosti A, et al.
S1 guideline for diagnostic evaluation in androgenetic
Figure 85-3 Female pattern androgenetic alopecia, alopecia in men, women and adolescents. Br J Dermatol. 1497
grade III according to the Ludwig classification. 2011;164[1]:5-15.)

Kang_CH085_p1495-1506.indd 1497 03/12/18 10:24 am

16 Sinclair scale for grading female pattern hair loss
Figure 85-5 Sinclair scale for grading female pattern hair loss (5-point scale). (Redrawn from Blume-Peytavi U, Blumeyer A,
Tosti A, et al. S1 guideline for diagnostic evaluation in androgenetic alopecia in men, women and adolescents. Br J
Part 16
Dermatol. 2011;164[1]:5-15.)
have recognized 12 genetic regions associated with
::
AGA. Candidate genes include genes for the androgen
Disorders of the Hair and Nails
receptor (AR), histone-deacetylases (HDAC) 4 and 9,
and the WNT molecule WNT10A.13
In men, AGA is an androgen-dependent trait.14 Dihy-
drotestosterone is the androgen chiefly responsible for
the follicular pathology. Dihydrotestosterone probably
acts primarily on dermal papilla, the predominant site of
androgen receptor and type II 5α-reductase expression
within the hair follicle. A number of signaling molecules
have been implicated in the inhibition of hair growth
in AGA including transforming growth factor (TGF)-β1
and transforming growth factor-β2,14 dickkopf 1 (a mem-
ber of the WNT signaling family),15 and interleukin-6.16
There is also evidence for involvement of prostaglan-
dins in AGA. The enzyme prostaglandin D2 synthase
and its product prostaglandin D2 are elevated in bald-
ing scalp skin; prostaglandin D2 has an inhibitory effect
on hair growth in animal and in in vitro experiments.17
WOMEN
Less is known about the etiology of AGA in women.
There is an increased frequency of balding in
Olsen scale
Male pattern Diffuse Frontal accentuation
(Hamilton) (Ludwig) (Olsen)
Figure 85-6 Olsen scale: Christmas tree pattern in female
pattern hair loss. (Redrawn from Blume-Peytavi U,
Blumeyer A, Tosti A, et al. S1 guideline for diagnostic
1498 evaluation in androgenetic alopecia in men, women and
adolescents. Br J Dermatol. 2011;164[1]:5-15.)
Kang_CH085_p1495-1506.indd 1498
first-degree male relatives of women with AGA, which
suggests there is at least some genetic commonality
between female and male AGA.18 Case-control gene-
association studies have found a weak association
between the AR/EDA2 locus and early-onset female
AGA, but no association with the 11 autosomal loci
that associate with male AGA.19-21 There is a weak asso-
ciation with the gene for estrogen receptor 2 (ESR2),
which suggests the involvement of estrogenic path-
ways in female AGA.22,23 As of this writing there have
been no genome-wide studies in women.
The role of androgens in female AGA is also less certain
than in men. Nevertheless, there is a subset of women
with AGA and associated hormonal dysregulation.
DIAGNOSIS
Generally, AGA is a clinical diagnosis. Depending on
patient history and clinical evaluation, further diag-
nostics may be necessary.
PATIENT HISTORY
Patient and family history of the first manifestation
of hair loss and of the course of hair loss (chronic or
intermittent) should be documented. Patients with
AGA usually complain about a longstanding, slowly
progressing reduction of hair density, sometimes even
without noticing significant hair loss. Patients typi-
cally describe hair thinning with an accentuation of the
frontal, parietal, or vertex region, but diffuse thinning
is possible as well. Pruritus and trichodynia may pres-
ent as initial signs of AGA. The family history for AGA
is often positive. A positive family history for other
hair disorders may facilitate differential diagnostic
conclusions and lead to further diagnostic procedures.
In women, especially in those with peripheral signs
of hyperandrogenism (Fig. 85-7), a gynecologic history
is recommended, including among other possibilities,
menstrual cycle disturbances and intake of hormonal
contraception.
Furthermore, a detailed patient history should be
performed to rule out other causes for the hair loss or
03/12/18 10:24 am

