16

Disorders of the PA RT
Hair and Nails

Chapter 85 :: Androgenetic Alopecia

:: Ulrike Blume-Peytavi & Varvara Kanti

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

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16 CLINICAL FEATURES FEMALE PATTERN
MALE PATTERN HAIR LOSS HAIR LOSS

MALE PATTERN, HAMILTON- FEMALE PATTERN,

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

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.)

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 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.)

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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 first-degree male relatives of women with AGA, which
::

AGA. Candidate genes include genes for the androgen suggests there is at least some genetic commonality
Disorders of the Hair and Nails

receptor (AR), histone-deacetylases (HDAC) 4 and 9, between female and male AGA.18 Case-control gene-
and the WNT molecule WNT10A.13 association studies have found a weak association
In men, AGA is an androgen-dependent trait.14 Dihy- between the AR/EDA2 locus and early-onset female
drotestosterone is the androgen chiefly responsible for AGA, but no association with the 11 autosomal loci
the follicular pathology. Dihydrotestosterone probably that associate with male AGA.19-21 There is a weak asso-
acts primarily on dermal papilla, the predominant site of ciation with the gene for estrogen receptor 2 (ESR2),
androgen receptor and type II 5α-reductase expression which suggests the involvement of estrogenic path-
within the hair follicle. A number of signaling molecules ways in female AGA.22,23 As of this writing there have
have been implicated in the inhibition of hair growth been no genome-wide studies in women.
in AGA including transforming growth factor (TGF)-β1 The role of androgens in female AGA is also less certain
and transforming growth factor-β2,14 dickkopf 1 (a mem- than in men. Nevertheless, there is a subset of women
ber of the WNT signaling family),15 and interleukin-6.16 with AGA and associated hormonal dysregulation.
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- DIAGNOSIS
ing scalp skin; prostaglandin D2 has an inhibitory effect
Generally, AGA is a clinical diagnosis. Depending on
on hair growth in animal and in in vitro experiments.17
patient history and clinical evaluation, further diag-
nostics may be necessary.

WOMEN
PATIENT HISTORY
Less is known about the etiology of AGA in women.
There is an increased frequency of balding in 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
Olsen scale
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.
Male pattern Diffuse Frontal accentuation
(Hamilton) (Ludwig) (Olsen) In women, especially in those with peripheral signs
of hyperandrogenism (Fig. 85-7), a gynecologic history
Figure 85-6 Olsen scale: Christmas tree pattern in female is recommended, including among other possibilities,
pattern hair loss. (Redrawn from Blume-Peytavi U, menstrual cycle disturbances and intake of hormonal
Blumeyer A, Tosti A, et al. S1 guideline for diagnostic contraception.
1498 evaluation in androgenetic alopecia in men, women and Furthermore, a detailed patient history should be
adolescents. Br J Dermatol. 2011;164[1]:5-15.) performed to rule out other causes for the hair loss or

