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Characteristics of Androgenetic Alopecia in Asian
Vol. 24, No. 3, 2012
243
Corresponding author: Won-Soo Lee, M.D., Ph.D., Department o
f
Dermatology and Institute of Hair and Cosmetic Medicine, Yonsei
University Wonju College of Medicine, 20 Ilsan-ro, Wonju 220-701,
Korea. Tel: 82-33-741-0622, Fax: 82-33-748-2650, E-mail: leewonsoo@
yonsei.ac.kr
T
his is an Open Access article distributed under the terms of the
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Ann Dermatol Vol. 24, No. 3, 2012 http://dx.doi.org/10.5021/ad.2012.24.3.243
REVIEW ARTICLE
Characteristics of Androgenetic Alopecia in Asian
Won-Soo Lee, M.D., Ph.D., Hae-Jin Lee, M.D.
Department of Dermatology and Institute of Hair and Cosmetic Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea
Androgenetic alopecia (AGA), or pattern hair loss, is a
common disorder in Asian men and women, with a reported
incidence of up to 73% among general population. There are
several descriptions regarding the characteristics of AGA in
patients of European descent. Asian patients with AGA have
different types of hair loss and family histories from
Europeans, which may affect treatment response. Therefore,
in this review, prevalence, hair loss patterns, familial factors,
androgen receptor gene polymorphisms of Asian AGA
patients, and management based on algorithmic guidelines
for AGA are discussed. This review may be useful for
dermatologists in clinical practice for diagnosing and
designing management approaches for Asian patients with
AGA. (Ann Dermatol 24(3) 243∼252, 2012)
-Keywords-
Androgenetic alopecia, Asians
INTRODUCTION
The term “androgenetic alopecia (AGA)” was introduced
by Orentreich
1
in 1960, but the same condition in men
has also been termed male pattern alopecia, common
baldness, male pattern baldness, and male pattern hair
loss (MPHL). Androgen dependence and hereditary factors
are less obvious in affected women than in affected men,
thus the term pattern hair loss, which is a much broader
concept, is preferred for women. AGA is the most
common type of alopecia that occurs after puberty in both
sexes. Patients typically present with progressive thinning
and shortening of hair in affected areas. AGA is clearly a
stressful experience for both sexes, but it may be
substantially more distressing for women. In this review,
Asian characteristics of prevalence, hair loss patterns,
familial factors, androgen receptor (AR) gene polymor-
phisms, and management of AGA will be discussed.
PREVALENCE OF AGA IN ASIAN
There are population differences in the prevalence and
types of AGA. In individuals of European descent, the
prevalence of AGA has been well documented by
Hamilton
2
and Norwood
3
. A study of European-American
men in the USA revealed a predominance for frontal bald-
ness (Type A variant in Norwood-Hamilton classification)
in 12% and a Type III or worse pattern in 16% of males
aged 18∼29 years old, which increased progressively to
53% in those aged 40∼49 years old
4
. A study of 20∼50
year old Norwegian men most commonly reported Type I
(31%), followed by Type II (26%) and Type V or worse
(20%)
5
.
AGA is also a common disorder in Asian people.
Takashima et al.
6
and Kakizo
7
studied AGA in Japanese
and found that it was minimal before the age of 40 and
that, although the incidence increased with age, it
remained lower than in Europeans. Japanese men develop
AGA approximately one decade later than Europeans, and
the prevalence is 1.4-fold lower in each decade of life
6
. In
Korean men, the prevalence of AGA (Norwood III or
above) at all ages was 14.1% and increased steadily with
advancing age, but remained lower than that of Europeans:
2.3% in the third decade, 4.0% in the fourth decade,
10.8% in the fifth decade, 24.5% in the sixth decade,
34.3% in the seventh decade and 46.9% over 70 years.
Type III vertex involvement was the most common type in
the third decade to the seventh decade in Korean men;
over 70 years, type VI was most common. A ‘female
W
S Lee and HJ Lee
244 Ann Dermatol
pattern’ was observed in 11.1% of cases
8
. In Korean
women, the prevalence of AGA (Ludwig I or above) at all
ages was 5.6%, and also increased steadily with advan-
cing age: 0.2% in the third decade, 2.3% in the fourth
decade, 3.8% in the fifth decade, 7.4% in the sixth
decade, 11.7% in the seventh decade and 24.7% over age
70 years. Type I was the most common type up to the
sixth decade; over 60 years, Type I and II were similar in
prevalence. Type III was not observed
8
.
The age specific prevalence of AGA in Taiwanese men
was compatible to that among Korean men but was lower
than that among individuals of European descent
9
.
Smoking status, current amount of cigarette smoking, and
smoking intensity were statistically significant factors for
AGA after controlling for age and family history
9
. A
population-based cross sectional study was carried out in
7,056 subjects (3,519 men and 3,537 women) in Shang-
hai, China
10
. The prevalence of AGA in Chinese men was
19.9%, and the prevalence of female pattern hair loss
(FPHL) in men was 0.1%. The most common type of hair
loss in men was type III vertex (3.5%). The prevalence of
AGA in Chinese men was lower than in European men
but was similar to that in Korean men. However, over the
age of 60 it approached the prevalence in European men
and was higher than in Korean men. The prevalence of
AGA in Chinese women was 3.1%, while MPHL in
Chinese women was found in those aged over 50 years
(0.4%), and the most common type was Ludwig type I
(1.4%). Interestingly, the prevalence of AGA in Chinese
women was lower than that in Korean women and
European women, and type I was the most common
type
10
.
In Singapore, Tang et al.
