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Postępy Dermatologii i Alergologii 4, August / 2014 207
Original paper
Address for correspondence: Małgorzata L. Kmieć MD, PhD, Department of General Dermatology, Esthetic and Dermatosurgery, Medical
University of Lodz, 1 Hallera St, 90-647 Lodz, Poland, phone: +48 42 678 90 41, +48 696 450 708, e-mail: malgorzata.kmiec@umed.lodz.pl
Received: 25.06.2013, accepted: 20.08.2013.
Assessment of the usefulness of dihydrotestosterone
in the diagnostics of patients with androgenetic alopecia
Izabela Urysiak-Czubatka, Małgorzata L. Kmieć, Grażyna Broniarczyk-Dyła
Department of General Dermatology, Esthetic and Dermatosurgery, Medical University of Lodz, Poland
Head of Department: Prof. Grażyna Broniarczyk-Dyła MD, PhD
Postep Derm Alergol 2014; XXXI, 4: 207–215
DOI: 10.5114/pdia.2014.40925
Abstract
Introduction: Androgenetic alopecia (AGA) is the most common form of hair loss. Clinically observed hair loss is
due to the continuous miniaturization of aected hair follicles. Genetic factors and androgenic factors especially
dihydrotestosterone (DHT), which is a testosterone tissue metabolite, play major roles in the pathogenesis of AGA.
However, expert opinions about the usefulness of DHT in the diagnosis of this type of alopecia are divided.
Aim: To evaluate the usefulness of DHT level in patients with androgenetic alopecia compared with the control
group.
Material and methods: The study comprised 49 subjects: 19 women and 9 men with androgenetic alopecia.
The control group consisted of 17 healthy women and 4 men without hair loss.
Results: Increased serum concentrations of DHT were observed in patients with androgenetic alopecia (17 women,
5 men), but also in the control group. The dierences in mean values of DHT were not signicant according to
the types of alopecia and the control group. Increased serum concentrations of DHT were not correlated with the
advance of alopecia.
Conclusions: Dihydrotestosterone is the most inuential androgen and seems to play a very important role in the
pathogenesis of androgenetic alopecia. Based on the results of our study and others, the most important factors
would appear to be the genetically-determined sensitivity of the follicles to DHT and their dierent reactions to
androgen concentration.
Key words: androgenetic alopecia, dihydrotestosterone, diagnostic.
Introduction
Alopecia (hair loss, shedding) is a dysregulation of the
balance between hair loss and regrowth. The hair follicle
from which the hair grows is inuenced by endogenous
and exogenous factors. The hair cycle within the human
scalp is asynchronous: adjacent follicles are in various
hair cycle periods, and each of them has a microscopic
structure characteristic of the current phase. In the devel-
opment cycle of the hair follicle, there are three phases:
active growth (anagen), inhibition of growth and atrophy
of the hair follicle (catagen) and resting (telogen). The
life cycle of the hair follicle can be compromised in any
of its phases. In the human life, the hair follicle passes
hair cycle probably on average 20–30 times [1–3]. Hair
loss is a physiological process. Daily loss should not ex-
ceed 70–100 hairs, but individual variations may exist
and increased hair loss is seen in autumn and spring [4].
However, a problem occurs when hair loss exceeds 100
per day and lasts longer than a few weeks. The clinical
picture of diseases of the scalp is varied, and the type of
hair loss depends on factors that play a role in its patho-
genesis.
Alopecia can be divided into non-scarring and scar-
ring forms. Non-scarring alopecia, unlike scarring alope-
cia, leads to hair loss without destroying hair follicles.
The most common types of non-scarring hair loss are
male and female androgenetic alopecia, telogen euvi-
um and alopecia areata. This group includes also some
less common variations: hair pulling alopecia, trichotil-
lomania, alopecia syphilitica, and mycosis of the scalp.
Androgens are known to be associated with the
mechanisms of hair growth and renewal. The hair folli-
cle is the site of androgen-tissue interaction, and is also
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Izabela Urysiak-Czubatka, Małgorzata L. Kmieć, Grażyna Broniarczyk-Dyła
the peripheral organ for the synthesis of substantial
amounts of androgens from cholesterol [5, 6].
Androgens
Androgens are hormones synthesized from choles-
terol. Under physiological conditions, they are present
in both sexes, but their concentration is higher in men.
