CASE REPORT DOI 10.1111/J.1365-2133.2004.06279.

Androgenetic alopecia in children: report of 20 cases

A. Tosti, M. Iorizzo and B.M. Piraccini
Department of Dermatology, University of Bologna, Via Massarenti 1, 40138 Bologna, Italy

Summary

Correspondence Androgenetic alopecia (AGA) is the most common type of hair loss in adults.
Antonella Tosti. Although there are differences in the age at onset, the disease starts after puberty
E-mail: tosti@med.unibo.it when enough testosterone is available to be transformed into dihydrotestoster-
one. We report 20 prepubertal children with AGA, 12 girls and eight boys, age
Accepted for publication
17 June 2004 range 6–10 years, observed over the last 4 years. All had normal physical devel-
opment. Clinical examination showed hair loss with thinning and widening of
Key words: the central parting of the scalp, both in boys and girls. In eight cases frontal
androgenetic alopecia, children, hair loss, accentuation and breach of frontal hairline were also present. The clinical diagno-
prepubertal onset
sis was confirmed by pull test, trichogram and dermoscopy in all cases, and by
scalp biopsy performed in six cases. There was a strong family history of AGA in
Conflicts of interest:
None declared all patients. The onset of AGA is not expected to be seen in prepubertal patients
without abnormal androgen levels. A common feature observed in our series of
children with AGA was a strong genetic predisposition to the disease. Although
the pathogenesis remains speculative, endocrine evaluation and a strict follow-up
are strongly recommended.

Hair loss in children may become evident shortly after birth,
due to congenital or hereditary diseases, or later, during child-
hood. Alopecia areata and trichotillomania are the most com-
mon forms of alopecia in childhood, typically producing
patchy hair loss. Other causes of hair loss include the loose
anagen hair syndrome, where diffuse alopecia may be associ-
ated with areas of marked thinning due to traumatic extraction
of the loosely attached hair.
Androgenetic alopecia (AGA) is the most common type of
hair loss in adults. Although there are differences in the age at
onset, in both sexes the disease starts after puberty, when
enough testosterone is available to be transformed into dihyd-
rotestosterone. The onset of AGA is therefore not expected to
be seen in prepubertal patients without abnormal androgen
levels.1 Both androgenic hormones and genetic predisposition
are necessary for the development of AGA, at least in men.2
The disease does not affect males castrated before puberty and
is less frequent and less severe in females.3 Genetic predisposi-
tion to the disease is well known, but the genes responsible
have not yet been identified. Polymorphism in the androgen
receptor gene has recently been detected.4 A strong family his-
tory predisposes to early development and rapid progression
of AGA. AGA clinically appears with hair thinning involving
the androgen-dependent areas of the scalp (temporoparietal
region and the vertex), with male and female patterns that are
well known.5
Male pattern baldness is classified using the Hamilton
scale, based on frontotemporal recession and vertex thinning.
Female pattern hair loss is not as easily classifiable as in
men; three different clinical patterns have been described:
the Ludwig pattern, the Hamilton pattern and the Christmas
tree pattern. The first emphasizes the preservation of the
frontal fringe and a reduction in hair density affecting
mainly the crown region of the scalp. The second is the typ-
ical male pattern of AGA that can also be observed in post-
menopausal women.5 The third has been recently described
by Olsen6 as a hair loss that increases towards the front of
the scalp with an encroachment and sometimes a breach of
the frontal hair line. It is more common when the disease
has a very early age at onset.
Diagnosis of AGA is usually easy, only necessitating a clin-
ical examination. Dermoscopy is useful to evaluate hair diam-
eter diversity in affected areas. More than 20% hair diameter
diversity is an early sign of AGA.7 Scalp biopsy is usually
unnecessary, except in doubtful cases.
Case reports
Over the last 4 years we have observed 20 prepubertal cauca-
sian children with AGA, 12 girls and eight boys, age range 6–
10 years. Data from our patients are reported in Table 1. In
both boys and girls, clinical examination showed hair loss
with thinning and widening of the central parting of the scalp
(Fig. 1). In eight cases frontal accentuation and breach of
frontal hairline were also present (the Christmas tree pattern)
(Fig. 2). The pull test, trichogram and dermoscopy were per-
formed in all cases to exclude other forms of hair loss occur-
ring in children.