11
reported a prevalence of 63%
for Norwood type I to VII. The prevalence increased with
age from 32% among young adults aged 17 to 26 years to
almost 100% for those in their eighties. In Thailand,
Pathomvanich et al.
12
conducted a randomized study
including 1,124 Asian men (local Thai and Chinese)
between the ages of 18 and 90. The prevalence of
baldness was reported as 38.52%; this figure approached
that of Europeans, rather than the one fourth to one third
reported in previous studies of Asians
6
. The prevalence
increased with age, affecting 11% of young adults aged
over 20 years and reaching 61.78% at 70 years of age.
There are, however, two limitations of this survey. First,
the small number of men included over 80 years of age
(31 men) might have affected the results when compared
to the Norwood study of the same age group. In addition,
there were two Asian subgroups involved in this study,
Thai and Chinese.
According to these studies mentioned, the prevalence of
AGA in Chinese and Korean men was similar to, but
significantly lower than, the prevalence in Thailand. The
highest prevalence among the Asian groups studied was
the 63% observed in Singapore; this discrepancy may be
attributed to the diverse populations residing in the
country or the inclusion of the almost normal Norwood
type I in the Singapore study. In contrast, type II was the
most common pattern among Indian males until the sixth
decade, followed by type III Vertex after the sixth decade.
The type A variant was only seen in 1% of Indian males,
and FPHL was only observed in 0.2% of Indian males.
These results suggest a less extensive balding pattern in
Indian male population than in other Asian populations
13
.
In summary, Asian men with AGA have different charac-
teristics from those of men of European descent. There are
similar increases in prevalence with age among all the
Asian groups studied. This high prevalence in older men
suggests that this form of hair loss may be a normal
consequence of aging. However, particularly in younger
men, hair loss can have significant psychosocial manifes-
tations, and can in turn have a significant economic
impacts on household health expenditures
14
. The wide
variation in prevalence rates in the current Asian studies
would require a more standardized protocol.
AR GENE POLYMORPHISM IN AGA
Balding scalps are characterized by high levels of the
potent androgen dihydrotestosterone (DHT) and increased
expression of the androgen receptor gene. Most AGA
patients have an androgen dependent trait, although it is
thought to be under the control of multiple genes, such as
genes for the AR, insulin-like growth factor-1, and DHT
regulations
15,16
. The human AR gene is on the X
chromosome at Xq11-12. The AR is a structurally
conserved member of the nuclear receptor superfamily.
The amino terminal domain is required for transcriptional
activation and contains a region of polyglutamine that is
encoded by CAG trinucleotide repeats. In humans, the
number of CAG repeats is polymorphic. Expansion of
CAG repeats in the AR has clinical implications for human
disease
17
. A low number of CAG repeats in the AR gene
implies increased risk factors for coronary heart disease
18
and prostate cancer
19
. In recent studies, neurotrophic
factors, especially brain-derived nerve factor, were found
to have potential importance mediating the effects of
androgens on hair follicles, serving as negative regulatory
control signals
20
. These findings suggest that other regula-
tory signals may affect the pathogenesis of AGA, as well as
AR gene polymorphisms.
The ubiquity of the AR gene Stu I restriction site, and the
Characteristics of Androgenetic Alopecia in Asian
Vol. 24, No. 3, 2012
245
higher incidence of shorter triplet repeat haplotypes in
bald men, suggests that these markers are very close to a
functional variant that is a necessary component of the
polygenic determination of male pattern baldness. A
meta-analysis study by Zhuo et al.
21
suggests that the G
allele of the AR Stu I polymorphism might be a potential
risk factor for AGA, especially in subjects of European
descent. Functional mutations in or near the AR gene may
explain the high reported levels of expression of this gene
in the balding scalp
22
. Shorter CAG repeat lengths may be
associated with the development of androgen mediated
skin disorders such as AGA, hirsutism, and acne in men
and women
23
. These findings suggest that the CAG repeat
length in AR may affect androgen mediated gene expres-
sion in hair follicles and sebaceous glands in men and
women with androgenic skin disorders
14,23
. Interestingly,
when the number of triplet repeats (CAG+GGC) was
plotted against degree of symptom improvement after
treatment with finasteride, a broad correlation between
these variables was observed
24
. The smaller the repeat
number, the greater the improvement with finasteride. The
group of patients with shorter repeat regions in the AR
gene responded better to finasteride than did those with
longer repeat regions, although patients with shorter
repeats tended to have severe initial symptoms. The
determination of such polymorphisms is thought to be
useful in drug choice for AGA patients
24
.
Jung et al.
25
compared CAG repeat numbers within the AR
genes of 64 male Korean AGA patients with those of 40
normal male controls in a preliminary study. There was no
significant difference in the number of CAG repeats
between the Korean AGA patients and controls. There
were no correlations between CAG repeat numbers and
age of onset or severity of AGA in Korean AGA patients.
These results suggests that AR receptor CAG polymor-
phisms in the Korean male population might not play a
major role in AGA susceptibility. Nevertheless, a more
extensive study to clarify whether there are real population-
based differences in AR gene polymorphisms is needed.
Recently, advanced genetic studies of AGA have been
published. Hayes et al.
26
reported that the gene locus of
E211A is significantly lower in proportion in the vertex
and vertex balding group and frontal balding group com-
pared with the no balding group. Therefore, the AR-E211
A allele, in linkage with the functional repeat sequences,
is associated with a lower risk of metastatic prostate
cancer and a lower risk of alopecia. Moreover, a study
using genome-wide linkage study revealed a locus
associated with AGA on chromosome 3q26
27
.
Hillmer et al.