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 16

Chapter 85 :: Androgenetic Alopecia

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 like lichen planopilaris or frontal fibrosing alopecia,
systemic and newly diagnosed diseases (eg, infections, which can mimic AGA, should be considered (see
thyroid function disorders, and surgical procedures) that section “Differential Diagnosis”). Balding scalp exami-
occurred 6 months to 1 year prior to the first signs of hair nation should include checking for photodamage and
loss, and nutritional behavior (especially chronic deficient field cancerization. Thus, clinical examination of the
diet or rapid significant weight loss) possibly leading to scalp should focus on possible signs of inflammation,
diffuse effluvium (see section “Differential Diagnosis”). like erythema, scaling, or hyperkeratosis, and signs of
Lifestyle procedures, such as special hairstyles causing scarring, such as skin atrophy and loss of hair follicle
traction, and environmental factors like smoking and ostia. However, atrophy of scalp skin also may be pres-
ultraviolet radiation exposure should be considered.1 ent in longstanding AGA.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
HAIR EXAMINATION
antithyroid action, intake of anabolic steroids, or supple- Scalp Hair: Hair should be parted to assess scalp
mental androgens. Allergies and intolerances should be hair density. Part width should be compared between
recorded as they might be important for the choice of the the frontal, occipital, and temporal regions to exam-
appropriate therapy (eg, contact dermatitis caused by ine the distribution of alopecia (see Figs. 85-1 through
propylene glycol in topical solutions)1 as well as cosmetic 85-6, Hamilton-Norwood, Ludwig, and Olsen scales).
habits (eg, hair care and color, hair style). Dermoscopy/trichoscopy can be helpful in assessing
hair follicle openings to exclude scarring alopecia and
in identifying short and fine miniaturized hairs. Hair
CLINICAL EXAMINATION caliber variations might also be present.
The hair pull test (Sabouraud maneuver) can be
implemented to provide information on hair shed-
Clinical examination should involve the scalp skin and ding. For this test, approximately 50 to 60 hairs are
hair, facial and body hair, and skin, as well as the nails. grasped between the thumb, index, and middle fingers
from the base of the hairs near the scalp and firmly,
SCALP EXAMINATION but not forcefully, tugged away from the scalp. If more
than 10% of the grasped hairs are pulled away from
The scalp skin usually appears normal in AGA, but fre- the scalp, this constitutes a positive pull test and con-
quently associated findings include seborrhea and/or firms active hair shedding.1 In AGA, the hair pull test
seborrheic dermatitis.1 Inflammatory or infectious dis- may be positive in the frontal region, while it is typi- 1499
eases, as well as alopecia areata and scarring alopecia cally negative in the occipital region.

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16 Facial and Body Hair Examination: Facial and
body hair density and/or distribution changes can be
cases to rule out other differential diagnoses or comor-
bidities.1 The trichogram should only be performed by
found as a result of ethnic hypertrichosis, hypertrichosis dermatologists who are familiar with this technique
caused by medications, or hirsutism. Signs of acne, seb- and perform it routinely.
orrhea, oily skin, and obesity might present peripheral
signs of hyperandrogenism. Even though some women
with AGA complain of reduction of eyebrows or eye- BIOPSY
lashes, this finding points to other types of alopecia, like
A biopsy, mostly performed as a deep, 4-mm, cylindri-
alopecia areata or frontal fibrosing alopecia (see section
cal punch, is indicated in AGA only in cases where the
“Differential Diagnosis”)24 rather than to AGA.
diagnosis is uncertain, such as where scalp changes
are suggestive of cicatricial alopecia or diffuse alopecia
NAIL EXAMINATION areata. Scalp biopsies should be evaluated by derma-
topathologists who are experienced in hair pathology
Nail abnormalities are not characteristic for AGA, but using both vertical and horizontal sectioning. The pre-
Part 16

may contribute to differential work up of alopecia ferred area for biopsy is the central scalp in an area
areata, certain deficiencies, and lichen planus.1 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

DIAGNOSTIC TOOLS of AGA.1 Histologically AGA presents an increased
Disorders of the Hair and Nails

number and proportion of miniaturized (vellus-like)

hair follicles with a typically less than 3:1 ratio of ter-
DERMOSCOPY minal to vellus-like hair follicles, compared with a
greater than 7:1 ratio in the normal scalp. Other fea-
Dermoscopy, a noninvasive technique, improves exami-
tures include an increased telogen-to-anagen ratio and
nation of scalp skin and hair shafts by magnification (eg,
an increase in the number of follicular stelae (tracts
assessment of hair follicle openings, hair shaft caliber
beneath miniaturized follicles). A mild perifollicular
variations). The findings can be saved for future com-
lymphohistiocytic infiltration, primarily around the
parison using videodermoscopy. In AGA, hair diameter
upper hair follicle, also may be present, as well as peri-
variations, loss of trio groups with single terminal hairs,
follicular fibrosis, in longstanding AGA.
and an increased number of vellus hairs can be seen.