Figure 85-7 Female pattern androgenetic alopecia, facial hypertrichosis, and seborrhea oleosa in an adolescent 15-year old girl.
aggravating factors. Patient interview should include
systemic and newly diagnosed diseases (eg, infections,
thyroid function disorders, and surgical procedures) that
occurred 6 months to 1 year prior to the first signs of hair
loss, and nutritional behavior (especially chronic deficient
diet or rapid significant weight loss) possibly leading to
diffuse effluvium (see section “Differential Diagnosis”).
Lifestyle procedures, such as special hairstyles causing
traction, and environmental factors like smoking and
ultraviolet radiation exposure should be considered.1
A drug history should be taken to identify a possibly
drug-related hair loss, such as after treatment with che-
motherapeutic agents, hormones with proandrogenic or
antithyroid action, intake of anabolic steroids, or supple-
mental androgens. Allergies and intolerances should be
recorded as they might be important for the choice of the
appropriate therapy (eg, contact dermatitis caused by
propylene glycol in topical solutions)1 as well as cosmetic
habits (eg, hair care and color, hair style).
CLINICAL EXAMINATION
Clinical examination should involve the scalp skin and
hair, facial and body hair, and skin, as well as the nails.
SCALP EXAMINATION
The scalp skin usually appears normal in AGA, but fre-
quently associated findings include seborrhea and/or
seborrheic dermatitis.1 Inflammatory or infectious dis-
eases, as well as alopecia areata and scarring alopecia
Kang_CH085_p1495-1506.indd 1499
16
Chapter 85 :: Androgenetic Alopecia
like lichen planopilaris or frontal fibrosing alopecia,
which can mimic AGA, should be considered (see
section “Differential Diagnosis”). Balding scalp exami-
nation should include checking for photodamage and
field cancerization. Thus, clinical examination of the
scalp should focus on possible signs of inflammation,
like erythema, scaling, or hyperkeratosis, and signs of
scarring, such as skin atrophy and loss of hair follicle
ostia. However, atrophy of scalp skin also may be pres-
ent in longstanding AGA.1
HAIR EXAMINATION
Scalp Hair: Hair should be parted to assess scalp
hair density. Part width should be compared between
the frontal, occipital, and temporal regions to exam-
ine the distribution of alopecia (see Figs. 85-1 through
85-6, Hamilton-Norwood, Ludwig, and Olsen scales).
Dermoscopy/trichoscopy can be helpful in assessing
hair follicle openings to exclude scarring alopecia and
in identifying short and fine miniaturized hairs. Hair
caliber variations might also be present.
The hair pull test (Sabouraud maneuver) can be
implemented to provide information on hair shed-
ding. For this test, approximately 50 to 60 hairs are
grasped between the thumb, index, and middle fingers
from the base of the hairs near the scalp and firmly,
but not forcefully, tugged away from the scalp. If more
than 10% of the grasped hairs are pulled away from
the scalp, this constitutes a positive pull test and con-
firms active hair shedding.1 In AGA, the hair pull test
may be positive in the frontal region, while it is typi- 1499
cally negative in the occipital region.
03/12/18 10:24 am
16 Facial and Body Hair Examination: Facial and
body hair density and/or distribution changes can be
found as a result of ethnic hypertrichosis, hypertrichosis
caused by medications, or hirsutism. Signs of acne, seb-
orrhea, oily skin, and obesity might present peripheral
signs of hyperandrogenism. Even though some women
with AGA complain of reduction of eyebrows or eye-
lashes, this finding points to other types of alopecia, like
alopecia areata or frontal fibrosing alopecia (see section
“Differential Diagnosis”)24 rather than to AGA.
NAIL EXAMINATION
Nail abnormalities are not characteristic for AGA, but
Part 16
may contribute to differential work up of alopecia
areata, certain deficiencies, and lichen planus.1
::
DIAGNOSTIC TOOLS
Disorders of the Hair and Nails
DERMOSCOPY
Dermoscopy, a noninvasive technique, improves exami-
nation of scalp skin and hair shafts by magnification (eg,
assessment of hair follicle openings, hair shaft caliber
variations). The findings can be saved for future com-
parison using videodermoscopy. In AGA, hair diameter
variations, loss of trio groups with single terminal hairs,
and an increased number of vellus hairs can be seen.
GLOBAL PHOTOGRAPHY
Global photographs are helpful tools for the objective
evaluation of the course of hair growth, hair volume,
and hair density in clinical studies, and for long-term
followup in daily practice. For followup assessment,
a standardized technique should be implemented, for
example, by using a stereotactic device assuring a con-