In women, androgens are precursors of female sex hor-
mones and are converted to estrogens.
Androgens can be classied based on the site of pro-
duction: whether they are synthesized in the testes as
testosterone (T), dihydrotestosterone (DHT) or androste-
rone, in the ovaries as DHT or androstenedione, or in the
adrenal cortex as T or dehydroepiandrosterone (DHEA).
Androgen receptors are present in almost all organs,
which then are inuenced by the hormones in both men
and women [7]. Secondary sexual features are formed in
the uterus, spermatogenesis occurs and muscle mass de-
velops under the inuence of androgens. They also have
a signicant impact on the development and function of
the sebaceous glands, and the functioning of the pilose-
baceous unit [8]. The response of hair follicles to andro-
gens varies according to body area. More than 200 types
of androgenic activity in cells have been reported [9].
The presence of high levels of sex hormones is known
as hyperandrogenism. Most often, this is a consequence
of excessive production of endogenous hormones by
dysregulation of the hypothalamic-pituitary-adrenal cor-
tex, polycystic ovary syndrome (PCOS) or by hormonal-
ly-active tumors. Less frequently it arises as a result of
exogenous hormone delivery into the body by doping or
iatrogenic causes. Hyperandrogenism in women is asso-
ciated with characteristic features such as formation of
a male body type, change in voice tone, the appearance
of the male pattern hair, impaired fertility, clitoromegaly,
breast atrophy and androgenetic alopecia, while in men,
elevated androgen levels usually lead to androgenic alo-
pecia. However, in both sexes, severe seborrhea and acne
vulgaris may appear [10].
Dihydrotestosterone
Dihydrotestosterone is a tissue metabolite of testos-
terone. It is formed under the inuence of the 5a-reduc-
tase enzyme, which exists as two isoforms. Type 1 5a-R
is mainly found in the sebaceous glands and the epider-
mis, but is also present in sweat glands, hair follicles, en-
dothelial cells and Schwann cells in the myelin sheaths
of nerves [11–14], while type 2 5a-R is mainly located in
the hair follicles (inner layer, infundibulum, sebaceous
glands) [15]. The conversion of circulating testosterone
into DHT is mainly performed by isoenzyme 5a-R type 2
[16]. Dihydrotestosterone has the ability to bind to sex
hormone binding globulin (SHBG) more than three times
higher than testosterone. In men, approximately 70% of
DHT is formed from the conversion of testosterone, while
in women, the substrate is androstenedione. While el-
evated concentrations of DHT can be observed in men
with androgenetic alopecia or Klinefelter’s syndrome, as
well as in approximately 40% of women with idiopathic
hirsutism and approximately 35% with PCOS, decreased
concentrations occur in men with azoospermia and anor-
chia. Determination of DHT concentration is helpful for
antiandrogen therapy in patients with prostate cancer or
androgenetic alopecia [17].
Androgenetic alopecia
Androgenetic alopecia concerns both men and women.
Male androgenetic alopecia (MAGA) is the most com-
mon form of hair loss that occurs in men. It can begin at
dierent stages of life, but its incidence increases with
the patient’s age. It usually applies to 25% of men aged
25 years, 40% of those in their 40 and over 50% of men
aged 50 [16]. While the total incidence of the active form
of MAGA in Caucasians over 40 is estimated at 50%, the
symptoms are not as apparent in Asian, Native American
and African/Caribbean men [18, 19]. It is estimated that
of all patients experiencing hair loss, androgenetic alope-
cia is recognized in 95% of them [3, 20, 21].
Female androgenetic alopecia (FAGA) is one of the
most common forms of hair loss in women. Its incidence
increases with age; it is estimated that excessive hair loss
relates to 12% of women before 29 years of age, 25% un-
der 49 and over 50% before the age of 79 years. Only 43%
of women aged 80 years show no signs of hair loss [22].
The precise etiology and pathogenesis of androge-
netic alopecia is still unclear, but genetic and androgenic
factors play denite roles.
The genetic factor
The inheritance of male androgenetic alopecia
(MAGA) is not fully understood. However, it is probably
an autosomal dominant [23] with variable gene pene-
trance and multigenic eects dependent on many fac-
tors [24, 25]. The probability of MAGA depends on the
number of rst and second degree relatives who have
experienced this type of alopecia. An unfavorable prog-
nostic factor is the presence of androgenetic alopecia
(AGA) in the patient’s mother or sisters [3]. Garton et al.