GLOBAL PHOTOGRAPHY
Global photographs are helpful tools for the objective LABORATORY TESTING
evaluation of the course of hair growth, hair volume,
and hair density in clinical studies, and for long-term In men, laboratory testing for the diagnosis of AGA is
followup in daily practice. For followup assessment, not necessary, except if the history or clinical exami-
a standardized technique should be implemented, for nation indicate another underlying disorder or asso-
example, by using a stereotactic device assuring a con- ciated disease. Literature data indicate a possible
stant view, magnification, and lighting. positive association between AGA and insulin resis-
tance, metabolic syndrome, hypertension, and benign
prostate hyperplasia in men.25 Furthermore, laboratory
AUTOMATIC DIGITALIZED testing might be indicated before introducing specific
SYSTEM FOR HAIR DENSITY therapies (eg, measurement of the prostate-specific
antigen value before introducing finasteride therapy;
AND ANAGEN/TELOGEN HAIRS see section “Medications”).
(PHOTOTRICHOGRAM) In women, an extensive endocrinologic workup is not
necessary, except if the history and clinical examination
These systems allow measurement of hair density and indicate androgen excess. In this case, an interdisciplin-
the anagen-to-telogen ratio for diagnostic and followup ary approach involving gynecologists, endocrinolo-
purposes, but they are mainly used for standardized and gists, and dermatologists is recommended to rule out/
reproducible tools in clinical studies. Typical findings in distinguish between the different causes associated with
AGA are reduced hair density in a pattern distribution hyperandrogenism, such as polycystic ovary syndrome,
compared to the occipital area. The anagen-to-telogen congenital adrenal hyperplasia, androgen-secreting
ratio is normal or decreased when comparing frontal or tumors, or Cushing syndrome. For this purpose the free
vertex to the occiput. These techniques are helpful for androgen index, sex hormone-binding globulin, and
long-term followup and quantification of hair density. prolactin should be determined and further laboratory
testing (eg, 17-OH-progesterone, follicle-stimulating
TRICHOGRAM hormone, estradiol, or cortisol) should be considered.
The measurements should be optimally taken between
1500 The trichogram is not indicated as a routine diagnostic 8:00 and 9:00 am, ideally between the second and fifth
tool in AGA. It should only be considered in individual day of the menstrual cycle, in order to standardize and

Kang_CH085_p1495-1506.indd 1500 03/12/18 10:24 am

 facilitate interpretation. Furthermore, it is advisable to
perform blood hormone testing at least 2 months after
with premature onset of AGA, an interdisciplinary
approach involving the dermatologist and pediatric
16
stopping any hormonal intake, including oral contra- endocrinologist should be taken. If significant psycho-
ception, as estrogens lead to elevated sex hormone- logical distress is observed, especially in women and
binding globulin levels and consequently falsify the young patients with early onset of AGA, psychological
outcome of the free androgen index.1 referral should be considered for the development of
Measurement of ferritin level or thyroid- coping strategies.
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 DIAGNOSTIC ALGORITHM
treatment of diffuse androgen-dependent alopecia in
women, even though contradictory data also have A diagnostic evaluation form for AGA has been pro-
been published.1 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.)

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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-

ral band like recession, loss of eyebrows, perifollicular
DIFFUSE ALOPECIA AREATA erythema and hyperkeratosis (see Fig. 85-10C, D). The
detection of clinical and histologic signs consistent
Diffuse alopecia areata typically does not follow a with a lymphocytic scarring alopecia aid in diagnosis.
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 TRACTION ALOPECIA
Traction alopecia occurs as a result of chronic tension
on the hair shaft (see Fig. 85-10B). Although the hair
TABLE 85-1 loss is reversible initially, hair loss may become perma-
Differential Diagnoses for Androgenetic nent if tension on the hair follicles continues. History
Alopecia 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

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 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
of libido, depression, suicidal ideation, impaired cogni-
tion, fatigue, and decreased penile sensitivity, probably
has an often underestimated psychosocial impact on occurring in men with a history of sexual dysfunction
the affected patients.26 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-

MANAGEMENT sion or current sexual dysfunction.

