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Transcript
Atopic dermatitis.An Approach to
an Allergic Enigma Sttntntttty
ii:,
'\s
.
i
Dr A Morris
35 Finsbun'Aver-ruc
NEWLANDS
7700
Curriculum vitae
Adrian Morris gradr-rated
fiom UCT Medic:rl
at
School in 1983. Alier his hor.rseuranship
Groote Schuur Hos;rital, his SHC) posts
inch.rdedpaediatricsat Red Cross Childrens'
Hospital ;rnd emergcr.rcvnrcclicineat Grootc
Schuur Hospital. He ther-rcomplctecl (iP
Vocational training in Surrcy, (England) befbre
returning to Cape Torvn in l9ll8, to join a
group family practicc in Ncwlancls.He
o b t a i n e dt h e l ) C H ( S A ) i n 1 9 8 9 a n d t h e
MFGP (SA) in 1990. Allergy and clinical
ir.nmunologvare his speci;rlintcrcsts. He is ir
member of the Britislr Socictv fbr Allcrgv ancl
Clinical Immunology, and wils a dclegite at
their I99I ar-rd1992 annnll coufbrenccs.
While in Iingland, hc attended the BSACI (iP
training course ir.rAllcrgv. He rvaselecteclorrto
the executivecommittee of the Allerg,vSocictl
of Sor,rthAfi'icrrin 1992.
Atooic Derntrttitis or Infinrile
Eciema is one ol'the nlost coi11tl1oi1
relapsing skin disorders of chilclhoocl
and onc of the ntost dillicult to trcat.
l)espite tu1ever increasing incidence,
the exact aetiologrr and tliagnostic
Ibatures of Atopic Dentatitis rentain
LrrTclear.The dry hypet'-irriteble skin
and the misery/associatcdwith this
conditiotl, clisrupts the lili of both
the alfected child and his or her
lamily. Treatntent is ainted at
controlling the st,ntptottts until
nantral reso]Lttioil occurs.
S Alr Fant Pract )993; 14: 255-62
I(EYWORDS:
Dermatitis,Atopic; Physici.rr,
Family; Infant; Allergy and
Immunology.
AI Moris
age. By puberry 40% ofcaseshave
completely resolved.
Atopic Dermatitis appearsto be
inherited as an autosomal dominant
trait with poor penetrance.2
Patientswith atopic dermatitis have a
greater predisposition to associated
pityriasisalba, forefbot dermatitis,
perioral eczema,icthyosislulgaris,
anterior subcaosularcataractsand
often later devilop occupational
irritant dermatoses.3Only allergic
contact dermatitis seemsto be less
c()mmon in the atopic dermatitis
suffercr (with the exceDtionof nickel
allergy).
I0% o1'childrenrvith sevcreatooic
dernrltitis are growth retardedon
accolult of, either dre debilitating
llature of tl-rediseaseitself, chronic
steroid adrninistration or even
restrictivediets which may have been
instituted.
Pathophysiology
"It's not the crttption that itches, but
the itch that erLtpts."
This conditiorl \vas originally
describedby Besnicrin 1892, but the
term "Atopic Dermatitis" was onlv
introduced b)'Wise and Sulzberger in
1933.
The ir-rcidenccof Atooic Dermatitis
(AD) or Infantile Eczerna(synonyms:
Prr.rrigoBesnier,Ncurodermatitis
Constitutionalis) variesfrom 3 to
l0% of the population, rvith an everincreasingincidence over the past 30
years.r This l-rasbeen ascribedto
progressiveurbanisation and
increasedlevelsofirritants and
pollutar.rtsir.rthe home. It commonly
appearsafter about 3 months of age
ar-rdbegir.rsto clear by 3 to 5 yearsof
255
SA Hrn'rilvPracticeTune 1993
An underlying immr-rneabnormality
rvill predispose
or dysregr-rlation
certain ir-rdividualsto develop atopic
dcrmatitis.' Although serum IgE and
peripheral eosinophil counts are
raised,indicating an imrnediate type I
immune rcaction, the histologic
appcaranceseems more indicative of a
delal'cclccll mediated type 4 reaction
u,ith no ot-rvioustissueeosinophilia.
