vol28 i1 alopecia areata

5/20/2018 Vol28 i1 Alopecia Areata

1/8

A

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

usually 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 ;


2/8

/20-0323H-see %ront matter 1 223 Elsevier Inc. All rights reserved. 15

doi:/2./2/G9.sder.22./.22


3/8

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 //.


4/8

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

receiving 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 universalis respond poorly.

vol28 i1 alopecia areata

Documents