28
investigated the signatures of genetic
variants of AR and their relationships to the AGA risk
haplotype. Haplotype homozygosity suggested that the
AGA risk haplotype was driven to high frequency by
positive selection in Europeans, although a low meiotic
recombination rate contributed to high haplotype homo-
zygosity. Further, they detected high levels of population
differentiation and a series of fixed derived alleles along
an extended region centromeric to AR in the Asian
HapMap sample.
RACIAL DIFFERENCES IN PATTERNS OF
HAIR LOSS IN AGA AND THE BASP
CLASSIFICATION FOR AGA
Asian men with AGA display different characteristics
compared with men of other ethnicity. However, there is
an increase in prevalence with age among all the Asian
groups studied similar to that observed in other ethnic
population
8-12,29
. The reason for this increase rate in the
prevalence of AGA compared to Europeans remains
unknown, but a transition toward a more Western diet
and lifestyle may play a role.
There are also populational differences in the patterns of
hair loss in AGA. In a previous study, FPHL was observed
in 11.1% of Korean males with AGA
8
. In a Chinese study,
MPHL was found in 13 of 108 (12%) women with AGA,
all of whom were over 50 years of age
10
. In an Indian
study, although it was possible to classify 80% of cases of
AGA and II (28%) and III (15%) were the most common
types of AGA, 27 patients of 150 male subjects (18%) did
not fit into specific patterns according to the Norwood
Hamilton classification
30
. In addition, the type ‘a’ variant
was noted in 20% of patients, clearly indicating the
limitations of the existing classifications. There is consider-
able overlap in types IV, V and VI in the Norwood
classification, with the ‘a’ variants further confusing the
picture
30
.
Various classification methods have been proposed for
describing AGA. In 1950, Beek
31
published a classification
system, based on 1,000 males of European descent, which
used two evolutionary aspects: frontal and frontovertical
baldness. In the following year, the first systematic
classification of AGA was established by Hamilton
2
, who
sub-classified patterns of baldness based on frontoparietal,
frontal recession, and vertex thinning, then evaluated a
large group of men and women for the presence of
specific patterns of hair loss from the prenatal period
through the tenth decade of life. In 1975, Norwood
3
refined Hamilton’s classification by emphasizing temporo-
frontal or vertex only subcategories of hair loss into seven
types with a type A variant and reported the incidence of
male pattern baldness at various ages in 1,000 adult male
W
S Lee and HJ Lee
246 Ann Dermatol
Fig. 1. The Norwood-Hamilton classification of male balding
defines two major patterns and several less common types.
Thinning starts in both temples as well as the crown/vertex and
slowly progresses to encompass the entire top of the scalp (cited
from Ref. 3).
Fig. 3. The BASP classification system includes four basic types
(L, M, C, and U) and two specific types (V and F). The basic
types represent the shape of the anterior hairline, and the specifi
c
types represent the density of hair on specific areas (frontal and
vertex). The final type is decided by the combination of the basi
c
and specific type (cited from Ref. 37).
Fig. 2. The Ludwig pattern of hair loss (3-point). There are thre
e
main classes, each with increasing hair loss (cited from Ref. 35).
subjects of European descent. An additional pattern was
introduced as the Norwood-Hamilton classification in a
clinical trial of finasteride in MPHL
32
. Olsen
33,34
proposed
assigning separate designations (temporal, frontal, mid and
vertex) to areas of the scalp that bald at different rates in
different individuals with MPHL. Ludwig
35
presented quite
a different picture of hair loss in women from that
described by Hamilton
2
. He emphasized preservation of
the frontal fringe despite progressive centrifugal loss over
the top of the scalp and arbitrarily designated three
gradations of hair loss. Olsen
36
proposed that frontal
accentuation (or the ‘‘Christmas tree’’ pattern) should be
considered an additional pattern of hair loss in women,
which helps to distinguish AGA from potential hair loss
mimicries in women. Presently, the Norwood-Hamilton
classification
32
for MPHL and the Ludwig classification
35
for female AGA are the most commonly used classification
methods for assessing AGA worldwide.
Each of these existing classifications has substantial
limitations in clinical setting. The Norwood-Hamilton
classification (Fig. 1)
3
is very detailed and is less stepwise
classifications in its descriptions, making it difficult to
memorize for common use. It does not list some non-typical
types of baldness, such as FPHL in men. Additionally,
many women with MPHL cannot be classified using the
Ludwig classification system (Fig. 2)
35
. For most of these
classification systems, clinicians must use different classi-
fication systems for each gender in order to correctly
classify patterns
34
.
Thus, a more widely accepted, accurate, and stepwise
method for classifying AGA would be of great benefit. Lee
et al.
37
devised a new classification system, named the
Basic and Specific (BASP) classification (Fig. 3), which is
comprehensive and systematic regardless of population or
gender. The BASP classification
37
was based on observed
patterns of hair loss. The basic (BA) types represent the
shape of the anterior hairline, and the specific types (SP)
represent the density of hair on distinct areas (frontal and
vertex). There are four basic types (L, M, C, and U) and
two specific types (F and V). The final type is assigned
according to a combination of the assigned BA and SP
types.
A total of 2,213 Korean subjects, comprised of 1,768
males and 445 females, were classified according to the
BASP classification
37
. According to the severity of the
Characteristics of Androgenetic Alopecia in Asian
Vol. 24, No. 3, 2012
247
phenotype, both the basic and specific types were
subclassified into subtypes in order to generate a more
stepwise and systematic classification. It is possible to
describe patterns of hair loss in detail using the BASP
method, and, thus estimate the further extent of hair loss
and therapeutic response to a certain therapy. For both
sexes, the majority of patients enrolled in the study were
in the third and fourth decades of life (65.1% of males and
56.68% of females). In males, the older as well as the
younger group were more likely to have little recession of
the frontal hairline (classified as type M1-2) and diffuse
thinning over the top of the scalp (type F1-2). The women
in the study developed typical female AGA.