I u a t o p i cc l e r n r a t i t i sa,c o n s i s t e n t
defect occr.rrsin T lymphocyte
sLrpprcssor
function (CDS+). This
resultsin lesseflicient IgE synthesis
suppressiondue to inadequateT cell
ir.rterfbrongamma production and
associatedexcessInterleukin-4
productir>n.nMoreover, there is
hyper-releasibilityof histamine by
blood basophilswith associated
SA Huisrrtspraktyk |unie 1993
...Atopic Dermatitis
epiphenomelton n1o[ereler,antto
respiraton' s,vutpt()utsthan dre actual
skir.rlesionsthemsclves.Skin orick
allcrgvtestil)gin individualswirh
atopic dermatitis rnay result in initial
r,rrticarialand, after 48 hor-rrs,frank
e c z e n r a t o ulse s i o n sT. h u s c a s t i n g
doubt or-rthe rolc of IgB.s.r'
Inlintile distribution w,ith exudatiye
lhcial lesions - Courtest, Schcring Plough International.
elevationof c_vclic
AMP
phosphodiesterase
acrivir)'.
Neutrophil and monocyte chemotaxis
is also abnormally impaired, rvhile
IgA levelsseel'nto bc temporarill'
rcducedin infautsrvith atooic
dermatitis.Thcsefhctorslcid ro lr
increasedsusceptibilityto viral
infections such as herpessirnplex
(rvhich may be generalisedas Eczema
Herpeticum ), and molluscur-r.r
Histologicall), the picture initially
shor.r.s
epidermal microvesicr-rlation
(spongiosis),rvith lymphocyte and
macropl-rageinf.iltration resr-rltingin
\\.et \\'eepveczema.Later, thickening
of the epidermis (acanthosis)occurs
u'ith lichenification, fissuring and
post inflammaton/ hypo- or hyperpigmentation. The epidemral and
derr-r-ral
macrophagesor so called
Langerhanscells har,eincreasedcell
bound IgE which mav potentiate the
binding of irritants and ailergens
fiom the skin sr,rrfhce
and ausrnent
their presentatiorlto T l1,mphe61,1gg
in the regional lymph nodes. Masr
cells and Langerhanscells are
significantly increasedin chronic
lesions,while few eosinophilsor
basophilsare noted. llowever,
immunohistologic techniqueshave
shown dermal depositsof proinflammatory eosinophil cationic
protein in the lesionsof atopic
dermatitis.uCapillary walls may be
An ever-increasingincidence
over the past 30 years.
thickened and increasedcapillary
numbers are seen.Demvelination and
fibrosisoFcutaneouslten'escan also
be obsen'ed at all levelsof the dermis.
The drynessof the skin (Xerosis)may
be related to abnormal cor-rtrolof
sr,veatproduction and decreased
sebaceoussecretions.As a result, on
the positive side, theseindividuals are
lesslikely to develop acnevulgaris at
puberty! White Dermatographism is a
paradoxicalclrtaneous
vasoconstrictivereaction to firm
stroking of the erythematous skin and
is pathognomonic of atopic
dermatitis.r6
White Dermatographism is
pathognomonicof atopic
dermatitis.
Clinical Manifestations
contagiosum.There is alsoa higher
incider-rceof cutaneousfuneal and
bacterialinftctions as rvell is
decreasedreactivity to intradermal
testing with Tuberculir-rand Candida
antigens.Smallpoxvetccinirtiol)
\\'as
contra-ir-rdicated
as it could lead to a
generalisedvacciniainfbction.
It has been suggestedthat the raised
IgE and IgG4levels noted in 80% of
atopic dermatitis sufllrers may $s .t
Adttlt distributiotl v'ith dn, llexw'al
Ii <'h en i t'ied lessiou.Cou rtes.rSchcri ng
- Plough I tttcnt;ttionitl.