[26] demonstrated the dependence of MAGA occurrence
on the polymorphic gene encoding ornithine decarboxy-
lase, which plays a role in the regulation of the hair cycle.
Other studies suggest that genetic variants present in
or near the gene encoding the androgen receptor (AR)
(chromosome Xq12) may have an impact on the occur-
rence of MAGA [27–29].
In 2008, Prodi et al. [30] showed that the EDA2R gene
(an A2 ectodysplasia receptor), located on chromosome
X, is associated with MAGA frequency. Although studies
suggesting a relationship between MAGA and chromo-
some X may conrm the impact of genetic factors inher-
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Assessment of the usefulness of dihydrotestosterone in the diagnostics of patients with androgenetic alopecia
209
ited from the mother, these results do not explain the
observed inheritance of MAGA from the father.
Also in 2008, Hillmer et al. [31] and Brent et al. [32] in-
dependently discovered closely related variants of genes
on chromosome 20. Men diagnosed with the newly-dis-
covered variant and the other susceptibility locus for
the
androgen receptor are seven times more likely to experi-
ence alopecia. Their presence is dependent on latitude,
which explains the ethnic variation of MAGA. Studied
variants are located near genes PAX1 and FOXA2. How-
ever, their role in hair loss is still not fully understood.
Other studies based on genome mapping indicate a re-
lationship between MAGA and chromosome 3q26 [33].
Also, the inheritance of female androgenic alopecia
(FAGA) is not fully understood. It may well be of an au-
tosomal dominant nature, with either variable expres-
sion of genes or polygenic eects. The wide variation in
phenotypic variability, prole of women aected, degree
of disease progression and range of hair loss proles ap-
pears to conrm this [34, 35]. As in men, the pathogene-
sis of FAGA is based partly on the genes responsible for
the production of androgens and their conversion to DHT,
as well as the vulnerability of the respective receptors.
The androgen-sensitive miniaturization of the hair
follicles is a pathognomonic symptom in both men and
women. The presence of two copies of the androgen re-
ceptor in women, one of which is randomly inactivated,
has raised some controversy about the role of AR in FAGA
[36]. So far, only a few genes involved in this form of alo-
pecia have been reported. One of them is the CYP17 gene
(10q24.3chromosome) encoding P450 aromatase, which
is responsible for, among other things, the release of es-
tradiol and conversion of androgens to estrogens within
the hair follicle. The gene was found in numerous studies
to be present in patients with PCOS and their brothers,
who demonstrated early androgenetic alopecia [19, 36,
37]. Yip et al. [35] also report an increased incidence of
the rs4646C allele in women with FAGA: the allele is
found within the CYP19A1 gene, which also encodes the
aromatase P450. Another gene identied in families with
AGA is located on chromosome 3q26 [33].
Inuence of androgen
Two peripherally-circulating androgens which may
have an inuence on androgenic alopecia are dehydroe-
piandrosterone sulfate (DHEAS) and androstenedione,
which are produced by the adrenal glands. Testoster-
one and dihydrotestosterone, on the other hand, are
synthesized primarily within the gonads [38]. The most
important androgen in males is testosterone, formed in
the interstitial cells of the testes. However, the major
role in the pathogenesis of androgenic alopecia is played
by the metabolite dihydrotestosterone, which has a far
more potent androgenic action, and is formed by the
5a-reductase enzyme (5a-R). 5a-R is present as two
isozymes: type 1 5a-R is encoded by the SRD5A1 gene
located on chromosome 5 (p15), while the type 2 SRD5A2
gene is located on chromosome 2 (p23) [39]. In men with
genetically determined 5a-R2 deciency, MAGA is absent
[40]. Moreover, in men with this form of hair loss, not
only is 5a-R more active, but a higher level of DHT can
also be found in the frontal compared with the occipi-
tal lobe, which is important proof of the participation of
this enzyme in the pathogenesis of MAGA [18]. Grin
and Wilson [41], and Sawaya and Price [42] do not sup-
port the theory which assumes that elevated levels of
androgens play a major role in MAGA, assigning great-
er signicance to the genetically-determined increased
sensitivity of hair follicles to the hormones. The level of
androgen receptors is 1.5 times higher in the frontal scalp
compared to the occipital region. Male pattern alopecia
never occurs in the temporal area and the region below
the occipital area.
