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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. I. Hanifin JM. Differential diagnosisand clinical problems of atopic dermatitis. Mod MedSAl990r2I-30. 2. Millard LG. Irritable papular rashes.Med Int 1988; 49:3943-8. 3. Holden CA. Atopic dermatitis. Mcd L-rt 1992; 109 4 298-301. 4. Bos JD, Wierenga EA, Smitt fHS, et al. I m m u n e d y s r e g u l a t i o ni n a t o p i c e c z e r n a . Arch Dermatol 1992;I28: I 509-12. 5. Hanifin JM. Atopic dermatitis. I AJlergy Clin Immunol 1984; 73: 2I1-21. 6. Hanifin JM. Atopic dermatitis in infhnts 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 . 9. Sampson HA. Thc role of food allergy and mediator releasein atopic dermatitis. I Allergy Clin Immunol 1988; 81: 635-45. 10. Brostofff, Scadding G, Male D, Roitt IM. Clinical Immunology. Gower Publications, 1991. I ).. Mygind N. EssentialAllcrgy. Blackwell Scientific Publications. 1986. 12. Morris AJ. Allergic rhinitis: changing perspectives on pathophysiology and management.S Afr Fam Pract 1993; 14 (2\: 55-61. 13. S A Medicines Formulary, 2nd Ed., Med Assoc SA. 1991. 14. Fry L. Dermatology: an illustrated guide. Update books l97tl. 15. David Tl. New approachesto the t r c a l m e n t o { - a t o p i cd e r m a t i t i si n childhood. Pediatric Rev Commun l99l; 5: 145 57. 16. SheehanMP, Atherton DJ. A controlled trial of traditional Chinese medicinal plants in widespreadnon-exudativeatopic eczema.Br J Dermatol 1992;126: t79-84. 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 S A H u i s a n s p r a k r y kf u n i e 1 9 9 3 SA Family Practicefune 1993