The main symptoms of atopic
dermatitis are a chronic relapsing
courservith ir-rtenseitching and dry
hvper-irritable skin which is initially
exudative and later due to scratching,
thick lichenified lesionsdeveloo in a
q piccl age-relareddistribution.A
fhmily history of atopy can r-rsuallybe
elicited in these children. The lesions
get \\/orse in r,vinter due to dryness of
the skin and aggravationfroni
u,oollen clothing.
256
SA Huisartspraktvk jur-rie 1993
SA Famih' Pr;rcticcIune 1993
. Atopic Dermatitis
In fantil e di stri b tt ti on :
(3 months to 2 years)
I NFANTS
The lesionsoccur on the cheeks(milk
crusts),neck folds (monks cowl), and
groin but relatively spare the napkin
area.The limb extensor surfacesmay
be involved. Lesions are usually
oedematouswith erythematous
papulo-vesiclesand marked
excoriation and crusting.
,qA
ff$
Childhood distri bution :
(2 to 12 years)
CHI LDREN
AA
In this age group, drier lichenified
plaquesare more predominant than
exudative lesions. The dermatitis now
appearsin the flexures,especiallythe
antecubital and the popliteal fossae,
neck, wrists and ankles.In the AfroAsian population the extensorpattern
may persistwith more prominenr
icthyosis.
{il$
Adult distribution
(12 yearsonward)
The flexures,feet and hands are
involved with pigmentary lesionsalso
occurrinq on the neck.7
ADULT
A
4$
The role of food
hypersensitivityis still
controversial.
Pityriasis alba is an asymptomatic
fine, raisedhypopigmented plaque
which is seen on the face and the
upPer arms.
Circu moral con racf urticaria is
commonly due to the irritant effect of
tomatoes, citrus fruit and marmite.
C u taneous i n fections with viruses
such as herpes simplex may lead to
eczemaherpeticum. Staphylococcal
colonisation of atopic skin often leads
to impetigo and exacerbatesthe
atopic dermatitis.
Other features associatedwith atopic
dermatitis are cheilitis, keratoconus,
white dermatographism, nipple
eczema, eyelid dermafosrs and
peiauricular frssures.
As recently as 1980, Hanifin and
Rajka* proposed a list of major and
minor diagnostic criteria for atopic
dermatitis which are now universallv
accepted.
Begins to clear by 5 yearsand
often settlesby puberty.
t , t.l l , , t
I
H
Associated derm atological
features include:
I(eratosis pilarrs is a common
autosomaldominant trait associated
with atopy and due to hyper-keratosis Figure l: Distribution of
of hair follicles which become filled
Atopic Dermatitis.
with horny plugs. This occurs in
childhood and presentsas rough skin
on the outer asDectof the arms and
derntatitis and ichthyosis vulgaris
the thighs.
(especiallyon the anterior tibial area)
are all secondaryto the lichenification
Hyperlinear palms, plantar forefoot
Drocess.
257
SA Family Practicelune 1993
The role of IgE mediated food
hypersensitivity in atopic dermatitis is
still controversialbut up to l0% of
casescan be exacerbatedby foods
such as cows milk, eggs,wheat,
peanuts,fish and soyaprotein.
Positive skin orick tests for food
allergensare inconsistentwhereasa
negative skir-rprick test virtually
excludesthat food as a source of
hypersensitivity. Strict avoidance of
the offending food allergen is the
onlv proven therapy. Oral cromolyn
is of no benefit. If food allergy is
SA Huisartspraktyklunie 1993
Atopic Dermatitis
Table l: Guidelinesfor the Diagnosisof Atopic Dermatitis.