In both men and women with a genetic predisposi-
tion, DHT binds to specic androgen receptors. The sub-
sequently-formed complex enters the nucleus of the hair
cell and combines with the DNA, thus prompting the ac-
tivation of genes and production of proteins responsible
for the gradual transformation of normal hair follicles to
the involutional “miniaturized follicles” [2, 18]. This trans-
formation takes place by shortening the anagen phase
and lengthening the telogen. Gradually, the number of
thin telogen hairs increases, while the terminal hairs be-
come thin follicle-type hairs known as vellus hairs [42,
43]. The response of the hair follicles to androgens is var-
ied. The DHT can stimulate the growth of the hair follicles
on the face, chest and genital area, while inhibiting the
growth of hair in the skin of the scalp. The progression
of hair loss varies. It can be very gradual and continuous,
but it is often episodic.
In women with a genetic predisposition, andro-
gen-sensitive hair follicles are either over-stimulated or
inhibited depending on the part of the body. However,
androgen levels in these women may be elevated or
normal [44, 45]. It is estimated that FAGA occurs in only
every fourth woman with signs of virilization and elevat-
ed levels of androgen [46, 47]. The relationship between
the occurrence of FAGA and excessive secretion of Δ4-an-
drostenedione by the ovaries or the adrenal gland, and
increased concentrations of dehydroepiandrosterone
(DHEA) and its sulfate (DHEAS), which are synthesized
in the adrenal glands,
has been demonstrated [4, 45–49].
Androstenedione and DHEA are metabolized circumfer-
entially to testosterone (T), which in turn, is converted
to 4 other metabolites, the most important role being
played by DHT.
Numerous enzymatic proteins are involved in the en-
zymatic conversion of androgens, including steroid sulfa-
tase (DHEAs to DHEA), 3β-hydroxysteroid dehydrogenase
(DHEA to androstenedione) and 17β-hydroxysteroid ox-
idoreductase. The latter converts DHEA to androstenedi-
ol and the androstenedione to testosterone. In turn, the
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Izabela Urysiak-Czubatka, Małgorzata L. Kmieć, Grażyna Broniarczyk-Dyła
5a-reductase in the cells of the hair follicle is responsible
for the conversion of free testosterone to DHT.
While the process of hair loss in men is associated
primarily with the excessive activity of 5a-R type 2, both
isoenzymes are present in women, but predominant-
ly 5a-R type 1. An important role is also played by aro-
matase cytochrome P-450, located in the outer sheath
of the hair root, which catalyzes the conversion of an-
drostenedione to estrone and testosterone to estradiol,
resulting in lower circulating and tissue levels of T and
DHT. This action explains the clinical dierences of andro-
genetic alopecia in men and women. The concentration
of aromatase in women is between 2 and 5 times higher
in the skin of the scalp, particularly in the frontal region,
which probably determines the retention of hair. In men,
lower levels of this enzyme seem to aect hair loss in this
region [4, 48–50].
Another hormone which probably takes part in the
pathogenesis of FAGA is prolactin. It has been shown that
hyperprolactinemia increases DHEAS by its eect on the
adrenal cortex [48]. Furthermore, lowered SHBG levels
should also be considered as a factor in the pathogenesis
of FAGA, insofar that it may be the cause of the increased
amount of free testosterone. Some authors believe that
a simultaneous reduction in the amount of SHBG and an
increase in the 3a-glucuronide androstenediol, is a bio-
chemical marker of FAGA. However, other authors consid-
er a combination of decreased SHBG and an increase of
T/SHBG ratio to be more signicant [16, 51].
The clinical picture
Several classications have been developed to assess
the severity of androgenetic alopecia in men. A scale pro-
posed in 1951 by Hamilton [52] distinguishes 8 degrees of
hair loss: I degree indicates completely preserved hairs of
the head, II – slight thinning of hair in the leading corners,
III – visible thinning of hair in the leading corners (receding
hair), IV – deep bend with frontal hair loss and thinning at
the top of the head, V – signicant hair loss in the frontal
area and within the top of the head, VI – partial merging
of frontal alopecia lesions and top of the head, and VII and
VIII – clear fusion of the two foci of alopecia.