556
2005 British Association of Dermatologists • British Journal of Dermatology 2005 152, pp556–559
 Androgenetic alopecia in children, A. Tosti et al. 557

Table 1 Data from our patients

Age at Sibling ⁄ stage DHEA-S
Patient Sex ⁄ age onset Parent affected ⁄ stage (age at levels
no. (years) (years) (age at onset, years) onset, years) (lg dL)1)
1 F ⁄ 10 6 Mother ⁄ L III (25) – 120Æ20
2 F ⁄ 10 7 Mother ⁄ L II (30) – 98Æ50
3 F ⁄9 6 Father ⁄ H IV (27) Sister ⁄ L I (16) 148Æ20
Mother ⁄ L III (25)
4 F ⁄ 10 9 Father ⁄ H IV (30) – 99Æ20
5 F ⁄ 10 10 Father ⁄ H III (35) – 103Æ10
6 F ⁄6 6 Father ⁄ H V (26) – 45Æ60
Mother ⁄ L II (28)
7 F ⁄ 10 9 Father ⁄ H IV (32) – 111Æ30
8 F ⁄8 6 Father ⁄ H V (30) Brother ⁄ H II (17) 92Æ20
Mother ⁄ L III (23)
9 F ⁄8 7 Father ⁄ H V (28) – 79Æ60
Mother ⁄ L II (27)
10 F ⁄9 7 Mother ⁄ L II (25) Brother ⁄ H II (15) 105Æ20
11 F ⁄7 7 Father ⁄ H III (28) – 61Æ50
Mother ⁄ L II (23)
12 F ⁄6 6 Father ⁄ H V (27) – 80Æ20
Mother ⁄ L III (20)
13 M ⁄ 10 8 Father ⁄ H III (30) Brother ⁄ H II (17) 250Æ60
Mother ⁄ L I (26)
14 M ⁄ 10 7 Father ⁄ H IV (30) Sister ⁄ L I (17) 201Æ5
Mother ⁄ L III (20)
15 M ⁄ 10 8 Father ⁄ H IV (27) Brother ⁄ H I (15) 182Æ5
16 M ⁄6 6 Father ⁄ H V (20) – 35Æ20
Mother ⁄ L III (25)
17 M ⁄8 7 Father ⁄ H III (30) – 77Æ60
Mother ⁄ L I (25)
18 M ⁄9 6 Father ⁄ H IV (30) – 91Æ10
Mother ⁄ L II (28)
19 M ⁄9 8 Mother ⁄ L II (20) – 80Æ50
20 M ⁄9 8 Mother ⁄ L II (30) – 75Æ20

DHEA-S, dehydroepiandrosterone sulphate (normal range: preadrenarche, 2Æ80–85Æ20;

postadrenarche, 33Æ9–280; after puberty, 65Æ10–368 lg dL)1); L, Ludwig pattern; H,
Hamilton pattern.

There was a strong family history of AGA in all patients.
One or both parents of our patients were affected by AGA clas-
sified according to the Hamilton (in men) and Ludwig (in
women) scales.5 Nine patients (six girls and three boys) had
one parent affected, most frequently the mother, and 11 (six
girls and five boys) had both parents affected. A wider family
history, including siblings and grandparents, revealed that
eight of our patients had siblings, one per patient. Clinical
examination revealed that six of the eight siblings were affec-
ted by AGA. Evaluation of the maternal and paternal grandpar-
ents was more difficult to perform and we were able to visit
the grandparents of only five children. The grandfather from
the paternal side was affected by severe AGA in 15 cases (three
documented by us, 12 reported by the family), the grandfather
from the maternal side in 10 cases (two documented by us,
eight reported). Hair thinning was reported in only one grand-
mother, from the maternal side of an 8-year-old girl.
Laboratory examinations were performed in all our patients,
including routine blood cell count and biochemical studies,
sex hormone assays [follicle-stimulating hormone, luteinizing
hormone, oestradiol, progesterone, 17-hydroxyprogesterone,
prolactin, testosterone, dehydroepiandrosterone sulphate
(DHEA-S), androstenedione], thyroid function, adrenocortico-
trophic hormone, cortisol and growth hormone-releasing hor-
mone. All results were within the normal range in relation to
age and sex. DHEA-S levels were within the postadrenarche
levels in 12 patients (Table 1).
Paediatric referral confirmed normal physical development
according to the Tanner scale and growth parameters. No
patients showed any evidence of pubic or axillary hair. No
breast development was seen in the girls. The boys’ genitalia
(penis and testes) were normal in volume. No signs of acne
or hirsutism were seen.
A 4-mm punch biopsy from the affected scalp was per-
formed in six cases and specimens were sectioned both hori-
zontally and vertically. In the horizontal sections a normal
hair density (mean 41 hairs, range 38–45) was observed.
Terminal follicles were reduced in number (mean number

2005 British Association of Dermatologists • British Journal of Dermatology 2005 152, pp556–559
558 Androgenetic alopecia in children, A. Tosti et al.
Fig 1. Androgenetic alopecia in a 9-year-old boy: the picture shows
hair loss with thinning and widening of the central parting of the
scalp.
Fig 2. Androgenetic alopecia in a 7-year-old girl: hair loss with
frontal accentuation and breach of frontal hairline.
for section ¼ 28), while intermediate and vellus-like follicles
were increased, with a terminal ⁄vellus ratio always < 3 : 1
(Fig. 3). The anagen ⁄telogen ratio was 88 : 12. In the verti-
cal sections, collapsed connective sheaths were evident under
the miniaturized hair follicles. No signs of inflammation
were seen.