stant view, magnification, and lighting.
AUTOMATIC DIGITALIZED
SYSTEM FOR HAIR DENSITY
AND ANAGEN/TELOGEN HAIRS
(PHOTOTRICHOGRAM)
These systems allow measurement of hair density and
the anagen-to-telogen ratio for diagnostic and followup
purposes, but they are mainly used for standardized and
reproducible tools in clinical studies. Typical findings in
AGA are reduced hair density in a pattern distribution
compared to the occipital area. The anagen-to-telogen
ratio is normal or decreased when comparing frontal or
vertex to the occiput. These techniques are helpful for
long-term followup and quantification of hair density.
TRICHOGRAM
1500 The trichogram is not indicated as a routine diagnostic
tool in AGA. It should only be considered in individual
Kang_CH085_p1495-1506.indd 1500
cases to rule out other differential diagnoses or comor-
bidities.1 The trichogram should only be performed by
dermatologists who are familiar with this technique
and perform it routinely.
BIOPSY
A biopsy, mostly performed as a deep, 4-mm, cylindri-
cal punch, is indicated in AGA only in cases where the
diagnosis is uncertain, such as where scalp changes
are suggestive of cicatricial alopecia or diffuse alopecia
areata. Scalp biopsies should be evaluated by derma-
topathologists who are experienced in hair pathology
using both vertical and horizontal sectioning. The pre-
ferred area for biopsy is the central scalp in an area
representative of the hair loss process. Biopsies should
not be taken from the bitemporal area as miniatur-
ized hairs may be present in this region independent
of AGA.1 Histologically AGA presents an increased
number and proportion of miniaturized (vellus-like)
hair follicles with a typically less than 3:1 ratio of ter-
minal to vellus-like hair follicles, compared with a
greater than 7:1 ratio in the normal scalp. Other fea-
tures include an increased telogen-to-anagen ratio and
an increase in the number of follicular stelae (tracts
beneath miniaturized follicles). A mild perifollicular
lymphohistiocytic infiltration, primarily around the
upper hair follicle, also may be present, as well as peri-
follicular fibrosis, in longstanding AGA.
LABORATORY TESTING
In men, laboratory testing for the diagnosis of AGA is
not necessary, except if the history or clinical exami-
nation indicate another underlying disorder or asso-
ciated disease. Literature data indicate a possible
positive association between AGA and insulin resis-
tance, metabolic syndrome, hypertension, and benign
prostate hyperplasia in men.25 Furthermore, laboratory
testing might be indicated before introducing specific
therapies (eg, measurement of the prostate-specific
antigen value before introducing finasteride therapy;
see section “Medications”).
In women, an extensive endocrinologic workup is not
necessary, except if the history and clinical examination
indicate androgen excess. In this case, an interdisciplin-
ary approach involving gynecologists, endocrinolo-
gists, and dermatologists is recommended to rule out/
distinguish between the different causes associated with
hyperandrogenism, such as polycystic ovary syndrome,
congenital adrenal hyperplasia, androgen-secreting
tumors, or Cushing syndrome. For this purpose the free
androgen index, sex hormone-binding globulin, and
prolactin should be determined and further laboratory
testing (eg, 17-OH-progesterone, follicle-stimulating
hormone, estradiol, or cortisol) should be considered.
The measurements should be optimally taken between
8:00 and 9:00 am, ideally between the second and fifth
day of the menstrual cycle, in order to standardize and
03/12/18 10:24 am
 facilitate interpretation. Furthermore, it is advisable to
perform blood hormone testing at least 2 months after
stopping any hormonal intake, including oral contra-
ception, as estrogens lead to elevated sex hormone-
binding globulin levels and consequently falsify the
outcome of the free androgen index.1
Measurement of ferritin level or thyroid-
stimulating hormone may be considered depending
on patient history, especially when diffuse effluvium
is suspected. Literature data indicate a possible sup-
portive role of adequate serum ferritin levels during
treatment of diffuse androgen-dependent alopecia in
women, even though contradictory data also have
been published.1
with premature onset of AGA, an interdisciplinary
approach involving the dermatologist and pediatric
16
endocrinologist should be taken. If significant psycho-
logical distress is observed, especially in women and
young patients with early onset of AGA, psychological
referral should be considered for the development of
coping strategies.
DIAGNOSTIC ALGORITHM
A diagnostic evaluation form for AGA has been pro-
posed by the European Consensus Group that includes