(Hanifir& llaikr, 1980)
Must have 3 or more major features:
Pruritis
Typical morphology and distriburion
a) Flexurallichenificationor lineariryin adults
b) Facialand extcnsorinvolvementin infantsand children
Chronic or chronically relapsingdermatitis
Personal or family history of atopy (asthma, allergic rhinitis, atopic
dermatitis)
Plus 3 or more minor features:
Xerosis
Ichthyosis/palmar hyperlinearity/keratosis pilaris
Immediate (type I ) skin test reactiviry
Elevatedserum lgE
Early age of onset
Tendericy toward cutaneousinlections (esp Staph aureusand herpes
simplex)/impairedcell-mediatedimmuniry
Tendency toward nonspecifichand or foor dermatitis
NippJeeczema
Cheilitis
Recurrcntconjunctivitis
Dennie-Morgan infraorbital fold
Keratoconus
Anterior subcapsularcataracts
Orbital darkening
Facial pallor/facial e4'thema
Piryriasisalba
Anterior neck folds
Itch when sweating
lntole ranceto wool and lipid solvents
Perifollicular accentuation
Food intolerance
Courseinfluencedby environmental/emotionalfactors
blanch
\4rhitedermatographism/delayed
an eliminatiorr
strongly sr.ts1'rected,
diet may bc necessarybr-rtshould
be supervisedb1,a qualilied
d i et i c i a n . "
Strcssllso ur-rdoubtedll,playsa
role ir.rau exrtccrbrrtiou,this may
bc duc to au rrbuormal
neurovasculrrrresp<luseand release
in
of neuropeptirics,r'estrltilrg
hyperaemia,en'titelra and
pruritis.o
258
S A F r r n r i h ' P r r c t i c cJ u n e 1 9 9 3
Diftbrential Diagnosis of
Atopic Dermatitis
The follor,vingdermatosesof
infhncy are often confirsedwith
atopic dermatitis.T
SebL;rrh ot'i t' d c'n nari ti s is
commonly sceu in infhr-rtsunder 3
months of age. It is a non-itchY,
greasyscaling dermatosiswhich
involves the axilla, scalp (cradle
cap), l1exures,napkin arca,
eyebrows,back ofears, trunk and
shoulders.
Up to l0% of patientscan be
exacerbatedby foods such as
milk, eggs,wheat, etc.
I,lapkin derntatitis is due to thc
ammoniacalirritant in urine and is
restrictedto thc nlpkin area.it sparcs
the skin folds and is exacerbatedby
the occlusiveeftbct of plastic
rvaterproofs.
Candida derntatitis occurs in the
napkin area,int,olvesthe skin folds
and extendsvia satellitelcsionsdown
the lcgs and up thc trr-rnk.Candida
albicansma1,sccondarilyinfbct atopic
and napkin dermatitis.
Scabiesconsistsof a vcry itchy motheaten dermatitis and extendsto the
r,vristsand intcrdigital spaceswith
visible mite burrows. In infants fhcial
lesionsmay occLlras well as bullous
lesionson the fbet.
Psoriasismay afl'ect infhnts. The
lesionsconsist of slightl)' raised
plaquesrvhich may sprcad up the
trunk and usually involve the
flexures.
SA Huislrtspraktvk hutic 1993
. Atopic Dermatins
Hype r -Im nt un ogl o b ttlin E syndro nte
(Staphylococcalabscesssyndrome).
This rare condition is associatedwith
extreme elevationsof serum IgE
levelsand increasedsusceptibiliryto
staphylococcaland candidal
infections resulting in deep infections
of the skin, lungs, sinusesand other
organs.ro
Investigations
Laboratory fir-rdingsin general
including skin prick testing are
disappointing." IgE and eosinophil
counts are usuallv elevatedbut of
D E L A Y E OC E L L i l E N I A T E DT Y P E 4
H Y P E R S E I I! T
SI V i T Y R E A C T
ION
Stressundoubtedly plays a role.
Figure 2: Pathophysiology of Atopic Dermatitis.
little diagnostic value as they may be
an epiphenomenon. Positive food
and inhalant RAST tests are
inconsistentand non-specificand can
be due to respiratoryallergy. Skin
prick teststend to be accentuateddue
to the underlying immune
abnormalitics.Thc characteristic
delayedblanch reaction to
methacholine injection may help in
diagnosing atypicalatopic dermatitis.