In 1975, this scale was modified by Norwood, who
widened its scope, highlighting also the type of angle
and peak alopecia (Hamilton-Norwood scale). This scale
is the most widely used for clinical assessment of the
severity of hair loss in men [53].
In 2007, Lee et al. [54] developed a universal scale to
assess the severity of hair loss in men and women: the
BASP (basic and specic classication). This classication
is based on observation of dierent types of alopecia.
The basic feature (basic-BA) is estimated from the frontal
hairline, and the specic type of hair loss (specic-SP)
is determined by the density of the hair in the various
regions (frontal, top of the head). There are four basic
patterns (L, M, C, and U) and two specic types (F and V)
of hair loss. The nal assessment of the type of hair loss
is a compilation of the basic features and characteristic
patterns. The clinical course of FAGA can proceed accord-
ing to either the female or male pattern or sometimes
both.
The female alopecia pattern is more common before
menopause, and usually relates to women aged 20 to 40
years. Androgen levels are often normal or only slight-
ly elevated [48]. In two thirds of cases, it coincides with
polycystic ovary syndrome. This is probably related to
the increased production of androgens and their eects
on the target tissues [55, 56]. Hair loss in FAGA women
is often widespread. An important clinical symptom is
the presence of a parting like “pine branches”. Androgen
stimulation is responsible for concomitant seborrhea.
The Ludwig classification is most commonly used
in assessing the severity of FAGA, and this distinguish-
es three levels of severity [57]. The rst degree is visible
thinning in the central part of the scalp while maintain-
ing 2- to 3-centimeter strands of hair on the forehead. In
stage II, clear thinning can be seen in the central part of
the scalp, and in stage III, alopecia occurs while main-
taining the hair in the frontal region. Total hair loss has
never been seen.
Another method is the three-point classication de-
veloped by Olsen [58], which represents the severity of
female androgenetic alopecia, especially in the frontal
midline. Androgenetic alopecia in women can also be
carried by a male pattern assessed by the 7-point Hamil-
ton-Norwood scale. This pattern of loss is more common
in women after the menopause: hair loss is gradual and
occurs towards the temporal and parietal area, however,
the frontal hair line is preserved [52, 53]. Other less fre-
quently-used scales are the 5-point Ebling and Sinclair
scale, 8-point Savin scale and a universal BASP classi-
cation [51, 54, 59].
Other theories on MAGA pathogenesis
Among other theories regarding the pathogenesis
of androgenetic alopecia, Randall et al. merits particular
interest [60]. Their theory assumes that the eect of an-
drogens concerns only one component of the hair folli-
cle – the hair papilla. According to this theory, androgens
acting directly on the papilla cells are associated with the
androgen receptor, which initiates the expression of the
genes for the regulatory factors that in turn, aect other
target cells. They take an active role in the paracrine ef-
fect and extracellular matrix factors, and inuence size
changes of the hair papilla and hair follicle.
Ustuner [61] reports that the presence of androge-
netic alopecia is a consequence of ischemia and pres-
sure placed on the skin by the hair follicle, which is then
pressed against the skull. Over time, in humans, the
thickness of the fat decreases and hence, its protective
eect on the follicles. In response to the hair loss, the
synthesis of testosterone, 5a-R, DHT and DHT receptor
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Assessment of the usefulness of dihydrotestosterone in the diagnostics of patients with androgenetic alopecia
211
increases. According to the author, the increase in DHT is
not the cause, but the consequence of hair loss, and its
action on the hair follicle is limited to transforming the
vellus in terminal hair.
Diagnosis of androgenetic alopecia
In the diagnosis of androgenetic alopecia, data from
interview and a characteristic clinical picture are usual-
ly sucient. The most useful criteria in the diagnosis of
MAGA include whether hair loss began after puberty, the
location of its loss and the presence of thin hair around
the top of the head. It is also important to determine its
genetic predisposition in closer or more distant relatives.
In doubtful cases, a trichogram, consisting of the exam-
ination of the roots of the hair, can be performed. As-
saying the most important androgen hormones such as
testosterone, free testosterone and total dihydrotestos-
terone is sometimes helpful [62]. Other diagnostic meth-
ods include trichoscopy, contrast-enhanced phototricho-
gram (CE-PTG), a daily assessment of the hair loss, wash
test, reective confocal laser scanning microscopy in vivo
(R-CSLM) and trichogram unit area measurement.