In men, regardless of age, 1,434 of the 1,768 males were
classified as type M, accounting for 81.1% of cases.
Among the subtypes and according to the severity of
baldness, the majority of subjects below 50 years of age
were classified as type M1, whereas most subjects over
the age of 50 were classified as type M2. The incidence of
Type L (9.3%) tended to decrease with age, but those of
types C (5.8%) and U (3.8%) tended to increase. In
women, type L showed the highest frequency in all age
groups, accounting for 210 (47.2%) of 445 female
subjects. Regardless of age, types M, C, and U were the
next most common in order, observed in 121 women
(27.2%), 111 women (25.0%), and 3 women (0.6%) of the
445 subjects, respectively. Type C0 was the second most
common subtype in female subjects between the second
and fourth decade of life, and its incidence decreased with
age. In men, type F, which is identical to FPHL in the
Ludwig classification, was observed in 42.4% (749/1,768)
of male subjects, and type V was observed in 19.8%
(350/1768). The grades of both types increased slightly
with age. In women, type F was observed in 70.6%
(314/445) of female subjects with AGA.
The BASP classification is a stepwise, systematic, and
universal classification system for AGA, regardless of race
or sex. It is an easily available comprehensive classification
system. The BASP classification may prove particularly
useful in communicating the exact amount and distribution
of hair loss in those with AGA
37
. For these reasons, we use
the basic and specific (BASP) classification in this review.
FAMILIAL FACTORS IN AGA
Family history plays an important role in the onset of
AGA, which is believed to be influenced by genetic
factors. However, the exact mode of inheritance has not
been well characterized. Although there are some reports
regarding the prevalence of AGA in male paternal family
members, reports regarding the maternal side are rare. The
AGA prevalence in male family members of patients
(30.3%) was higher than those of controls (8.5%)
38
. AGA
prevalence on the paternal side was greater than on the
maternal side. However, no differences were found
between paternal and maternal AGA prevalence, analyzed
according to the age of onset and severity of AGA. These
results suggest that AGA expression might be influenced
by familial AGA prevalence and that paternal AGA pre-
valence has a greater effect in general on AGA expression
than maternal AGA prevalence
38
.
In another Korean study, a family history of baldness was
present in 48.5% of men and 45.2% of women with
AGA
8
. In a Chinese study, a family history of AGA was
present in 55.8% of men and 32.4% of women with
AGA
10
. In contrast to the Korean study, the proportion of
Chinese men with a positive family history was higher,
suggesting that genetic background is important for
determining the prevalence of AGA in Chinese men, and
confirming that subjects with positive family histories are
at greater risk of developing severe AGA
9
. The proportion
of Chinese women with positive family histories was
lower, further indicating that AGA is a polygenetic heredi-
tary disease. In a Singaporean study, a positive family
history of AGA was recorded in 58.9% (151/256) of
subjects. Male patients tend to be more likely to have a
father or male sibling with a similar problem, whereas
female patients tend to be more likely to have a mother or
female sibling with AGA
39
. In an Indian study of 150
subjects, positive family histories were found in 127
(85%) of subjects, paternal in 101 (67%), maternal in
seven (5%) and both in 19 (13%). In 23 (15%) patients, no
family history could be elicited.
In a Taiwanese study, an association was detected between
moderate or severe AGA and family history of AGA from
paternal relatives, whereas there was no corresponding
association with maternal relatives
9
. Moderate or severe
AGA was associated with a family history of AGA among
first degree and second degree relatives but not among
third degree relatives after adjusting for age. In addition,
family histories of AGA among paternal relatives were
predictive of moderate or severe AGA after adjusting for
age. These findings do not support an association between
moderate or severe AGA and a family history of AGA
among maternal relatives. Moreover, a family history of
AGA is associated with the risk of early onset AGA. This
implies that those with a family history of AGA may have
a higher risk of early onset AGA and a higher risk of
developing severe AGA. Most importantly, early onset
AGA showed a dose dependent association with AGA
grade after adjusting for age and family history. From a
clinical point of view, this suggests that patients with early
W
S Lee and HJ Lee
248 Ann Dermatol
onset AGA should receive early advice to prevent further
deterioration
9
. These results of various epidemiologic familial
studies suggest that AGA expression is influenced by
familial AGA prevalence and, particularly, that paternal
AGA prevalence has more effect on AGA expression than
maternal AGA prevalence.
A recent study by Lee et al.
40
using the BASP classification
revealed that familial factors affecting the morphology of
AGA in Asians differ between males and females, and for
each BASP subtype. Parental influences on anterior
hairline shape in men were predominantly from the
paternal side, whereas these effects were less notable in
women. In patients without family histories of AGA, a
higher frequency of early-onset AGA than late-onset AGA
was identified in men but not in women. Basic types of
hair loss had a higher degree of heritability from the
paternal side of the family, regardless of the specific type.
This study provides detailed information indicating that
each hair loss pattern according to the BASP classification
has different familial factors in Asians
40
. Therefore, we can
provide appropriate information to patients if we obtain
careful personal and familial histories of AGA.