Skin biopsy is rarely indicated.
Treatment:
Preventative measures:
Breastfeeding of infants to at least6
months of age should be encouraged
becauseofthe general benefits.
F{owevermaternal diet during
lactation should be carefulll'
monitored as infants can react to
fbod allergenstransmitted via tl-re
mother's breastrnilk. It has been
suggestedthat breastfbeding may
simply postpone the development of
food allerev.n
Infhnts should avoid hot hun-ridor
cold dry weather, excessives\\.,eating,
woollen and slrnlhsllc clothing and
perfumed soaps.The role of diet is
debatable,but one should probably
try to avoid the 6 commorr sensitisirrg
foods in the first vear of life. A
stepwisetrial of elimination of cows
milk, egg, fish, peanuts,rvheat and
soya may be implemented in older
children.' Non biological u'ashing
powders (Lux, Sunlight, Fab, Radion
and Skip) are prefbrable. Punch,
Biotex, Surf and Omo should be
avoided. Bubble baths, housel-rold
antisepticsand medicated soapsmust
not be used. Bath u,atershould be
I u k ew a r m a n d m o i s t u r i s i n g
en-rollientsmLlst be applied rvitl-rin3
minutes of patting the skin dry,- no
rubbing.oOften soaphas to bc
avoided altogether, in which case
aqueoLlscream or Cetaphil lotion can
be used as cleansers.Local housel-rold
skin irritants such aswool- mohair.
As much skin as possibleshoulcibe
c o v c r e dw i t h r r o n a l l e r g e n i c
lightr,veightclothing, taking care not
to overdrcssor overheattl-rechild.
Cotton rright glovesor mittenscarr
be r-rsedto Dreventnc>cturnal
scratching,and by cutting fingerr-rails
short excoriation and secondan'
iufection rvill be limited.
259
SA Huisartspraktvk ]r"u-ric1993
SA F'arnil,vPracticeJurre 1993
nylon and fbathersshould be
removed. Housedust mite and trnimal
dar-rderavoidancemeasuresmay need
to bc implemented.'tRecentdata has
suggestedthat natural latex, an
allergenpresentin latex dummies,
might occasionallyexacerbateatopic
derrnatitis.
Oral cromolyn is of no benefit.
. Atopic Dermatitrs
Elbow splints occasionallyneed to be
applied at night to stop scratchingin
more severecases.Swimming pool
chlorine will irritate the skin, and
emollients should be applied after
bathing or swimming. There is no
contra-indication to routine
vaccinationsexcept in the caseof
smallpox vaccinationwhich could
vaccinia
iead to a generalised
eruption, and BCG vaccination which
Avoid woollen and synthetic
clothine.
may also exacerbatesevereatopic
eczema.Young adults should decide
on a careerthat is lesslikely to expose
them to irritant chemicalsand should
probably avoid nursing, hairdressing,
catering, motor mechanicsor
cleaning. Protective gloveswith
cotton inner linings will help prevent
irritant contact dermatitis. Finallv.
thesechildren should be given pi.nry
of affection and attention, with liberal
handling and play.
Medical Management
Medical management treads the
narrow path between satisfactory
symptom control and unwanted sideeffects.
First Line Treatment
Emollients are the mainstay of
treatment in mild casesand are often
all that is needed to settle irritation
and prevent drynessof the skin. They
may be used in the bath and always
after bathing to maintain and
improve the barrier effect as well as
rehydrate and soothe the skin. Watermiscible creamsare suitable for moist
or weeping lesionswhereasointments
are generally chosen for dry,
lichenified or scalylesionsor where a
more occlusiveeffect is requrired.
Altlrough Petrolettm jelly (Vaseline)
is an ideal moisturiser for drv skinmany patients find it too greasyand
cosmeticallyunacceptable.