The dierentiation of male pattern alopecia relates
mainly to telogen euvium, which, however, has a more
rapid course and includes areas not typically aected by
MAGA. A diagnosis of androgenetic alopecia in women
can cause many diculties. In order to establish the di-
agnosis, an interview in needed to determine the rate of
hair loss and its duration, as well as record any applied
treatment and the presence of other dermatological
diseases. It is also important to exclude endocrine and
gynecological diseases as causes, as well as the intake
of any hormone preparations, especially contraceptives.
In dierentiating the condition from telogen euvium,
it is important to take into consideration any completed
surgical interventions or the use of restrictive diets.
In an examination of patients with androgenetic al-
opecia, the presence of characteristics associated with
the coexistence of hyperandrogenism, such as hirsutism,
acne, obesity or menstrual disorders, should be noted.
If they are present, it is important to record the serum
concentrations of free and total testosterone, DHT, DHEA,
androstenedione, estradiol and prolactin and SHBG. In
order to evaluate the thyroid function, it is also recom-
mended that the concentrations of TSH, FT4 and FT3 are
determined. Some authors suggest that further deter-
mination of LH, FSH and PSA in serum should then be
performed [48, 63–67].
Suitable tests for the diagnosis of FAGA are tricho-
grams, trichoscopies, contrast-enhanced phototricho-
gram (CE-PTG), and a histopathological examination for
the dierentiation with CTE. Other less frequently-used
methods include an assessment of the daily hair loss,
wash test, reective confocal laser scanning microscopy
examination (R-CSLM) or trichogram unit area measure-
ment [68–70].
Aim
The aim of this study was to evaluate the usefulness
of DHT concentrations in patients with androgenetic
alopecia (male and female) compared with the control
group.
Material and methods
The study comprised 49 people. The study group
consisted of 28 patients experiencing hair loss, receiving
treatment from the Department of General Dermatology,
Esthetic and Dermatosurgery, Medical University of Lodz,
who volunteered during the period from January 2007 to
February 2009. The initial diagnosis of alopecia was de-
termined by history and clinical examination. The study
group consisted of 19 women and 9 men aged between
17 and 63 years. Children and adolescents under 16 years
of age, pregnant women, people with fungal infections of
the skin, parasitic infections and immune systemic dis-
eases were excluded from the study.
The control group consisted of 21 healthy volunteers
without hair loss, 17 of whom were female and 4 were
male. The age of the patients in the control group ranged
from 21 to 63 years. A careful history based on the au-
thor’s own inquiry was taken in all patients, consisting of
personal data, age of the patient at the onset of hair loss,
the duration and pattern of hair loss (patchy, diuse),
the presence of key factors in determining the cause of
hair loss, such as past medical history, stress, lifestyle,
improper hair care, medications and family history of
alopecia, as well as any details concerning the applied
treatment and its ecacy.
During the clinical study, the scalp, hair and skin of
the patients were examined, noting signs of seborrhea
and the coexistence of hirsutism. The degree of alopecia
in men with MAGA was determined based on the 7-point
Hamilton-Norwood scale, while in women with FAGA, the
determination was based on the 3-point Ludwig classi-
cation. In all patients and in the control group, the serum
concentrations of dihydrotestosterone were evaluated.
The concentration of DHT in the serum was assessed
using a 4132 EIA enzyme immunoassay, reagent kits and
DRG International analyzer. The results are given in Table 1.
Statistical analysis
The results were statistically analyzed using the
following tests of significance: the Shapiro-Wilk test,
Bartlett’s test, one-way ANOVA without replication, the
Schee multiple comparison test, Mann-Whitney-Wilcox-
on test, Fligner-Policello test, logistic regression, χ
2
inde-
pendence test and Fisher’s exact test. The condence in-
terval was set at 95% (95% condence interval – 95% CI).
The results were considered statistically signicant
for a p-value of less than 5 percent (p < 0.05).
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Izabela Urysiak-Czubatka, Małgorzata L. Kmieć, Grażyna Broniarczyk-Dyła
Results
Results of a clinical trial
The Ludwig classication was used to assess the se-
verity of hair loss in women with FAGA. On this basis,
5 women were noted as being at stage I, 11 stage II, and
3 stage III alopecia.
Men with MAGA were evaluated with the Hamil-
ton-Norwood classication. Of the nine men examined,
3 were found to be at stage II, 3 other at stage IIIa, and
the remaining 3 at stage IV of alopecia.