MANAGEMENT OF AGA IN ASIAN
General consideration
AGA is often related to poor self-image and low self-
respect. The problem must be viewed in perspective; an
emphatic approach is important, as different people are
affected in various ways when they lose hair. Patients
should avoid hair-care products likely to injure the scalp
and/or hair. Patients should maintain adequate diet,
especially with adequate protein. The National Institutes
of Health of the United States recommended daily
allowance for protein is 0.8 g/kg
41
. Topical medications
act only where the medication is applied; therefore, the
whole area at risk of hair loss (the top of the scalp) should
be treated with a given topical agent. If possible, any
drugs that could negatively affect hair growth should be
stopped and alternative substitutes used. Any underlying
scalp disorders, such as seborrheic dermatitis or scalp
psoriasis, should be treated as these conditions can affect
the ability to use topical treatments for hair loss without
irritation.
The typical man with MPHL who seeks treatment has
significant concerns about the condition and has already
engaged in considerable efforts to obtain information and
at times even resorted to self-medication. Individualized
consideration of attitudes, concerns, self-treating efforts,
and expectations is crucial for effective management of
men seeking medical treatment for MPHL
42
. Research has
shown that most men and women who have unwanted
hair loss have distressing experiences that diminish their
body image
43
. Because of the psychological impact of hair
loss, patients may seek inappropriate and unproven thera-
pies. However, they must also appreciate the real goals
and true limitations of each form of therapy. It is important
that misconceptions should also be corrected. Some
patients mistakenly think that their hormone levels are too
high. Others erroneously place too many restrictions on
their hair and grooming (e.g., hair styling, teasing, hair
spray, washing frequency, hair color or permanents)
44
.
Knowledge and understanding of the genetic and
physiological basis of AGA may help allay misconceptions
and anxiety about its occurrence, and indirectly influence
patient willingness to seek treatment for this condition
45
.
Clinicians should follow the progress of their patients
periodically to identify problems, utilizing photographic
records of treatment results.
Medical treatment
A reduction in hair loss is usually seen after 3∼6 months
of medical treatment, and visible hair regrowth is
observed after 6∼12 months. Continuous treatment is
needed to ensure sustained benefits. Unfortunately,
available medical treatments are not curative. Ensuring
that patients understand the limitations of these treatments
is an important aspect of the management of AGA.
Patients should be counseled that treatment for AGA will
not restore hair growth to its prepubertal density and that
the main aim is to prevent further progression of hair loss.
Currently there are two agents, topical minoxidil and oral
finasteride (only for males), approved by the United States
Food and Drug Association (FDA) for the treatment of
AGA.
1) Male
(1) Topical minoxidil solution
Topical minoxidil solution is administered at a dosage of
1 ml twice daily. Its mechanism of action is unknown.
However, the main benefit appears to be a prolongation
of the anagen phase and hair shaft diameter, irrespective
of the underlying cause of baldness. It is well established
that 5% minoxidil is more effective than 2% or 3%
solution. Patients should be warned that during the initial
2∼8 weeks, a temporary telogen effluvium may occur in
some patients, which is self-limiting and subsides when
subsequent anagen regrowth begins, and should not be a
cause for treatment cessation
46
.
A recent advancement in the use of minoxidil as a hair
loss treatment is the development of a 5% topical foam.
Placebo controlled, double-blind trials have demonstrated
Characteristics of Androgenetic Alopecia in Asian
Vol. 24, No. 3, 2012
249
that the hydroalcoholic foam is efficacious, safe, and well
accepted cosmetically by patients
14
.
(2) Oral finasteride
Oral finasteride, a potent type II 5α-reductase inhibitor,
should be administered at a daily dosage of 1 mg. In
clinical trials over a 2-year period in men aged 18∼41
years, the number of responding hairs was established
after 1 year and continued treatment increased the length,
diameter, and pigmentation of these hairs so that the
coverage of the scalp increased over time. On stopping
finasteride, the balding process resumed. An extension of
the above study to 5 years showed that finasteride 1
mg/day was well tolerated, and led to durable improve-
ments in scalp hair growth
47
.
Finasteride is generally well tolerated, side effects are
typically mild and do not require discontinuation of
therapy. Rare side effects may include some loss of libido
and erectile function. At present, there is no proven
benefit for finasteride in women. A placebo-controlled
study in postmenopausal women with AGA given
finasteride 1 mg/day over 1 year showed no significant
benefit
47
.
2) Female
(1) Topical minoxidil solution
Topical minoxidil solution is administered at a dosage of 1
ml twice daily. The 5% solution was compared with the
2% solution in 2 studies involving 493 women. On the
basis of hair-count data, the 5% solution was not sig-
nificantly more effective than the 2% solution
48
. Patients
should be warned that in the initial 2∼8 weeks, a tem-
porary telogen effluvium may occur in some patients,
which is self-limiting and subsides when subsequent
anagen regrowth begins, and should not be a cause for
treatment cessation
46
. Side effects include hypertrichosis
which occurs in 6% of women using 2% minoxidil, and
14% among those using the 5% solution
46
. This occurs on
the face and resolves within 1∼6 months after drug
discontinuation. However, hypertrichosis diminishes or
disappears after about 1 year, even with continued use of
minoxidil.
(2) Oral antiandrogens
Cyproterone acetate, spironolactone and flutamide can be
used as alternatives to minoxidil, but most of the anti-
androgen therapies have not been rigorously studied in
FPHL
49
. In general, better results are seen in women with
hyperandrogenism. Side effects are generally greater with
cyproterone acetate and spironolactone
41
.