Chapter 85 :: Androgenetic Alopecia

Interdisciplinary evaluation must be decided indi- history, clinical examination, laboratory and hair
vidually, based on age, clinical findings, and associ- examination tests, diagnostic techniques and clinical
ated findings. Especially in children and adolescents documentation (Fig. 85-8).1

Clinical algorithm for the diagnosis of androgenetic alopecia

Hair loss

YES NO No primary
Classify Pattern
pattern distribution? suspicion of AGA
check DD

Perform
Negative test Positive

No active hair loss Active hair loss Check DD in

addition

YES
Examine Further suspicion
scalp skin of AGA?

Normal Pathologic

Men Women
Men
Seborrheic Other scalp Check
dermatitis disorders DD

Women

Women
Check for signs of hormonal dysregulation
(menstrual cycle, body hair examination, acne, seborrhea)

Normal Pathologic Perform hormonal

laboratory tests

Women
Women Suspicion of
AGA Normal Pathologic hyperandrogenism
refer to
endocrinologist

Figure 85-8 Clinical algorithm for the diagnosis of androgenetic alopecia (AGA). DD, differential diagnosis. (Adapted from
Blume-Peytavi U, Blumeyer A, Tosti A, et al. S1 guideline for diagnostic evaluation in androgenetic alopecia in men, women 1501
and adolescents. Br J Dermatol. 2011;164[1]:5-15, with permission. Copyright © 2011 John Wiley & Sons.)

Kang_CH085_p1495-1506.indd 1501 03/12/18 10:24 am

16 DIFFERENTIAL DIAGNOSIS diagnosis. A biopsy is useful for confirming the diag-
nosis if clinically not distinct (see Fig. 85-9A).
Table 85-1 outlines the differential diagnosis of AGA.
Multiple hair and scalp disorders may present with
clinical features that resemble or coexist with AGA.
CENTRAL CENTRIFUGAL
CICATRICIAL ALOPECIA
TELOGEN EFFLUVIUM Central centrifugal cicatricial alopecia is a scarring alo-
pecia of the vertex region that most commonly occurs
Telogen effluvium is an acute or chronic diffuse hair
in women of African descent (Fig. 85-10A). The der-
loss caused by an increased number of hair follicles
moscopic detection of loss of follicular ostia confirms
in telogen, possibly leading in the time course to a
the scarring type. Biopsies can be useful to confirm the
reduced hair density over the entire scalp. Telogen
diagnosis.
Part 16

effluvium is usually associated with a precipitating

event, like a severe illness or psychological trauma,
crash diet or certain medications, and the results of the FRONTAL FIBROSING ALOPECIA
hair pull test are diffusely positive (Fig. 85-9B).
::

Frontal fibrosing alopecia is a frontotemporal band-

Disorders of the Hair and Nails

like scarring alopecia, characterized by frontotempo-

DIFFUSE ALOPECIA AREATA
Diffuse alopecia areata typically does not follow a
patterned distribution. Although not always present,
a personal or family history of alopecia areata, the
detection of patchy or total hair loss, hair loss in other
body sites, and nail abnormalities offer support to this
TABLE 85-1
Differential Diagnoses for Androgenetic
Alopecia
ral band like recession, loss of eyebrows, perifollicular
erythema and hyperkeratosis (see Fig. 85-10C, D). The
detection of clinical and histologic signs consistent
with a lymphocytic scarring alopecia aid in diagnosis.
TRACTION ALOPECIA
Traction alopecia occurs as a result of chronic tension
on the hair shaft (see Fig. 85-10B). Although the hair
loss is reversible initially, hair loss may become perma-
nent if tension on the hair follicles continues. History
of tight braiding of the hair is useful for diagnosis.

