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Symposium

Current Treatment Strategies in Pediatric Alopecia Areata

Etienne Wang, Joyce SS Lee, Mark Tang
National Skin Centre, 1 Mandalay Road, Singapore

Abstract
Alopecia areata (AA) is a non‑scarring autoimmune disease of the hair follicle that can present at any age. Pediatric cases are commonly
seen in a dermatology clinic, and management can potentially be challenging, with a small proportion of cases experiencing a chronic
relapsing course marked by distressing hair loss that can bring about significant psychosocial morbidity. We review the established
treatments for pediatric alopecia areata, alongside second and third line therapies that have shown to be efficacious. We also offer a
treatment algorithm as a guide to the treatment of pediatric AA.

Key Words: Alopecia areata, pediatric, treatment

Introduction even fewer studies on childhood AA and hence, much

Alopecia areata (AA) is a chronic inflammatory disorder,
characterized by a T‑cell autoimmune‑mediated attack
on the hair follicle, and occasionally on the nails. This
leads to patches of non‑scarring alopecia on the patient’s
scalp, face, and other hair‑bearing skin of the body. The
reported lifetime risk of developing AA has been estimated
to be 1.7% and accounts for up to 2% of new cases in a
dermatology clinic in the West.[1]
Pediatric Alopecia Areata
Pediatric alopecia areata is not uncommon. Up to one‑third
of newly diagnosed AA cases have been reported in
patients aged 20 years and below, in both Singapore[2]
and India.[3] The majority of pediatric AA patients present
with localized mild disease affecting less than 50% of the
scalp.[2‑5] Pediatric AA has been associated with atopy, nail
changes, including the twenty nail dystrophy syndrome and
a positive family history. In some studies, pediatric AA has
also been associated with a guarded long term prognosis,
with patients having multiple relapses and progression to
alopecia totalis (AT) or universalis (AU).[6,7]
Up to 50% of AA patients have spontaneous regrowth of
their hair within a year without treatment,[8] thus making
watchful waiting a reasonable option for young children
with limited disease. For patients with more extensive or
progressive disease, it would be important to discuss with
the parents the various treatment options available, bearing
in mind the child’s ability to accept and tolerate more
invasive procedures.
Treatment Options in Pediatric Alopecia Areata
A Cochrane Review of AA treatments in 2008 concluded
that there is a paucity of well‑designed randomized trials
to guide treatment.[9] Evaluation of efficacy is also difficult
in AA where spontaneous remission is common, and
great disease heterogeneity exists. Significantly, there are
Address for correspondence: Dr. Mark Tang, National Skin Centre,
1 Mandalay Road, Singapore 308205. E‑mail: marktang@nsc.gov.sg
of the evidence pediatric is extrapolated from adult AA
data. Long‑term safety data is also less well‑established
in children, for example with the use of topical
immunotherapy.
Management of pediatric AA is particularly challenging
given the chronicity of the condition. It is crucial to evaluate
the impact of the disease on the child’s physical and
emotional well‑being, including issues like self‑confidence,
self‑image, and acceptance by peers. Parental anxiety,
frustration, guilt, and expectations must also be proactively
managed to ensure an overall holistic management of the
patient.
We review the various established treatments, as well as off
label and new therapies for AA below.
Treatment options with strength of
recommendation B
Topical corticosteroids (Quality of evidence III)
Local application of potent topical corticosteroids has
been effective in the treatment of moderate‑to‑severe AA.
A 12‑week half‑head study of 0.05% clobetasol propionate
foam against placebo showed regrowth of at least 50% in
7/34 treated sites compared with 1/34 of the placebo‑treated
sites.[10] In patients with AT/AU, 29% (8/27) responded to
0.05% clobetasol propionate ointment under occlusion.[11]
In our center, topical steroid therapy is the first‑line treatment
for pediatric cases of AA, given its ease of use, convenience,
and lack of pain. We advocate using a highly potent
topical corticosteroid such as 0.05% clobetasol propionate
lotion, and subsequently, tailing down to a lower potency
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Wang, et al.: Pediatric alopecia areata
corticosteroid, such as 0.1% mometasone furoate or 0.1%
betamethasone valerate scalp lotion to avoid skin atrophy.
Topical minoxidil (Quality of evidence III)
Minoxidil (2, 4 dinitro‑6‑piperidinopyrimidine‑3‑oxide) is
an established topical treatment for non‑scarring alopecia
such as AA. One study showed 3% minoxidil under
occlusion led to more regrowth in extensive AA when
compared to placebo.[12] In another study, comparing
minoxidil at concentrations of 1% and 5% for extensive
AA, patients receiving 5% minoxidil experienced more
regrowth.[13] Both these studies included children, although
no subgroup analysis was done for pediatric cases. In
the latter study, Price included an anecdotal report of a
9‑year‑old girl with 100% regrowth after 48 months of
monotherapy with minoxidil.[13] Since minoxidil is unlikely
to have any immunomodulatory effect on the autoimmune
attack of the hair follicle,[14] it likely acts synergistically
with corticosteroids[15] to improve outcomes in AA.