Surgical management
Despite advances in medical therapy, hair transplantation
remains the only means of permanent hair restoration in
cases of severe AGA. It is contraindicated in patients with
systemic diseases such as hypertension, cardiac disease,
and diabetes mellitus, all of which must be controlled
before hair transplantation. Local diseases such as
cutaneous lupus erythematosus, morphea, alopecia areata,
and scalp folliculitis must be quiescent for at least 6
months before hair transplantation. Complications of hair
transplantation include ingrown hairs and foreign body
reactions, infections, cobblestoning, graft depression, epi-
dermal cysts, bleeding, headaches, scarring (keloid and
hypertrophic scars), poor hair growth, arteriovenous fistula,
osteomyelitis, wound dehiscence, telogen effluvium,
accelerated hair loss, delayed temporary marked thinning,
curly, lusterless hair, chronic mild folliculitis, and patient
dissatisfaction.
After 4∼6 months, the skin surfaces of the grafts have
usually blended in perfectly with the surrounding scalp. In
some patients, the grafts may be a shade lighter in color
until they are “aged” by sun exposure
50-52
.
Other alternative medical therapies
Dutasteride is a dual type I and type II 5a-reductase
inhibitor. In clinical trials, oral dutasteride showed
significantly greater efficacy than placebo according to
phototrichometric hair count, subject self-assessment, and
investigator and panel photographic assessment
53
. Dutas-
teride is generally well tolerated, with rare side effects that
may include some loss of libido and erectile function.
Dutasteride is only approved by the Korean FDA for the
treatment of AGA.
Topical alfatradiol may be an alternative, though reports of
its efficacy have variable results to treat AGA
54
. Under the
influence of 17alpha-estradiol (alfatradiol), an increased
conversion of testosterone to 17beta-estradiol and andro-
stendione to estrone improves hair growth
55
. Topical alfa-
tradiol is available in Europe, South America, and Korea.
Kim et al.
56
reported single center, open-label, non-com-
parative, phase IV study of the efficacy and safety of
alfatradiol (17α-estradiol) solution on female pattern hair
loss in Korean women. Hair counts and diameter from
baseline to 4 and 8 months after treatment were signifi-
cantly increased in treated patients.
Bimatoprost and latanoprost, which are prostaglandin (PG)
analogues, demonstrate stimulatory effects on hair growth
of eyebrows and eyelashes and pigmentation in a high
numbers of patients
57
. Currently bimatoprost is approved
as eyelash growth enhancer. It might be used for the
treatment of AGA off-label. The expressions of PG recep-
tors were examined in mouse skin hair follicles, and
mRNA was identified in dermal papilla and outer root
W
S Lee and HJ Lee
250 Ann Dermatol
sheath follicular structures during the anagen phase. In
addition, other studies have demonstrated the ability of
PG to stimulate movement from telogen to anagen in
mice.
Ketoconazole might also be used for the treatment of
AGA. The mechanism of ketaconazole is unknown, but
may involve inhibition of inflammation, or anti-androgenic
properties
58
. There is some evidence, both in humans and
in rodents, that this agent may stimulate hair growth
14
.
Prostaglandin analogues and ketoconazole are not appro-
ved for AGA treatment and further studies are needed to
investigate the therapeutic effect on AGA.
Other devices and non-medical aesthetic aids
Devices can be used as alternative tools for the treatment
of AGA. Laser hair comb (Low-level laser therapy)
59,60
and
Fractional photothermolysis laser
61
have been tried to treat
AGA. However, these treatments cannot be substituted for
the medical and surgical approaches previously men-
tioned.
Non-medical approaches can provide cosmetic relief to
both men and women with thinning hair, if medical
treatments are not indicated, not effective, or not desired
by the patient. Non-medical aesthetic aids include wigs,
hairpieces, hair extensions, and topical powder makeup.
They can also be used as adjuvant tools to medical or
surgical treatments
41
.
CONCLUSION
Although the clinical aspects of AGA are recognized in
both men and women and the role of DHT is well
documented, much remains to be determined regarding
the most appropriate treatments for AGA based on
genetics and pathophysiology. AGA is a disconcerting
experience for both sexes, but it may be substantially
more distressing for women. Therefore, dermatologists
should take into account the psychological well-being of
patients with AGA, which can lead to the choice of an
appropriate treatment. Moreover, most of the previously
published studies of AGA were conducted among only
patients of European descent. There are effective treatments,
medical or surgical, currently available for some men and
women with AGA. Compared to other populations, Asian
patients with AGA have different types of hair loss and
family histories, which may influence treatment response.
This review of AGA in Asians may be practical for
informing dermatologists regarding their approaches to
understand, diagnose and treat Asian patients with AGA in
clinical practice.
REFERENCES
1. Orentreich N. Pathogenesis of alopecia. J Soc Cosmet
Chemists 1960;11:479-499.
2. Hamilton JB. Patterned loss of hair in man; types and
incidence. Ann N Y Acad Sci 1951;53:708-728.
3. Norwood OT. Male pattern baldness: classification and
incidence. South Med J 1975;68:1359-1365.
4. Rhodes T, Girman CJ, Savin RC, Kaufman KD, Guo S, Lilly
FR, et al. Prevalence of male pattern hair loss in 18-49 year
old men. Dermatol Surg 1998;24:1330-1332.
5. DeMuro-Mercon C, Rhodes T, Girman CJ, Vatten L.
Male-pattern hair loss in Norwegian men: a community-
based study. Dermatology 2000;200:219-222.
6. Takashima M, Iju K, Sudo M. Alopecia androgenica: its
incidendce in Japanese and associated conditions. In:
Orfanos CE, Montagna W, Stutgen G, editors. Hair research
status and future aspects. Berlin: Springer-Verlag, 1981:287-
293.
7. Kakizo K. Correlation between cancer of the stomach and
alopecia. Kurume Med J 1969;32:1540-1565.