In the clinical study, clear seborrheic simultaneous
changes were found in almost half of the patients in the
group with MAGA and FAGA.
The laboratory results
Serum concentrations of DHT were found to exceed
the normal range in the majority of patients and control
group subjects. The DHT concentrations were elevated in
17 of 19 women with FAGA, in 5 of the 9 men with MAGA,
and in 12 of the 21 patients in the control group (1 man,
11 women) (Figures 1, 2).
Dierences in mean DHT concentration according to
the type of alopecia were not statistically signicant rel-
ative to the control group. Elevated levels of DHT did not
correlate with the progression of hair loss.
Discussion
Alopecia (hair loss, shedding) is a dysregulation of the
balance between hair loss and regrowth. Non-scarring al-
opecia leads to hair loss without destroying hair follicles.
The follicle development cycle may be impaired in any of
its phases. The hair follicle is aected by endogenous and
exogenous factors. The clinical picture of scalp diseases
is varied, the type of hair loss depends on factors that
play a role in its pathogenesis.
Despite the fact that every type of alopecia has many
characteristic features, their dierentiation is sometimes
dicult and the results are unclear. So far no reliable di-
agnostic tools have been developed which would be use-
ful both for evaluating and monitoring the response of
therapy in dierent types of alopecia. Typically, interview
data, clinical assessment, laboratory tests, and helper
methods such as the pull test, trichogram and trichosco-
py, as well as histopathological examination of vertical
and horizontal sections, are useful methods in the dier-
entiation of hair diseases. Histopathological examination
of the scalp often allows a diagnosis to be made, howev-
er, recommendations for its implementation should be
carefully considered because of its invasive nature.
Androgenetic alopecia is the most common type of
non-scarring hair disorder. Excessive hair loss has been
found to have a signicantly deleterious eect on the ap-
pearance of a patient, often causing distress and social
conict as well as aggravating their quality of life.
In the opinion of some authors, androgens are the
most important hormones regulating human hair growth,
apart from nutritional deciency and thyroid disease [71,
72]. There are few studies assessing the correlation be-
tween androgenetic alopecia and DHT concentrations in
serum samples from the patient. On the basis of studies
performed on 52 patients of both sexes with early andro-
genetic alopecia, Sreekumar et al. [73] found no increase
in androgen concentrations (DHT and T), but did note the
Table 1. Range of standard DHT concentration
measurement in serum of the patients*
Gender Concentration [pg/ml]
Female Premenopausal: 24–368
Postmenopausal: 10–181
Male 250–990
*The standard serum DHT concentrations indicated by the manufacturer were
determined only in the United States population.
Figure 1. The dierences in DHT mean serum in patients
with androgenetic alopecia and in the control group
DHT concentration [pg/ml]
1100
1000
900
800
700
600
500
400
300
200
100
0
0.8
0.7
0.6
0.5
0.4
0.3
0.2
0.1
0
Research group – FAGA
Research group – MAGA
Control group – Female
Control group – Male
547
420
894
1055
Control group MAGA FAGA
Figure 2. The dierences in DHT mean serum in patients
with androgenetic alopecia and in the control group
DHT norm
DHT above norm
12
12
4
2
5
17
Fraction
Postępy Dermatologii i Alergologii 4, August / 2014
Assessment of the usefulness of dihydrotestosterone in the diagnostics of patients with androgenetic alopecia
213
presence of a signicantly elevated ratio of DHT/T. How-
ever, Vierhapper et al. [74] report that the level of DHT
is signicantly higher in men with MAGA, and its deter-
mination is necessary before anti-androgen treatment.
In the present study, the androgen values exceeded the
norm, both in patients with androgenetic alopecia, and
also in the control group.
Among investigated women with androgenetic al-
opecia, increased values of DHT were most commonly
observed. However, increased levels of DHT did not cor-
relate with the progression of hair loss. The literature
reports that although the severity of hair loss may vary,
regardless of age, the severity of alopecia is not signif-
icant in most cases [34, 35, 41]. Many authors [20, 36,
37, 75] note the frequent occurrence of this form of hair
loss in immediate family members. In the present study,
more than half of the patients reported the occurrence
of androgenetic alopecia in their mothers, but this was
not statistically signicant. In some women with FAGA,
the coexistence of seborrhea was found, which is also
conrmed by other authors [37, 49, 53]. The literature
highlights the frequent presence of hirsutism in patients
with FAGA, which is also the cause of hyperandrogenism
[10, 49, 55, 63, 76]. However, all patients demonstrat-
ed the Ferriman-Gallweya criteria, which did not allow
for hirsutism recognition [63, 77]. The mean age of the
group of men with androgenetic alopecia was 25 years.