Telogen Effluvium
■ Associated with precipitating event
■ Hair pull test diffusely positive HYPOTRICHOSIS SIMPLEX
Diffuse Alopecia Areata
■ No pattern of distribution OR ECTODERMAL
■ Personal or family history of alopecia areata
■ Hair loss in other body sites
DYSPLASIA
■ Nail changes
It is important to differentiate between congenital or
Central Centrifugal Cicatricial Alopecia
■ Scarring alopecia of the vertex region
acquired hair loss in adolescents. Hereditary hypo-
■ Most commonly in women of African descent
trichosis simplex is characterized by diffuse and pro-
■ Dermoscopy and histologic evaluation shows scarring alopecia gressive hair loss of the scalp and the body, beginning
Frontal Fibrosing Alopecia
during early childhood. There are no anomalies of the
■ Frontotemporal, band-like scarring
skin, nails, or teeth. The group of ectodermal dyspla-
■ Associated with loss of eyebrows sias comprise a large, heterogenous group of inherited
■ Perifollicular erythema and hyperkeratosis disorders involving the skin, its appendages, nails, and
■ Histology shows lymphocytic scarring alopecia teeth. Delayed physical/psychological development
Early Traction Alopecia and sweating disorders may be present.
■ History of chronic tension in the hair shaft (tight braiding)
Hypotrichosis Simplex
■ Diffuse, progressive loss of scalp and body hair from early CLINICAL COURSE AND
childhood
■ No anomalies of skin, nails, or teeth PROGNOSIS
Ectodermal Dysplasia The course of AGA is naturally progressive, mean-
■ Skin, appendages, nails, and teeth associated ing that the main therapeutic aim is the improvement
■ Delayed physical/psychological development and sweating
1502 or even merely prevention of disease progression.
disorders
This can mainly be achieved during the early, mild to

Kang_CH085_p1495-1506.indd 1502 03/12/18 10:24 am

 16

Chapter 85 :: Androgenetic Alopecia

A

Figure 85-9 Differential diagnosis between female pattern androgenetic alopecia and (A) diffuse alopecia areata or
(B) diffuse effluvium may present a challenge; a detailed patient and family history, laboratory testing and/or biopsy
might be necessary.

A B C D

Figure 85-10 Hair disorders mimicking androgenetic alopecia. A, Central centrifugal cicatricial alopecia; B, traction alopecia;
C, frontal fibrosing alopecia; and D, coexisting frontal fibrosing alopecia and androgenetic alopecia Ludwig grade III in a 1503
postmenopausal woman.