8. Paik JH, Yoon JB, Sim WY, Kim BS, Kim NI. The prevalence
and types of androgenetic alopecia in Korean men and
women. Br J Dermatol 2001;145:95-99.
9. Su LH, Chen TH. Association of androgenetic alopecia with
smoking and its prevalence among Asian men: a community-
based survey. Arch Dermatol 2007;143:1401-1406.
10. Xu F, Sheng YY, Mu ZL, Lou W, Zhou J, Ren YT, et al.
Prevalence and types of androgenetic alopecia in Shanghai,
China: a community-based study. Br J Dermatol 2009;160:
629-632.
11. Tang PH, Chia HP, Cheong LL, Koh D. A community study
of male androgenetic alopecia in Bishan, Singapore. Singapore
Med J 2000;41:202-205.
12. Pathomvanich D, Pongratananukul S, Thienthaworn P,
Manoshai S. A random study of Asian male androgenetic
alopecia in Bangkok, Thailand. Dermatol Surg 2002;28:804-
807.
13. Grover S. A study of patterns of androgenetic alopecia in
men: an Indian perspective. Br J Dermatol 2005;152:572-
574.
14. Ellis JA, Sinclair RD. Male pattern baldness: current treat-
ments, future prospects. Drug Discov Today 2008;13:791-
797.
15. Nyholt DR, Gillespie NA, Heath AC, Martin NG. Genetic
basis of male pattern baldness. J Invest Dermatol 2003;121:
1561-1564.
16. Tang L, Bernardo O, Bolduc C, Lui H, Madani S, Shapiro J.
The expression of insulin-like growth factor 1 in follicular
dermal papillae correlates with therapeutic efficacy of
finasteride in androgenetic alopecia. J Am Acad Dermatol
2003;49:229-233.
17. Choong CS, Wilson EM. Trinucleotide repeats in the human
androgen receptor: a molecular basis for disease. J Mol
Endocrinol 1998;21:235-257.
18. Zitzmann M, Brune M, Kornmann B, Gromoll J, von
Characteristics of Androgenetic Alopecia in Asian
Vol. 24, No. 3, 2012
251
Eckardstein S, von Eckardstein A, et al. The CAG repeat
polymorphism in the AR gene affects high density lipopro-
tein cholesterol and arterial vasoreactivity. J Clin Endocrinol
Metab 2001;86:4867-4873.
19. Giovannucci E, Stampfer MJ, Krithivas K, Brown M, Dahl D,
Brufsky A, et al. The CAG repeat within the androgen
receptor gene and its relationship to prostate cancer. Proc
Natl Acad Sci U S A 1997;94:3320-3323.
20. Panchaprateep R, Korkij W, Asawanonda P. Brain-derived
nerve factor and neurotrophins in androgenetic alopecia. Br
J Dermatol 2011;165:997-1002.
21. Zhuo FL, Xu W, Wang L, Wu Y, Xu ZL, Zhao JY. Androgen
receptor gene polymorphisms and risk for androgenetic
alopecia: a meta-analysis. Clin Exp Dermatol 2012;37:104-
111.
22. Ellis JA, Stebbing M, Harrap SB. Polymorphism of the
androgen receptor gene is associated with male pattern
baldness. J Invest Dermatol 2001;116:452-455.
23. Sawaya ME, Shalita AR. Androgen receptor polymorphisms
(CAG repeat lengths) in androgenetic alopecia, hirsutism,
and acne. J Cutan Med Surg 1998;3:9-15.
24. Wakisaka N, Taira Y, Ishikawa M, Nakamizo Y, Kobayashi
K, Uwabu M, et al. Effectiveness of finasteride on patients
with male pattern baldness who have different androgen
receptor gene polymorphism. J Investig Dermatol Symp Proc
2005;10:293-294.
25. Jung JG, Park JW, Kim MH, Cinn YW. A study on CAG
repeat polymorphisms of the androgen receptor in Korean
androgenetic alopecia: preliminary report. Korean J Dermatol
2009;47:772-776.
26. Hayes VM, Severi G, Eggleton SA, Padilla EJ, Southey MC,
Sutherland RL, et al. The E211 G＞A androgen receptor
polymorphism is associated with a decreased risk of meta-
static prostate cancer and androgenetic alopecia. Cancer
Epidemiol Biomarkers Prev 2005;14:993-996.
27. Hillmer AM, Flaquer A, Hanneken S, Eigelshoven S, Kortüm
AK, Brockschmidt FF, et al. Genome-wide scan and fine-
mapping linkage study of androgenetic alopecia reveals a
locus on chromosome 3q26. Am J Hum Genet 2008;82:
737-743.
28. Hillmer AM, Freudenberg J, Myles S, Herms S, Tang K,
Hughes DA, et al. Recent positive selection of a human
androgen receptor/ectodysplasin A2 receptor haplotype and
its relationship to male pattern baldness. Hum Genet
2009;126:255-264.
29. Krupa Shankar D, Chakravarthi M, Shilpakar R. Male andro-
genetic alopecia: population-based study in 1,005 subjects.
Int J Trichology 2009;1:131-133.
30. Sehgal VN, Kak R, Aggarwal A, Srivastava G, Rajput P. Male
pattern androgenetic alopecia in an Indian context: a
perspective study. J Eur Acad Dermatol Venereol 2007;21:
473-479.
31. Beek CH. A study on extension and distribution of the
human body-hair. Dermatologica 1950;101:317-331.
32. Kaufman KD, Olsen EA, Whiting D, Savin R, DeVillez R,
Bergfeld W, et al. Finasteride in the treatment of men with
androgenetic alopecia. Finasteride Male Pattern Hair Loss
Study Group. J Am Acad Dermatol 1998;39:578-589.
