vol28 i1 alopecia areata
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Alopecia Areata: Evidence-Based Treatments
Seema Garg and Andrew G. Messenger
Alopecia areata is a common condition causing nonscarring hair loss. It may e patchy!
involve the entire scalp "alopecia totalis# or whole ody "alopecia universalis#. $atients may
recover spontaneously ut the disorder can %ollow a course o% recurrent relapses or result
in persistent hair loss. Alopecia areata can cause great psychological distress! and the
most important aspect o% management is counseling the patient aout the unpredictale
nature and course o% the condition as well as the availale e%%ective treatments! with details
o% their side e%%ects. Although many treatments have een shown to stimulate hair growth
in alopecia areata! there are limited data on their long-term e%%icacy and impact on &uality
o% li%e. 'e review the evidence %or the %ollowing commonly used treatments: corticosteroids
"topical! intralesional! and systemic#! topical sensiti(ers "diphenylcyclopropenone#! psor-
alen and ultraviolet Aphototherapy "$)*A#! mino+idil and dithranol.
Semin ,utan Med Surg :/0-/ 1 223 Elsevier Inc. All rights reserved.
lopecia areata "AA# is a chronic in%lammatory condition caus-
ing nonscarring hair loss. The li%etime ris4 o% developing the
condition has een estimated at /.56 and it accounts %or /6 to 6
o% new patients seen in dermatology clinics in the )nited 7ingdom
and )nited States./ The onset may occur at any age8 however! the
ma9ority "26# commence e%ore 2 years o% age. There is e&ual
distriution o% incidence across races and se+es. In recent decades!
the role o% genetic predilection has started to e e+plained.
Appro+- imately 26 o% a%%ectedpeople have a %amily history o%
the disease! suggesting a genetic predisposition.; A small twin
study %ound an inherited component in appro+imately 006 o%those a%%lictedy the disease! suggesting there is also a
contriution %rom environmental %actors.< Associations have een
reported with chromosome / "in- creased incidence in =own>s
syndrome#! ma9or histocompatiility comple+! and cyto4ine and
immunogloulin genes indicating apolygenic asis. A genome-
wide scan identi%ied additional loci that
also are implicated in other hair disorders and psoriasis.0
AA is considered a tissue-restricted autoimmune condition as
the result o% association with other autoimmune diseases! oth
within the a%%ected person and their %amily. ,irculating antiodies
against %ollicular components are detected more %re&uently in
people with AA.!5 A hallmar4 o% AA is a periular lymphocytic
in%iltrate that consists primarily o% activated T-lymphocytes.
E+periments using human hair %ollicles transplanted onto
immunoincompetent mice strongly implicate a T-cell?mediated
pathomechanism.3
A%%ectedpeople develop single or multi%ocal smooth! well-circum-
scried patches with short ro4en hairs at the periphery "e+clamation
mar4 hairs#. The pattern and severity o% hair loss varies greatly.
All hair-earing s4in may e involved! with appro+imately /26 o%
those
=epartment o% =ermatology! @oyal allamshire ospital! She%%ield! )nited
7ingdom.
Address correspondence to: A. G. Messenger! =epartment o% =ermatology!
@oyal allamshir e ospital ! Glosso p @oad! She%%ield S/2 C! )7. E-
mail:a.g.messengerDshe%%ield.ac.u4
with AA having nail involvement. @ecovery can occur spontaneously!
although hair loss can recur andprogress to alopecia totalis "total losso% scalp hair# or universalis "oth ody and scalp hair#. =iagnosis is
usu- ally made clinically! and investigations usually are unnecessary.
$oor prognosis is lin4ed to the presence o% other immune diseases!
%amily history o% AA! young age at onset! nail dystrophy! e+tensivehair loss! and ophiasis "AA o% the scalp margin#./2
AA can cause signi%icant psychologicalprolems. The unpredict-ale nature o% the condition! with apparent improvement %ollowed
y deterioration can e distressing. ne o% the most important as-
pects o% management is counseling the patient and the %amilymem- ers o% a young child aout the nature and course o% the
condition as well as the availale e%%ective treatments with details
o% what they involve and their side e%%ects.
Treatment
The hair %ollicle in AA is not destroyed. There%ore! there is potential
%or regrowth! although there is no cure and no treatment has een
shown to alter the course o% the disease. Many treatments can
induce hair growth. owever! assessing e%%icacy is di%%icult in patchy
AA as a result o% the %re&uency o% spontaneous recovery. n the
other hand! studies incorporating patients with severe disease are
hampered y the poor response to any %orm o% treatment in this
group o%patients.
There are %ew randomi(ed controlled trials o% treatments %or
AA!// although %or common treatment modalities none have shown
a signi%icant long-term ene%it compared with placeo. There are
numerous reports o% treatments %or AA that have assessed
e%%icacy with less-than-ideal criteria. Many o% these studies andreports are o% dout%ul value8 however! some treatments that have
not een eval- uated in randomi(ed controlled trials may ene%it
somepatients.