The response to treatment should be assessed at
6 months, although in some men it may not become
MEDICATIONS evident before 12 months. If successful, treatment
needs to be continued to maintain efficacy. In case
The best clinical evidence according to current study of ineffective treatment with 1 mg finasteride over
data concerns the topical application of minoxidil. Min- 12 months, the off-label use of the 5α-reductase inhibi-
oxidil prevents further progression of the disease and tor dutasteride, which inhibits the isoenzymes type 1
Part 16

leads to an increase in hair density and hair thickness and type 2, at a dose of 0.5 mg a day can be considered.
both in male patients older than 18 years of age with Finasteride is not indicated in women and is con-
mild to moderate AGA (2% to 5% solution; 1 mL or traindicated in pregnant women and women of child-
half a cap of 5% foam twice daily) and female patients bearing potential, because of the risk of feminization
::

older than 18 years of age (2% solution; 1 mL twice daily of a male fetus. Finasteride-treated men must avoid
Disorders of the Hair and Nails

or half a cap of 5% foam once daily). The response to donating their blood.27
treatment should be assessed at 6 months. If successful, In female postmenopausal patients, finasteride 1
treatment needs to be continued to maintain efficacy.27 mg failed to show efficacy; however, finasteride 5 mg
The patients should be informed about transitory may be effective in female normoandrogenic premeno-
increased telogen hair shedding, usually appearing pausal and postmenopausal patients. However, no
within the first 8 weeks of therapy initiation. Further- placebo-controlled trials are available in this popula-
more, after end of therapy with topical minoxidil, tion. In women of childbearing age, the use of a safe
increased hair loss follows. contraceptive method is indispensable.27
The main side effect of topical minoxidil is hypertri- Clinical studies on the efficacy of topical finasteride
chosis, mostly from local spreading or excessive con- preparations are currently underway.
tinuous topical application. To avoid contamination Antiandrogens and estrogenic drugs are being used
of the pillow with subsequent facial contact patients in the treatment of AGA, although evidence of effi-
should be advised to apply the drug at least 2 hours cacy for any of these treatments is insufficient. In male
before going to bed. Irritant and allergic contact der- patients, the use of systemic estrogens or androgen-
matitis may also occur. Irritation is more common with receptor antagonists is not recommended. In women
the 5% solution because of its higher content in propyl- with AGA and clinical or biochemical evidence of
ene glycol. Contact dermatitis resulting from propyl- hyperandrogenism, the use of oral antiandrogens
ene glycol or from minoxidil itself should be confirmed (chlormadinone acetate, cyproterone acetate, drospi-
by patch testing. It is recommended to pause topical renone, spironolactone, flutamide) in combination
minoxidil use during pregnancy and lactation, owing with an estrogen as an oral contraceptive pill can be
to the lack of data during this period.27 considered. Side effects of cyproterone acetate include
In male patients older than 18 years of age with depressive mood changes and liver toxicity. There is an
mild to moderate AGA, a systemic therapy with the increased risk of venous thromboembolism in patients
5α-reductase type 2 inhibitor finasteride (1 mg/day) taking estrogen-containing oral contraceptives, which
improves or to prevents progression of AGA. For may be greater in those taking cyproterone acetate
greater efficacy, the combination of oral finasteride than other oral contraceptives. Spironolactone 100 to
(1 mg once daily) and topical minoxidil can be consid- 200 mg per day taken continuously is an alternative
ered. Patients under treatment with finasteride should option because of its antiandrogenic effect, but should
be aware of reduction of prostate-specific antigen, also be combined with a safe contraceptive in women
which is important in prostate cancer screening in men. of childbearing age. Side effects include menstrual dis-
Further reported side effects of finasteride are impaired turbances and hyperkalaemia.27
sexual function, including erectile dysfunction, ejacula- As of this writing, there is insufficient literature evi-
tion dysfunction, reduced ejaculate volume, and loss of dence on the effect of topical alfatradiol, topical natural
libido. A possible negative impact of finasteride on those estrogens or progesterones, or topical fluridil.27
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 PROCEDURES
spermatogenesis in those men with preexisting condi-
tions relating to infertility should be mentioned. Post-
finasteride syndrome, defined as various symptoms
SURGERY
1504 persisting for months or years after discontinuation of In AGA, hairless or thinning areas can be cosmeti-
finasteride treatment, including sexual dysfunction, loss cally covered, albeit with a decreased density, using