33. Olsen EA. Female pattern hair loss. J Am Acad Dermatol
2001;45(3 Suppl):S70-80.
34. Olsen EA. Current and novel methods for assessing efficacy
of hair growth promoters in pattern hair loss. J Am Acad
Dermatol 2003;48:253-262.
35. Ludwig E. Classification of the types of androgenetic
alopecia (common baldness) occurring in the female sex. Br
J Dermatol 1977;97:247-254.
36. Olsen EA. The midline part: an important physical clue to
the clinical diagnosis of androgenetic alopecia in women. J
Am Acad Dermatol 1999;40:106-109.
37. Lee WS, Ro BI, Hong SP, Bak H, Sim WY, Kim do W, et al.
A new classification of pattern hair loss that is universal for
men and women: basic and specific (BASP) classification. J
Am Acad Dermatol 2007;57:37-46.
38. Jung JG, Kim MH, Cinn YW. Comparison of androgenetic
alopecia prevalence in paternal and maternal male family
members of male androgenetic alopecia patients. Korean J
Dermatol 2006;44:173-178.
39. Goh CL. A retrospective study on the characteristics of
androgenetic alopecia among Asian races in the National
Skin Centre, a tertiary dermatological referral centre in
Singapore. Ann Acad Med Singapore 2002;31:751-755.
40. Lee WS, Oh Y, Ji JH, Park JK, Kim do W, Sim WY, et al.
Analysis of familial factors using the basic and specific
(BASP) classification in Korean patients with androgenetic
alopecia. J Am Acad Dermatol 2011;65:40-47.
41. Olsen EA, Messenger AG, Shapiro J, Bergfeld WF, Hordinsky
MK, Roberts JL, et al. Evaluation and treatment of male and
female pattern hair loss. J Am Acad Dermatol 2005;52:
301-311.
42. Cash TF. Attitudes, behaviors, and expectations of men
seeking medical treatment for male pattern hair loss: results
of a multinational survey. Curr Med Res Opin 2009;25:
1811-1820.
43. Cash TF. The psychosocial consequences of androgenetic
alopecia: a review of the research literature. Br J Dermatol
1999;141:398-405.
44. Sawaya ME, Shapiro J. Androgenetic alopecia. New approved
and unapproved treatments. Dermatol Clin 2000;18:47-61.
45. Price VH. Treatment of hair loss. N Engl J Med 1999;341:
964-973.
46. Dinh QQ, Sinclair R. Female pattern hair loss: current
treatment concepts. Clin Interv Aging 2007;2:189-199.
47. Finasteride Male Pattern Hair Loss Study Group. Long-term
(5-year) multinational experience with finasteride 1 mg in
the treatment of men with androgenetic alopecia. Eur J
Dermatol 2002;12:38-49.
48. Olsen EA, Dunlap FE, Funicella T, Koperski JA, Swinehart
JM, Tschen EH, et al. A randomized clinical trial of 5%
topical minoxidil versus 2% topical minoxidil and placebo
in the treatment of androgenetic alopecia in men. J Am Acad
Dermatol 2002;47:377-385.
49. Ross EK, Shapiro J. Management of hair loss. Dermatol Clin
2005;23:227-243.
50. Avram MR. Laser-assisted hair transplantation - a status
W
S Lee and HJ Lee
252 Ann Dermatol
report in the 21st century. J Cosmet Dermatol 2005;4:135-
139.
51. Avram MR. Hair transplantation for men and women. Semin
Cutan Med Surg 2006;25:60-64.
52. Pathomvanich D. Donor harvesting: a new approach to
minimize transection of hair follicles. Dermatol Surg 2000;
26:345-348.
53. Eun HC, Kwon OS, Yeon JH, Shin HS, Kim BY, Ro BI, et al.
Efficacy, safety, and tolerability of dutasteride 0.5 mg once
daily in male patients with male pattern hair loss: a
randomized, double-blind, placebo-controlled, phase III
study. J Am Acad Dermatol 2010;63:252-258.
54. Trüeb RM. New and established methods in therapy of hair
diseases. Hautarzt 2003;54:732-740.
55. Hoffmann R, Niiyama S, Huth A, Kissling S, Happle R.
17alpha-estradiol induces aromatase activity in intact human
anagen hair follicles ex vivo. Exp Dermatol 2002;11:
376-380.
56. Kim JH, Lee SY, Lee HJ, Yoon NY, Lee WS. The efficacy and
safety of 17α-estradiol (ell-cranell
Ⓡ
alpha 0.025%) solution
on female pattern hair loss: single center, open-label,
noncomparative phase iv study. Ann Dermatol. In press
2012.
57. Law SK. Bimatoprost in the treatment of eyelash hypotrichosis.
Clin Ophthalmol 2010;4:349-358.
58. Hugo Perez BS. Ketocazole as an adjunct to finasteride in
the treatment of androgenetic alopecia in men. Med
Hypotheses 2004;62:112-115.
59. Avram MR, Rogers NE. The use of low-level light for hair
growth: part I. J Cosmet Laser Ther 2009;11:110-117.
60. Schweiger ES, Boychenko O, Bernstein RM. Update on the
pathogenesis, genetics and medical treatment of patterned
hair loss. J Drugs Dermatol 2010;9:1412-1419.
61. Kim WS, Lee HI, Lee JW, Lim YY, Lee SJ, Kim BJ, et al.
Fractional photothermolysis laser treatment of male pattern
hair loss. Dermatol Surg 2011;37:41-51.