More than half of the respondents with MAGA reported
a similar pattern of hair loss in their father or the mother,
which may support the theory of a genetic link for this
form of hair loss [3, 27–29]. All investigated men report-
ed a history of hormonal disorders. However, 2 patients
were taking formulations with carbohydrate-protein con-
taining, among other things, creatine, which causes mus-
cle growth. All patients were either classied as being in
stage II, IIIa or IV of hair loss by the Hamilton-Norwood
scale. Changes in the nature of acne vulgaris were seen
in almost half of the patients.
The results of the present study are consistent those
of other authors [56, 78–80], who consider that the lev-
el of androgens in women with FAGA may be increased
or normal. A retrospective study published in 2009 per-
formed on 228 women with symptoms of hyperandro-
genism, also showed higher levels of androstenedione,
DHEA and testosterone present in saliva. The SHBG
levels were also lower, although their mean values were
lower than those in women experiencing hirsutism. An
analysis of the results indicated a strong positive cor-
relation of hirsutism with markedly increased hormone
levels, particularly testosterone and negative with SHBG.
Average total testosterone levels were similar in patients
with hirsutism and FAGA [49].
It is noteworthy that biochemical markers of hyperan-
drogenism can be seen in women with an absence of clini-
cal features. Orme et al. note a complete lack of correlation
between FAGA and elevated androgen levels [81]. Schmidt
et al. [82] also report no increased androgen levels in pa-
tients with FAGA: the level of estrogen was usually within
normal limits. A recent Riedel-Baima and Riedel [83] study
assessing the concentrations of free and total testoster-
one, DHEAS, SHBG in 20 women with FAGA also shows
a normal range of concentrations of these hormones to
be present. Estradiol to free testosterone ratio levels and
estradiol to DHEAS ratio levels were found to be signi-
cantly lower in FAGA patients compared to the control
group. Estradiol to free testosterone ratio levels in women
with FAGA were almost always less than 10. Futterweit et
al. and Derksen et al. [55, 84] emphasize that the nding
of signicantly elevated levels of testosterone and DHEAS
may indicate the presence of androgen-secreting tumors
or of other diseases which require a precise gynecological
and endocrinal diagnosis. According to Price [76], the re-
sults of routine hormonal tests performed on women with
FAGA are often not much valuable.
According to Stanczyk [85], the determination of the
DHT level in serum is not helpful in assessing the prev-
alence of hyperandrogenism. However, its metabolites,
such as sulfate and glucuronide, androstenedione, ap-
pear to be clinically relevant markers in the recognition
of hirsutism, acne and androgenic alopecia.
Dihydrotestosterone has the most powerful androgen
action and seems to play an extremely important role
in the pathogenesis of androgenetic alopecia. However,
based on the present ndings and opinions of many oth-
er authors [6, 18, 27–29, 41, 42], the individual, genetical-
ly-based sensitivity of hair follicles to DHT concentrations
and their varied response to the action of androgens
seem to be the most signicant factors.
It is worth noting that blood serum DHT concentra-
tion is not routinely measured in Polish laboratories: the
standard serum DHT concentrations identified by the
manufacturers were determined only in the U.S. popu-
lation.
Conclusions
Dihydrotestosterone has the strongest androgenic
action and seems to play an extremely important role in
the pathogenesis of androgenetic alopecia. The useful-
ness of serum DHT level measurement in the diagnosis
of androgenetic alopecia is questionable, especially in
women with androgenetic alopecia. In the pathogene-
sis of androgenetic alopecia, the most important factor
seems to be the individual, genetically-based sensitivity
of hair follicles to DHT concentration and their varied re-
sponse to androgen action.
Conict of interest
Authors declare no potential conict of interest.
Postępy Dermatologii i Alergologii 4, August / 2014214
Izabela Urysiak-Czubatka, Małgorzata L. Kmieć, Grażyna Broniarczyk-Dyła
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