Kang_CH085_p1495-1506.indd 1504 03/12/18 10:24 am

 hair restoration surgery. Hair restoration surgery
involves hair transplantation, scalp reduction sur-
adenosine, prostaglandin analogs, herbal prepara-
tions, and nutritional supplements (eg, biotin, zinc,
16
gery, or a combination of both. Hair transplantation copper, amino acids, micronutrients and combination
is less invasive than scalp reduction surgery. Over preparations). For most of these products controlled
the last decades, hair transplantation has evolved clinical studies are scarce and largely of low evidence
into a microsurgical procedure. Follicular units of level. Detailed information on these products and
1 to 4 hairs are transplanted in large numbers and the available literature can be found in the current S3
high densities. Hair surgery, especially follicular unit guidelines for the treatment of AGA in women and
transplantation, can be considered to improve AGA in men.27 Based on currently available literature data
in suitable patients with sufficient donor hair supply no evidence-based recommendation can be given for
and medically controlled or spontaneously stabilized these miscellaneous products. Their use as a sup-
AGA, especially in the frontoparietal area. The result portive strategy within an individually tailored man-
greatly depends on the skills of the surgical team agement approach is at the discretion of the treating
and the adjustment of the surgical plan to individual dermatologist and the decision of the patient. Further

Chapter 85 :: Androgenetic Alopecia

patient characteristics. As hair surgery does not influ- controlled studies to prove the relevance of these and
ence progression of AGA, long-term results in early other new approaches in the treatment of AGA are
stages depend on spontaneous or medical stabiliza- needed.
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 COUNSELING
AGA is the most common hair loss disorder, affecting
NONPERMANENT HAIR both men and women. Taking into account the high
prevalence and the psychosocial burden and the often
REPLACEMENT MEASURES significant impairment of life of affected patients, the
Nonsurgical hair replacement methods include, in need for competent counseling and development of
addition to full and partial hair replacement mea- a trusting patient–physician relationship becomes
sures (wigs), various hair-binding techniques and hair apparent. To enhance therapy compliance, the patient
extension and supplementation techniques, either must be informed in detail about the therapeutic goal,
performed by the patients themselves (eg, sprinkle the possible treatment options, and their potential
hair) or by specialized personnel (eg, camouflage tech- side effects. The naturally progressive nature of the
niques, bonding).28 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
INTERVENTIONS disease in daily life should be offered. In individual
cases with high emotional overlay, particularly in
Low-Level Laser Therapy: Low-level laser women, professional psychological help might be
therapy, including the exposure of tissues to low lev- helpful. Overall, counseling dermatologists should
els of visible or near infrared light, can be used as an develop a therapeutic personalized plan for each
ancillary treatment for AGA. Low-level laser therapy patient based on clinical status, demands, needs, and
can be performed at home, using a LaserComb or complaints. The individualized concept should com-
wearing for a certain amount of time a helmet whose prise pharmacologic evidence-based recommenda-
power cord is plugged into a standard outlet. Dura- tions, hair care and cosmetic tips, and psychological
tion of therapy and frequency varies for the differ- counseling. The physician and patient must decide
ent devices. Current studies evaluating laser devices together on the best suited individualized therapy,
show inconsistent results thus providing low qual- considering the expected results, practicality, and
ity evidence.27 However, an improvement in total compliance.
hair count has been partly reported after using such
devices.29,30

SCREENING
MISCELLANEOUS Early diagnosis and treatment to prevent progression
of AGA is important in genetically predisposed fami-
Besides the above-mentioned evidence-based thera- lies. In patients with longstanding advanced AGA,
peutic approaches, there is a wide range of molecules, especially in male pattern baldness, scalp examina-
products, and interventions claiming to promote tion should include screening for benign and malig-
hair growth in AGA. These include platelet-rich nant skin lesions, such as actinic keratoses, squamous
plasma, mesotherapy, botulinum toxin injections, cell carcinoma or basal cell carcinoma as a result of
pulsed electromagnetic/static field devices, topically increased ultraviolet exposure of the balding scalp and 1505
applied caffeine, melatonin, retinoids, biochanin A, the lack of protecting full hair.

Kang_CH085_p1495-1506.indd 1505 03/12/18 10:24 am

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