2005 British Association of Dermatologists • British Journal of Dermatology 2005 152, pp556–559
Fig 3. Histopathological findings in a 4-mm punch biopsy specimen:
a variability in the hair density was observed, with a reduction in
numbers of terminal hairs and an increase in numbers of vellus-like
hairs (horizontal section, haematoxylin and eosin).
Discussion
The diagnosis of AGA in our children was supported by pat-
tern of alopecia, the presence of > 20% hair diameter diversity
by dermoscopy and by the pathological findings of a ter-
minal ⁄vellus hair ratio < 3 : 1.
Other forms of hair thinning were evaluated in the differen-
tial diagnosis, such as telogen effluvium, alopecia areata incog-
nita, hypotrichosis simplex and loose anagen hair syndrome.
Telogen effluvium and alopecia areata incognita produce a dif-
fuse hair thinning that also involves the parietal and the occip-
ital regions. The pathology of telogen effluvium shows
increased terminal telogen follicles in the absence of inflam-
matory changes. The terminal ⁄vellus hair ratio is not changed.
In alopecia areata incognita, hair shedding is severe, the pull
test shows a great number of telogen hairs and the pathology
shows an increased number of catagen follicles and perifolli-
cular infiltrates with eosinophils.
Hypotrichosis simplex is a familial syndrome with sparse or
normal hair at birth, very coarse hair regrowth in early child-
hood and hair loss, especially at the vertex, beginning at pub-
erty and leading to severe alopecia before the age of 20 years.
This patterned alopecia is similar to the one observed in our
patients, but is more severe. Examination of the parents of our
patients revealed that none of them had this pattern of hair loss.
Loose anagen hair syndrome was excluded by the patterned
hair loss seen in our patients and by the trichogram that never
revealed a number of loose anagen hairs exceeding 70%.8
The presence of normal physical and psychological
development, normal nails and teeth and no sweating abnor-
malities excluded ectodermal dysplasias. In ectodermal dyspla-
sias, moreover, hair thinning is severe and starts early in
childhood. Examination of the hair shafts by light microscopy
excluded alopecia due to hair shaft fragility.
Our 20 children were therefore affected by AGA with pre-
pubertal onset. The occurrence of AGA in prepubertal children

has rarely been reported in the literature, but it is probably
not exceptional. The adrenal secretion of androgen hormones
begins to increase 2–3 years before the onset of puberty,
through a process named adrenarche, reaching adult levels in
early to late puberty. Blood levels of DHEA-S and DHEA can
be utilized to establish the adrenal secretion of androgens. The
mechanisms responsible for regulating adrenarche are not
exactly known. In general, this process occurs independently
of gonadal maturation.9
Over the last century the mean age at onset of adrenarche
has become progressively lower and the same trend has been
reported for puberty. A hyperinsulinaemic diet, environmental
exposure to hormones, environmental sexual exposure and
parental mood disorders have been considered as possible cau-
ses of early adrenarche.10–14 In our children, the DHEA-S lev-
els were consistent with postadrenarche, but none of them
was affected by premature puberty, as demonstrated by phys-
ical and laboratory assessments.
A common feature observed in our series of children with
AGA was a strong genetic predisposition to the disease. Gen-
etic predisposition may induce an increased androgen sensi-
tivity of scalp follicles due to an abnormal activity of the
enzyme 5a-reductase type II or to an excessive expression of
the androgen receptor in the scalp. It is therefore possible
that adrenal androgens may be responsible for AGA in gen-
etically predisposed children. Another possible explanation for
the occurrence of AGA in prepubertal children may be that
this pattern of hair loss is not necessarily androgen
dependent.15
In all our children, both boys and girls, AGA presented with
a female pattern, consisting of selective involvement of the
central parting of the scalp, in some cases associated with
frontal accentuation. None of them had vertex balding or
recession of the temporal hairline, typical of male pattern
AGA. Female pattern AGA is typically observed in women and
has been reported to occur in the absence of circulating
androgens.15 As Orme et al. have suggested, other mechanisms
should be considered in the pathogenesis of this type of
AGA.15
AGA should therefore be considered in the differential diag-
nosis of children with hair loss, especially if there is a family

2005 British Association of Dermatologists • British Journal of Dermatology 2005 152, pp556–559
Androgenetic alopecia in children, A. Tosti et al. 559
history strongly positive for AGA. Although pathogenesis
remains speculative, endocrine evaluation and a strict follow-
up are strongly recommended.
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