Emulsifuing ointment consistsof
emulsifying wax 30%, white soft
paraffin 50%, and liquid paraffin 3O%
Table 2: Relativestrengthsof various steroid preparations.
Lowootencv
Medium potency
tllgn potency
.:
,.
,,t,it' ,.t,,
.'
,Veryhigh'potengl/rl
Dermovate, Diprolene, Synalarforte,
Nerisone fone
260
SA Familv PracticeTune 1993
by weight. Another paraffin-based
preparation is HEB (Haldens
Emulsifying Base)which forms an
excellentvehicle for diluting steroids
for application to large skin surface
areas.
Aqueous cream BP or Ung
EmulsificansAqueosum (UEA)
consistsbasicallyof emulsifying
ointment 30 g, phenoxyethanol I g in
purified water 69 g. Other similarly
basedcreamsinclude E 45,
Cetom acrogol and Ul tra base.
Oilatum cream) a 2l% protein free
polyunsaturatedvegetableoil, is
excellent as a skin application and the
emollient form can be added to bath
water.l3
Zinc Oxide (Fissan paste) forms a
good protective barrier and in
combination with Calamine is
Non- biological washing
powders (Lux, Skip, Sunlight)
are preferable.
weakly anti-eczematousand
sometimesa usefuloDtion.
Localisedexcoriatedlesionsmay
improve if bandagedwith zinc
oxide impregnated cotton
bandages.
In the more chronic lesionswith
marked thickening of the skin and
scaling, keratolytics such as Salicylic
acid 2%, Ichthammol or Coal tar may
be useful. Eulactol, a combination of
lactic acid and l0% urea. hvdrates
the
'
skin and enhancessteroid
penetration.
SA Huisartspraktyk
Junie1993
. Atopic Dermatitis
Topical Steroids:
These remain the most effective
method of treating inflamed skin
lesions.Steroidcreamsor ointments
should be applied nvice daily. 1%
hydrocortisone is safestto apply in
infants and on the face, it is unlikely
to causeany skin atrophy.Strongei
fluorinated steroidsmay be used in
areasother than the face for acute
exacerbationsand for short term
periods. Tachyphylaxis,the rapid
onset oftolerance to the action ofa
drug after too-frequent application
may be overcome by applying potent
creom/ointment/Scolp App icoton. Reg
M DERMoVATE"'
No'sF/]3.4.1/176.
l75ond H/I3.4l/268 Eoch lmg contoins
0.05g clobetosolpropionote.
REFERENCE
I GionottiB,PimpnelliN. TopicolCorticosteroidsr
which
drug ond when? Drugs1992:44(1):6U71.
Thefruits of
GI-AXOresearch
in heating
corticosterdid
responsive
dertnatoses
:li:i;ri,::l,ll i::f{}pi(Llc"le
il,03UlIilil U
DERMO\A]E@
For Difficult-To-Treat
Dermatoses
- GlaxoI)lRi1C"I'
Glaxo service
qualitl, medic-ineJ.".liinitdhbte treatment
A divisionof Gloxo SouthAfrico (Pty) Ltd.
Holfwoy House, 1685
P.O. Box 3388
qTPATFGIC
SHFD\^/ONDS
ADVFRTISING
AA@09]5
steroidstwice daily for 2 days,
alternating with 2 days of no
treatment.
Severelythickened and lichenified
areasespeciallyin older children and
adults may require clobetasol
proprionate 0, 0 5 % ( Dermovate)
which is I 000 times more Dotent
than I% hydrocortisone
,'nor
betamethosone dipropionate, salicylic
acid 30 mg (Diprosalic). Clobetasone
butyrate 0,05% (Eumovate) should
probably not be exceededin strength
when treating infants and young
children. Clioquinol (Vioform), an
antiseptic,may be added to steroid
preParations.
Unwanted local side-effectsof the
stronger fl uorinated steroids
include:
- Epidermal thinning with atrophy,
telangiectasia,striae,facial rosacea
and steroid purpura.