In our center, topical 2% or 5% minoxidil is used as an
adjunctive treatment, in combination with topical or
intralesional steroids. Hypertrichosis on the face and
neck may be more common in children, especially at
higher concentrations. As such, 2% topical minoxidil
may be preferred in children. Topical minoxidil may also
cause irritant contact dermatitis or aggravate pre‑existing
seborrheic or atopic dermatitis. Serious systemic, but
non‑fatal, side effects such as hypotension and tachycardia
were reported in a young girl who ingested 100 ml
of minoxidil hair lotion.[16] As such, parents should be
counseled to keep the medicines out of reach of children.
Intralesional corticosteroids (Quality of evidence III)
Injection of corticosteroids into the deep dermis and
upper subcutis of the affected areas is the treatment of
choice for localized AA in adults, achieving adequate
tissue concentrations with minimal systemic absorption.[17]
It has been shown to be effective in several uncontrolled
trials,[18‑20] including a Singapore study that reported a
significant improvement in up to 82% of patients with
limited AA treated with monthly intralesional triamcinolone
acetonide for 12 weeks.[21]
For scalp lesions, we use triamcinolone acetonide 10 mg/
ml, injecting 0.05‑0.1 ml per site, spaced 1 centimeter
apart. Triamcinolone acetonide should be diluted to
2.5‑5 mg/ml for the eyebrows and face. Side effects include
pain, skin depressions secondary to localized atrophy, and
hypopigmentation. Peri‑orbital injections may be associated
with complications such as glaucoma, cataracts, and retinal
vascular occlusion.
Usage of intralesional corticosteroids is limited in children
due to the fear of injections and pain. Some options to
reduce pain include the use of smaller gauge 30 G or 32
G needles, ice or cold compresses, ethyl chloride spray,
Indian Journal of Dermatology 2012; 57(6)
distraction therapy, and the application of topical anesthetic
creams. The use of topical anesthetic creams such as
EMLA (eutectic mixture of local anesthetics containing
lidocaine 2.5% and prilocaine 2.5%) is an important way
to decrease pain and increase patient acceptance. The
maximum dose and surface area of EMLA that can be used
safely in children varies according to age and can be found
in Annex 2. Potential side effects of EMLA would be local
irritation and rarely methaemoglobinaemia due to systemic
absorption of prilocaine, especially in neonates and very
young children.[22,23] An alternative is ELA‑Max cream,
which is prilocaine‑free, which has a similar efficacy to
EMLA cream and a good safety profile in children.[24]
Topical immunotherapy (Quality of evidence IIb)
Topical immunotherapy is indicated for chronic and
extensive AA where prolonged topical or intralesional
corticosteroid injections are impractical or ineffective. It
has been shown to modulate the local autoimmune attack
on the hair follicles,[25] with reported response rates ranging
from 9% to 87% in adult patients. Response rates have
been found to be comparable in the pediatric AA, with
about one‑third of patients experiencing regrowth.[26,27]
Relapse rates in pediatric studies varies from 25% to
90%,[28] with cases having more extensive disease having
a poorer prognosis. In our local series of Singaporean AA
patients, those aged between 4 and 20 years were found to
have a poorer response to topical immunotherapy.[21]
Contact sensitizers used today include
diphenylcyclopropenone (DPCP) and squalene acid dibutyl
ester (SADBE). The original sensitizer dintrochlorobenzene
(DCNB) is no longer in use as it has been found to be
potentially mutagenic in the Ames test. SADBE is a
strong sensitizer but is not stable in acetone and undergoes
hydrolysis in storage frequently. Hence, we favor the
use of DPCP, with a protocol described by Happle
et al.[29] The patient is first sensitized with 2% DPCP on
a 2 centimeter bald patch on the scalp. This is left on for
24 hours and washed off. Patients are reviewed 2 weeks
later. Sensitization to DPCP is successful if an eczematous
reaction is noted over that patch. Subsequently, DPCP,
starting at 0.0001% concentration, is applied weekly at
increasing concentrations with a goal to induce a mild
eczematous reaction and a tolerable itch that lasts 1‑2 days.
The DPCP is left on for 24 hours each time and washed off.
As DPCP is degraded by light, patients are advised to shield
the treated areas from light for 24 hours after application.
While topical immunotherapy has been used since 1983, with
no serious long‑term sequelae has been reported to date,[30,31]
parents and patients should be counseled carefully regarding
the common side effects of topical immunotherapy, especially
irritant contact dermatitis. In severe cases, patients may have
generalized eczema, regional lymphadenopathy, or urticaria.
Children with atopic dermatitis or seborrheic dermatitis may
be at higher risk of such side effects. Other reported cutaneous
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Wang, et al.: Pediatric alopecia areata
side effects include hyperpigmentation and hypopigmentation,
including vitiligo. DPCP is highly sensitizing and should be
applied by trained medical or nursing personnel who must be
protected to avoid sensitization. Adequate precautions should
be taken by family members as well.
Pulsed Systemic Corticosteroids (Quality of evidence Ib)
Pulsed systemic corticosteroid therapy is a treatment