Kang_CH085_p1495-1506.indd 1503 03/12/18 10:24 am

16 moderate stages of the disease. Irrespective of its clini-
cal progression, AGA provokes significant distress and
has an often underestimated psychosocial impact on
the affected patients.26
MANAGEMENT
MEDICATIONS
The best clinical evidence according to current study
data concerns the topical application of minoxidil. Min-
oxidil prevents further progression of the disease and
Part 16
leads to an increase in hair density and hair thickness
both in male patients older than 18 years of age with
mild to moderate AGA (2% to 5% solution; 1 mL or
half a cap of 5% foam twice daily) and female patients
::
older than 18 years of age (2% solution; 1 mL twice daily
Disorders of the Hair and Nails
or half a cap of 5% foam once daily). The response to
treatment should be assessed at 6 months. If successful,
treatment needs to be continued to maintain efficacy.27
The patients should be informed about transitory
increased telogen hair shedding, usually appearing
within the first 8 weeks of therapy initiation. Further-
more, after end of therapy with topical minoxidil,
increased hair loss follows.
The main side effect of topical minoxidil is hypertri-
chosis, mostly from local spreading or excessive con-
tinuous topical application. To avoid contamination
of the pillow with subsequent facial contact patients
should be advised to apply the drug at least 2 hours
before going to bed. Irritant and allergic contact der-
matitis may also occur. Irritation is more common with
the 5% solution because of its higher content in propyl-
ene glycol. Contact dermatitis resulting from propyl-
ene glycol or from minoxidil itself should be confirmed
by patch testing. It is recommended to pause topical
minoxidil use during pregnancy and lactation, owing
to the lack of data during this period.27
In male patients older than 18 years of age with
mild to moderate AGA, a systemic therapy with the
5α-reductase type 2 inhibitor finasteride (1 mg/day)
improves or to prevents progression of AGA. For
greater efficacy, the combination of oral finasteride
(1 mg once daily) and topical minoxidil can be consid-
ered. Patients under treatment with finasteride should
be aware of reduction of prostate-specific antigen,
which is important in prostate cancer screening in men.
Further reported side effects of finasteride are impaired
sexual function, including erectile dysfunction, ejacula-
tion dysfunction, reduced ejaculate volume, and loss of
libido. A possible negative impact of finasteride on those
who have a constitutive predisposition to psychological
disorders, leading to alteration of mood/depression has
been reported; gynecomastia; testicular pain; hyper-
sensitivity reactions; and possible negative impact on
spermatogenesis in those men with preexisting condi-
tions relating to infertility should be mentioned. Post-
finasteride syndrome, defined as various symptoms
1504 persisting for months or years after discontinuation of
finasteride treatment, including sexual dysfunction, loss
Kang_CH085_p1495-1506.indd 1504
of libido, depression, suicidal ideation, impaired cogni-
tion, fatigue, and decreased penile sensitivity, probably
occurring in men with a history of sexual dysfunction
or a personal or family history of psychiatric illness, are
also discussed in the literature. Consequently, finaste-
ride is contraindicated in patients with active depres-
sion or current sexual dysfunction.
The response to treatment should be assessed at
6 months, although in some men it may not become
evident before 12 months. If successful, treatment
needs to be continued to maintain efficacy. In case
of ineffective treatment with 1 mg finasteride over
12 months, the off-label use of the 5α-reductase inhibi-
tor dutasteride, which inhibits the isoenzymes type 1
and type 2, at a dose of 0.5 mg a day can be considered.
Finasteride is not indicated in women and is con-
traindicated in pregnant women and women of child-
bearing potential, because of the risk of feminization
of a male fetus. Finasteride-treated men must avoid
donating their blood.27
In female postmenopausal patients, finasteride 1
mg failed to show efficacy; however, finasteride 5 mg
may be effective in female normoandrogenic premeno-
pausal and postmenopausal patients. However, no
placebo-controlled trials are available in this popula-
tion. In women of childbearing age, the use of a safe
contraceptive method is indispensable.27
Clinical studies on the efficacy of topical finasteride
preparations are currently underway.
Antiandrogens and estrogenic drugs are being used
in the treatment of AGA, although evidence of effi-
cacy for any of these treatments is insufficient. In male
patients, the use of systemic estrogens or androgen-
receptor antagonists is not recommended. In women
with AGA and clinical or biochemical evidence of
hyperandrogenism, the use of oral antiandrogens
(chlormadinone acetate, cyproterone acetate, drospi-
renone, spironolactone, flutamide) in combination
with an estrogen as an oral contraceptive pill can be
considered. Side effects of cyproterone acetate include
depressive mood changes and liver toxicity. There is an
increased risk of venous thromboembolism in patients
taking estrogen-containing oral contraceptives, which
may be greater in those taking cyproterone acetate
than other oral contraceptives. Spironolactone 100 to
200 mg per day taken continuously is an alternative
option because of its antiandrogenic effect, but should
also be combined with a safe contraceptive in women
of childbearing age. Side effects include menstrual dis-