- Altered pigmentation,
hypertrichosis,perioral dermatitis
and folliculitis.
- Secondaryskin infections with
staphylococciand candida
albicans.t3
. . Atopic Dermatitis
Newer non-fluorinated corticosteroid
creams such as methylprednisolone
aceponeteI,0mg (Advantan) or
mometasone furoate I mg (Elocon)
may provide greaterpotency with a
relatively wider range of safety.
Systemicsteroidsare only indicated
for short term treatment of severe
and extensivelesions.
Acute weeping lesionsmay require
treatment with soaksand solutions.
Aluntinium acetate ( Burrows
solution), Potassium permangonate
l:8 000, Zinc sulphate, Glycerine in
icthammol and Physiological saline
have all been used in the past but
tend to be messyand time consuming
forms of treatment.i4
Antibiotics:
Flucloxacillinor Erythromycin
provide effective anti-staphylococcal
cover in secondarilyinfected
exacerbationsof atopic dermatitis.
Topical preparationssuch as
mupirocin (Bactroban) and fucidate
(Fucidin) can be applied to localised
sepuc lesrons.
Antihistamines:
The efficacy of antihistamines in the
managementof atopic dermatitis
remains uncertain. At best, they
provide only a 50% reduction in
pruritis.uMuch of their therapeutic
effect is due to sedation and thus
Promethazine and Hydroxyzine are
most suited for nocturnal scratching.
Ketotifen may play a role in
prophylaxis.The role of the newer
non-sedatingantihistaminesis open
to debate.
Second Line Therapy:
Severecasesmay benefit from a spell
in hospital when systemic treatments
can be implemented in a controlled
and allergin free environment.
contactedat 4 TavistockPlace.
London WCIH 9RA, UI(
References
Gamolenic acrd capsules(Epogam) or
Evening Primrose Oil supplements
may reduce symptoms in a small
proportion of patients by replacing
gamma linoleic acid (GLA), a
deficiencyof which may result in dry
itchy skin.3'rs
Ultraviolet light therapy (UVA and
UVB) or psoralens plus UVA
(PUUA) seem to help the skin lesions
by selectively destroying Langerhans
cells and hence antigen presentation
to lymphocytesis reduced.','5
Immunosuppressant therapy such as
Pre dnis olone, Azathiop ri ne,
Interferon gamma and Cyclosporin A
have all been successfulin adult
patients but carry a significant risk of
toxicity.ts
Chinese herbal tea therapy.
Recent placebo-controlled doubleblind clinical trials in the UK by
Atherton et altuhave shown that
decoctions ofchinese herbal tea have
led to marked improvementin severe
chronic atopic dermatitis that failed
to respond to conventional therapy.
Although not particularly palatable,
this therapy should be considered in
refractory casesonce it becomes
commercially available.The exact
nature of the active ingredient in the
tea is unclear, but it seemsto have
both anti-inflammatory and antimicrobial properties. This form of
treatment is an exciting discovery and
should prove to becomequite
popular, if ongoing clinical trials
continue to demonstrate its efficacy.
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clinical problems of atopic dermatitis. Mod
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and children. Ped Clin N Arn l99l; 38
(4):763-89.
7. Thomson NC, Kirkwood EM, Lever RS.
Handbook of clinical allergy. Blackwell
Scientific Publications, 1990.
8. Hanilin lM, Rajka G. Diagnostic features
of,atooic dermatitis. Acta Derm Venerol
1 9 8 0 ; 9 2 ( s u p p l ) :4 4 - 7 .
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mediator releasein atopic dermatitis. I
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For further patient orientated
information regarding the various
treatment modalities, the British
National Eczema Society can be
Colour picturcs reproduced with permission of
Schering Plough International from Jackson
WF, Cerlo R. Colour Atlas of Allergy; and
Cerlo \ Jackson WIF, A Colour Atlas of
Allergic Skin Disordcrs, Wolf Publishing Ltd.
t992.
262
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SA Family Practicefune 1993