option aimed at arresting the underlying inflammatory
process while attempting to avoid its long‑term side
effects.[32] Most clinical trials studying this treatment option
are uncontrolled, or adopt different dosing protocols,
making comparison and meta‑analysis difficult.[33,34] Pulse
intravenous methylprednisolone has been found to be
beneficial in several studies,[35,36] but significant risks such
as hypokalemia and cardiac arrhythmias necessitate careful
patient monitoring. In children with extensive patchy AA or
AT/AU, high dose pulse methylprednisolone was shown to
have a poor long‑term outcome, with 66% of patients having
less than 30% regrowth after a median of 12 months.[37] No
adverse effects were noted in this small case series.
Pulsed oral corticosteroids for AA have also been shown to
be effective in children without significant side effects.[34,38]
The dose tested in an uncontrolled case series of 16 young
patients was equivalent to oral prednisolone 5 mg/kg/month
for 3 months in patients aged 3‑11 years and 300 mg/month
for 3 months in patients aged 12‑18 years. All patients had
either extensive AA or AT, and 60% experienced excellent
results, even 3 months after the end of the treatment period.
The side effects reported were mild epigastric burning and
transient giddiness or headache in 2 patients.
Treatment options with strength of
recommendation C
Systemic corticosteroids (Quality of evidence III)
Although there are no trials examining the effects of daily
systemic corticosteroids in children, it has been shown to
be able to induce regrowth in adult AA.[39] However, the
well‑known adverse effects of long‑term corticosteroid
therapy, particularly growth retardation, metabolic
dysregulation and reduced bone mineral density, limits
its use in children. Hence, it is reserved for patients with
rapid onset or rapidly progressive extensive, active AA.
Oral prednisolone 0.5 mg‑0.8 mg/kg/day is prescribed, and
slowly tapered over 2 months, and not exceeding 3 months.
Dithranol (Quality of evidence IV)
Topical dithranol has been reported to be mildly effective
in several small studies[40,41] and has been postulated to act
by suppressing the local Th1 immune reaction at the hair
follicle. It is available in 0.2% to 0.5% cream or ointment
base and needs to be used for at least 3 months for clinical
effect. Contact dermatitis is common, and it can stain the
patient’s clothes. It may be useful in children who have
failed first‑ or second‑line therapies.
461
Phototherapy (Quality of evidence IIb)
Topical PUVA is a widely used modality with reported
success rates of 50‑70%.[42,43] However, most studies were
uncontrolled, and a retrospective analysis suggest that is
may be no better than the natural course of AA,[44] except
for the beard area.[45] Like dithranol, it may have a role
when combined with corticosteroids for extensive AA.[46]
In recalcitrant cases of adult AA, combination therapy
with oral prednisolone at 20 mg/day and twice‑weekly oral
PUVA resulted in good regrowth of terminal hairs for some
patients. No equivalent studies have been conducted in
children, but due to uncertain response rates and potential
side effects from cumulative UVA radiation including
photo‑aging, eye damage, and increased skin cancer risk,
PUVA should only be considered as third‑ or fourth‑line
treatment. Narrow‑band UVB (NBUVB) therapy has not
been shown to be effective in extensive AA. Only 20% of
patients achieved excellent responses with NBUVB in a
recent uncontrolled study, but these patients also received
systemic corticosteroids concurrently.[47] To our knowledge,
there have been no reports on the efficacy of UVA1 therapy
on childhood AA.
Laser therapy (Quality of evidence III)
The 308‑nm Excimer laser showed some efficacy in
treating AA in several small case series, mainly as an
adjuvant treatment in recalcitrant cases.[48,49] There has been
a case report of the use of fractional photothermolysis laser
to effectively treat AA in a patient who previously failed
topical minoxidil, topical steroids, and intralesional steroid
injections.[50]
Immunosuppressive agents (Quality of evidence III)
Corticosteroid‑sparing immunosuppressive agents such as
methotrexate, azathioprine, and cyclosporine have been
reported in several cases series to be effective in AA.
Methotrexate has been reported to produce 64% recovery
when used together with daily oral prednisolone for adult
patients with AT/AU.[51] A retrospective uncontrolled study
of children with severe AA treated with methotrexate for a
mean of 14.2 months had only 38.4% response.[52]
A pilot study of 20 patients (age range 8-57) treated with
azathioprine 2  mg/kg/day showed a significant regrowth
of 52.3% after a mean of 3 months.[53] Cyclosporine has
been postulated to be an ideal drug for the treatment of
AA due to its ability to suppress T‑helper cells, suppress
interferon‑gamma (IFN‑γ) production, with an additional
side effect of hypertrichosis. Reported efficacy of oral
cyclosporine range from 25% when combined with
low‑dose oral prednisolone[54] to 88.4% when combined
with weekly pulsed methylprednisolone.[55] In general, use
of these agents is limited in children because they require
frequent blood tests to monitor for potential side effects.
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Wang, et al.: Pediatric alopecia areata
Topical calcineurin inhibitors (Quality of evidence Ib)
Topical calcineurin inhibitors (TCIs) have been used in