Fo Treatment
Because there is a high proportion o% spontaneous recovery! with ;
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/20-0323H-see %ront matter 1 223 Elsevier Inc. All rights reserved. 15
doi:/2./2/G9.sder.22./.22
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16 S. Garg and A.G. Messenger
owever! the relapsing nature o% the disease needs to e discussed
withpatients. $atients with AA normally are highly motivated and
compli- ant! ut some patients may not want treatment or may not
respond and alternatives such as wigs! should also e discussed.
,orticosteroidsTopical ,orticosteroids
$otent topical steroids are widely used to treat AA! ut the
evidence %or their e%%icacy is limited. A /-wee4 within-patient
study "right vs. le%t side o% scalp# in moderate-to-severe disease with
a 2.206 clo- etasol propionate %oam %ormulation showed
regrowth o% at least
026 in 5 o% ;< o% the treated sites compared with / o% ;< on the
nontreated sites./; Aprevious study o% 2.206 cloetasolpropionateunder occlusion in patients with alopecia universalistotalis showed
that 36 "n # ene%ited8 however ; patients! relapsed in the
-month %ollow-up! giving a /5.6 overall long-term ene%it./< Ina
randomi(ed study comparing etamethasone valerate %oam to eta-
methasone dipropionate lotion in / patients with mild-to-moder-
ate AA! the %oam %ormulation produced signi%icantly greater re-growth at / wee4s./0 owever! a study y ,haruwichitratana et
al/ o% 2.06 deso+imetasone cream in moderate alopecia %ailed
to show signi%icant ene%it over placeo a%ter / wee4s o%
treatment.
Intralesional ,orticosteroids
Intralesional corticosteroids also are used %re&uently in AA. Their
use was %irst descried in /30 with the use o% hydrocortisone./5
Steroids with low soluility are pre%erred %or their slow asorption
%rom the in9ection site! promoting ma+imum local action with min-
imal systemic e%%ect. A study o% intralesional corticosteroids showed
the time %rom in9ection to visile hair growth was -< wee4s and
su- se&uent growth occurred at a constant linear rate. Tu%ts grew at
;; o% ;< sites in9ected with triamcinolone he+acetonide and at / o%
0 in9ected with triamcinolone acetonide./ The steroid is in9ected
into the upper su cutis every < to wee4s. $reparations used
include triamcinolone acetonide "0-/2 mgm# and hydrocortisone
acetate "0 mgm#. There are no randomi(ed controlled trials on
intralesional steroids. An uncontrolled study %rom Saudi Araia %ound
;6 o% patients receiving monthly triamcinolone in9ections showedcomplete regrowth. The out- come was more %avorale in younger
adults with less than 0 patches o% short duration "less than / month#
and less than ; cm diameter./3 Side e%%ects are minimal. S4in atrophy
is common ut resolves within a %ew months. The ris4 o% prolonged
atrophy can e reduced y the use o% smaller &uantities! limiting the
numer o% in9ections per site and ensur- ing the in9ection is not too
super%icial. Intralesional corticosteroids are most suitale %orpatchy!relatively stale hair loss o% limited e+tent. This modality is not
appropriate in rapidly progressive AA or in alopecia
totalisuniversalis.
Systemic ,orticosteroids
Systemic corticosteroids have een used in the treatment o% AA
since the /302s.2 There is little dout that systemic steroid
treatment will induce hair regrowth ut! in patients with more
severe %orms o% the disease! relapse is common when treatment is
discontinued. ,on- cerns over the side e%%ects o% long-term
treatment mean that many physicians are not prepared to use
systemic steroids to treat alopecia areata./ In an attempt to reduce
systemic side e%%ects! various high- dose pulsed therapy regimens
have een tried. @egimens includeprednisolone! g intravenoussingle dose or 2.0 g daily %or 0 days! alternating daily dose!/
tapering oral dose over wee4s!; intrave- nous
methylprednisolone 02 mg twice daily %or ; days< and ;22 mg
monthly %or at least < months.0 Most studies have reported a
good initial response to therapy! ranging %rom //.
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16 S. Garg and A.G. Messengerment. A randomi(ed controlled trial showed patients receiving 22mg prednisolone once wee4ly %or ; months were more li4ely to
develop signi%icant regrowth than were those given placeo. ow-
ever! 06 relapsed within ; months o% discontinuation o% treat-
ment. Two other studies %ound! a%ter an initial response! that
months to /0 months a%ter treatment there was no sustantialen-
e%it./! A %urther trial showed 6 mino+idil lotion %ollowing
wee4s o% tapering prednisolone may decrease the hair loss.;
$ulsed corticosteroids appear to e well tolerated. owever! those
receiv- ing daily or alternate day oral regimes developed the
e+pected side e%%ects! including: acne! oesity! mild
hypertension! impaired A,T reserve! and lenticular opacities./
ral steroids appear to wor4 well initially on recent-onset disease!
ut ophiasis and univer- salis respond poorly.