turbances and hyperkalaemia.27
As of this writing, there is insufficient literature evi-
dence on the effect of topical alfatradiol, topical natural
estrogens or progesterones, or topical fluridil.27
PROCEDURES
SURGERY
In AGA, hairless or thinning areas can be cosmeti-
cally covered, albeit with a decreased density, using
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 hair restoration surgery. Hair restoration surgery
involves hair transplantation, scalp reduction sur-
gery, or a combination of both. Hair transplantation
is less invasive than scalp reduction surgery. Over
the last decades, hair transplantation has evolved
into a microsurgical procedure. Follicular units of
1 to 4 hairs are transplanted in large numbers and
high densities. Hair surgery, especially follicular unit
transplantation, can be considered to improve AGA
in suitable patients with sufficient donor hair supply
and medically controlled or spontaneously stabilized
AGA, especially in the frontoparietal area. The result
greatly depends on the skills of the surgical team
and the adjustment of the surgical plan to individual
patient characteristics. As hair surgery does not influ-
ence progression of AGA, long-term results in early
stages depend on spontaneous or medical stabiliza-
tion of AGA. In men, a combination of finasteride
1 mg and/or topical minoxidil with follicular unit
transplantation may reduce postoperative progres-
sion of AGA.27
NONPERMANENT HAIR
REPLACEMENT MEASURES
Nonsurgical hair replacement methods include, in
addition to full and partial hair replacement mea-
sures (wigs), various hair-binding techniques and hair
extension and supplementation techniques, either
performed by the patients themselves (eg, sprinkle
hair) or by specialized personnel (eg, camouflage tech-
niques, bonding).28
INTERVENTIONS
Low-Level Laser Therapy: Low-level laser
therapy, including the exposure of tissues to low lev-
els of visible or near infrared light, can be used as an
ancillary treatment for AGA. Low-level laser therapy
can be performed at home, using a LaserComb or
wearing for a certain amount of time a helmet whose
power cord is plugged into a standard outlet. Dura-
tion of therapy and frequency varies for the differ-
ent devices. Current studies evaluating laser devices
show inconsistent results thus providing low qual-
ity evidence.27 However, an improvement in total
hair count has been partly reported after using such
devices.29,30
MISCELLANEOUS
Besides the above-mentioned evidence-based thera-
peutic approaches, there is a wide range of molecules,
products, and interventions claiming to promote
hair growth in AGA. These include platelet-rich
plasma, mesotherapy, botulinum toxin injections,
pulsed electromagnetic/static field devices, topically
applied caffeine, melatonin, retinoids, biochanin A,
Kang_CH085_p1495-1506.indd 1505
adenosine, prostaglandin analogs, herbal prepara-
tions, and nutritional supplements (eg, biotin, zinc,
16
copper, amino acids, micronutrients and combination
preparations). For most of these products controlled
clinical studies are scarce and largely of low evidence
level. Detailed information on these products and
the available literature can be found in the current S3
guidelines for the treatment of AGA in women and
in men.27 Based on currently available literature data
no evidence-based recommendation can be given for
these miscellaneous products. Their use as a sup-
portive strategy within an individually tailored man-
agement approach is at the discretion of the treating
dermatologist and the decision of the patient. Further
Chapter 85 :: Androgenetic Alopecia
controlled studies to prove the relevance of these and
other new approaches in the treatment of AGA are
needed.
COUNSELING
AGA is the most common hair loss disorder, affecting
both men and women. Taking into account the high
prevalence and the psychosocial burden and the often
significant impairment of life of affected patients, the
need for competent counseling and development of
a trusting patient–physician relationship becomes
apparent. To enhance therapy compliance, the patient
must be informed in detail about the therapeutic goal,
the possible treatment options, and their potential
side effects. The naturally progressive nature of the
disease should be pointed out, as well as the often
limited response to therapy, particularly in advanced
AGA. Practical counseling with tips on handling the
disease in daily life should be offered. In individual
cases with high emotional overlay, particularly in
women, professional psychological help might be
helpful. Overall, counseling dermatologists should
develop a therapeutic personalized plan for each
patient based on clinical status, demands, needs, and
complaints. The individualized concept should com-
prise pharmacologic evidence-based recommenda-
tions, hair care and cosmetic tips, and psychological
counseling. The physician and patient must decide
together on the best suited individualized therapy,
considering the expected results, practicality, and
compliance.
SCREENING
Early diagnosis and treatment to prevent progression
of AGA is important in genetically predisposed fami-
lies. In patients with longstanding advanced AGA,
especially in male pattern baldness, scalp examina-
tion should include screening for benign and malig-
nant skin lesions, such as actinic keratoses, squamous
cell carcinoma or basal cell carcinoma as a result of
increased ultraviolet exposure of the balding scalp and 1505
the lack of protecting full hair.
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