pediatric inflammatory conditions such as atopic dermatitis,
psoriasis, and vitiligo with success.[56] The main advantage
of TCIs lie in their steroid‑sparing effects and may be
an option for facial or eyebrow involvement in young
children. However, studies supporting their efficacy are
lacking. A recent randomized trial comparing intralesional
corticosteroids, topical corticosteroids, and TCIs in 78 adult
patients with localized AA showed topical tacrolimus to be the
least efficacious of the three.[57] Furthermore, one case report
reported no response in AA with topical pimecrolimus.[58]
Topical retinoids (Quality of evidence IIb)
There are limited published studies for topical retinoids in
the treatment of AA and none in children. An uncontrolled,
non‑randomized 3‑month trial of 80 patients with limited
AA showed a 70% response rate with topical steroids, 55%
with topical tretinoin 0.05%, and 20% in controls.[59] Topical
bexarotene, a retinoid X receptor agonist, was studied in
single‑blinded, half‑head study involving 42 patients, which
showed some efficacy.[60]
Treatment options with strength of
recommendation D
Prostaglandin analogues (Quality of evidence Ib)
A new and emerging treatment for non‑scarring hair loss is
the use of prostaglandin F2α analogues, such as latanoprost
and bimatoprost, which have been shown to cause eyelash
hypertrichosis. It is postulated to work by enhancing
conversion of hairs from telogen to anagen stage.[61]
However, topical latanoprost and bimatoprost were both
found to be ineffective in stimulating eyelash regrowth in
several randomized controlled studies of AA patients with
eyelash loss.[62,63] Although the safety of prostaglandin
analogues in the treatment of pediatric glaucoma is
well‑established,[64] this novel off‑label treatment for AA
has not been validated in children.
Biologics (Quality of evidence IIb)
Although tumor necrosis factor (TNF)‑α has been found
to be significantly elevated in the sera of AA patients,[65]
anti‑TNF‑α therapies have found to be ineffective in
AA.[66‑68] As such, biologics cannot be recommended for
treatment of AA at this juncture.
Holistic management of pediatric AA patients
Management of AA should also include an assessment of
the child’s psychosocial well‑being, emotional response, and
coping mechanisms to their disease, as well as the expectations
of the caregivers. AA has been associated with adjustment
disorder, anxiety, and depression in adults and children.[69]
Adolescents are particularly prone to body image disorders
due to their need for peer acceptance and establishment of
their identity. A small sample of 14 children and adolescent
Indian Journal of Dermatology 2012; 57(6)
patients with AA found a high rate of depression (50%)
and obsessive‑compulsive disorder (35.7%).[70] In addition,
both adult and pediatric AA patients have been found to
have heightened stress perception, causing them to handle
stressful life events less effectively than healthy subjects.[71]
This is important as AA has been reported to be triggered
by stressful events in the patient’s life,[68] and poor coping
mechanisms may perpetuate disease activity.
Patients with significant psychiatric co‑morbidities should be
co‑managed together with a psychiatrist.[72] Anti‑depressants
such as paroxetine, a selective serotonin re‑uptake inhibitor,[73]
and hypnotherapy[74] have been shown in small trials to help
hair regrowth over placebo in adults.[75] AA support groups
are important resource groups for patients and their caregivers
to gain further insight, emotional support, and acceptance of
their condition.[76] We have found that cosmetic camouflage
with wigs or “scalp prostheses” have been very helpful in
patients and should be proactively discussed.
Conclusions
Alopecia areata is a common yet challenging condition to
manage in the Pediatric Dermatology clinic. While many
patients with localized AA will respond well to first‑line
treatment with topical or intralesional corticosteroids,
some patients will require more aggressive or second‑line
therapy. Pediatric age of onset, more extensive disease
(scalp involvement more than 50%, ophiasis, or AT/
AU), and recalcitrance to initial therapies[7] may highlight
patients who will prove to be challenging to manage.
Some of these patients may benefit from a cocktail of
established therapies, whereby the synergy between
two or more established therapies proves to be better
than monotherapy.  [41]
Future studies focusing on such
combination therapies, as well as novel new treatments
not mentioned in this review because of lack of evidence
(non‑TNF‑α biologics, drugs directed against nerves like
capsaicin, and low‑level light therapy devices), will expand
the choices available to dermatologists, patients and their
parents in the treatment of pediatric AA.
We have included a treatment algorithm for pediatric cases
of AA (Annex 3) as a guide, but treatment will need to be
individualized and based on discussion with the child and
their parents.
Annex 1
Levels of evidence
Ia Evidence obtained from meta‑analysis of randomized
controlled trials.
Ib Evidence obtained from at least one randomized
controlled trial.
IIa 
Evidence obtained from at least one well‑designed
controlled study without randomization.
IIb 
Evidence obtained from at least one other type of
well‑designed quasi‑experimental study.
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Wang, et al.: Pediatric alopecia areata

III Opinions of respected authorities based on clinical • Pulsed systemic corticosteroids

experience, descriptive studies or reports of expert If hair loss still extensive, proceed to treatment for chronic
committees extensive AA
IV Evidence inadequate due to problems of methodology
(e.g. sample size or length of comprehensiveness of
Chronic extensive AA
follow‑up or conflicts of evidence). First‑line treatment:
• Topical steroids with topical Minoxidil lotion
Grades of recommendation
A There is good evidence to support the use of the Second‑line treatment:
procedure • Topical immunotherapy (DPCP)
B There is fair evidence to support the use of the Third‑line treatment:
procedure • Pulsed systemic corticosteroids
C There is poor evidence to support the use of the • Topical PUVA therapy
procedure • Azathioprine
D There is fair evidence to support the rejection of the use • Other miscellaneous therapies
of the procedure
E There is good evidence to support the rejection of the References
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How to cite this article: Wang E, Lee JS, Tang M. Current treatment
strategies in pediatric alopecia areata. Indian J Dermatol 2012;57:459-65.
Received: June, 2012. Accepted: July, 2012.
Source of support: Nil, Conflict of Interest: Nil.

Announcement

Dermatosurgery Registry of ACS(I)

Association of Cutaneous Surgeons (I) (www.acsinet.net) is happy to announce the launch of its online Dermatosurgery
registry (www.acsiregistry.in). This registry has been created to obtain data on dermatosurgical procedures being
performed by our members across the country. This is the first-of-its-kind effort to accumulate real-time scientific
data online w.e.f 1st June 2012. Nine different commonly performed procedures have been selected for the purpose of
documentation. The feedback from members of ACS(I) registered with the website will be pooled in the registry and
various information on these dermatosurgical procedures will be available as a ready reference. The registry is password
protected; the registry can’t be accessed by anyone not registered in the site.
We request participation by all to make this unique project successful and pave the way for an entirely new era of real-
time online documentation of scientific data on a large scale and nationwide basis.

465 Indian Journal of Dermatology 2012; 57(6)