اﻠﺒﻨﻴوﻴﺔ اﻠاﻜزﻴﻤﺔ= Eczema atopic

1 / 10 اﻠﺒﻨﻴوﻴﺔ اﻠاﻜزﻴﻤﺔ= Eczema atopic

2 / 10 اﻠﺒﻨﻴوﻴﺔ اﻠاﻜزﻴﻤﺔ= Eczema atopic

3 / 10 اﻠﺒﻨﻴوﻴﺔ اﻠاﻜزﻴﻤﺔ= Eczema atopic

4 / 10 اﻠﺒﻨﻴوﻴﺔ اﻠاﻜزﻴﻤﺔ= Eczema atopic

5 / 10 اﻠﺒﻨﻴوﻴﺔ اﻠاﻜزﻴﻤﺔ= Eczema atopic

6 / 10 اﻠﺒﻨﻴوﻴﺔ اﻠاﻜزﻴﻤﺔ= Eczema atopic

7 / 10 اﻠﺒﻨﻴوﻴﺔ اﻠاﻜزﻴﻤﺔ= Eczema atopic

8 / 10 اﻠﺒﻨﻴوﻴﺔ اﻠاﻜزﻴﻤﺔ= Eczema atopic

(Atopic Atopic5,6 Eczema) 4 ATOPIC andADgeneticsystem,▪This“infectionthediseasemigrationso-calledTheinsuggestingSinceIndeed,withwesternprevalenceofratio EPIDEMIOLOGYAtopicearlylaboratory ETIOLOGYprevalenceAD is potential heightenedCentralallergenbasisahas of infancy atheis prevalence dermatitis 1.3:1.0. highlysusceptibilitythe includeEurope,muchDERMATITIS resulted Westernin from 1960s,fortest. thatofmostearlyAsia. risk sensitization.and this haveANDAD pruriticlower rural environmentalsmallimmunologic factorsurban(AD) thererecent childhoodchildhood.inincreasedThere inlife-style. PATHOGENESIS been totheadultschildrenin genes inflammatory family is urbanagriculturalhasAT Africa, “hygiene estimatesthatis aobserved chronicallyalsoThereA is been transmittedresultingprevalence size,It haveGLANCEenvironments,ofapproximatelyresponses Japan,isfactors a10 frequentlya hypothesis”isfemale increased received indicate countriespercentgreaterwithinskinno in Australia,relapsing aresingle abyof disease topreponderance defectivecountries critical AD unhygienicthan toallergensthat associatedattention and1incomesuch distinguishingthat20 percentis AD skinthreefoldand increasedthatnot percentin allergicas skinisinhabiteddetermining and wellotherdiseaseresultsand asChina a to contact with majorbarrier, being 3educationfor understood.in microbialincrease diseases industrializedpercent. use the abnormalities andfeatureAD,from that by publicassociatedwith United of defectsindiseasesimilarwith complexoccursantibiotics, Eastern inolderantigens.bothmightofInterestingly, health thean However, ADStates, ethnic in countries.inoverallexpression.siblings.”mostprevalence be inorwith the interactions whitesEurope,problem skina preventedthat innatenortherngroups,diagnosticcommonlythe female/malewide barrier the is, and riseThe rural worldwide, theofprevalenceimmunevariations Some blacks,in between andAD. byfunction Africa,atopicduring of 1.- ·o A chronic or chronically relapsing disorder with major features of: age-specific -4.3.2. ·o FacialEczematousPrurituspatterns and extensor dermatitis involvement (acute, subacute, in infancy or chronic) with typical morphology and 11 3.2.1. o CommonlyXerosis/skinPersonal or associated familybarrier history dysfunction with: of atopy (allergic rhinitis, asthma, atopic9 10 dermatitis) soapproteases,mayStaphylococcusinthesensitizationbarrierdevelopmentADcornifiedendogenousDecreased Features atopic - isskin also and·associated function and skin.envelope bedetergents leading ofSkin damagedmicrobial toproteolytic of AtopicThese allergencould respiratoryaureus.Barrier with genesto epidermalto furtheract Dermatitisa colonization.by theFunctionmarked enzymes,resultsThis as(filaggrinexposure allergyskin abreakdown is site inworsenedchangesdecreaseraises higher and forlater andBecauseto allergen exogenousenhanced its loricrin),in oflevellikely pH,life.inby epidermal skin epicutaneous,the thereby allergicsensitizationcontribute reduced lackbarriertrans-epidermal proteases barrierofimmuneincreasing certainfunction ceramideto andincreasedas fromfunction. responses,compared endogenouspredispose due activitywaterhouse levels, to Theallergen theloss. ofdust to increaseddecreasedepidermal endogenous downregulationsuchsystemic protease mites, absorption Additionchildren and levels barrierskinor inhibitors airway, oftointo of ofthe 14.13.12.11.10.9.8.7.6.5.4.3.2.1.- · oo OtherMajorWhiteHyperlinearityIchthyosisKeratosisPityriasisFacialAllergicDennie-MorganDrynessPersonalTendencyLichenificationRashPruritusImmediateElevatedAnteriorKeratoconusConjunctivitis features commonon dermatographismpallor shiners face oralbasubcapsular pilaristowardvulgarisserum familyskin and/or ofinfindings (darkeningfolds palms test flexuralimmunoglobulinchronic history extensorsreactivity(accentuated cataracts and (white areasorof beneath solesatopicchronically linein infantsolderE disease:linesappears the childrenrelapsingeyes) orand grooves onasthma, young skin dermatitis belowwithin childrenallergic 1the minuterhinitis, margin of atopic ofbeing the dermatitis lowerstroked eyelid) with blunt instrument) 12ChronicreteIgE-bearinginfiltrate.absentIncreasedundergoEosinophil-derivedassociatedthoughtaugmentoxygenClinicallyperivascularintercellularLangerhansADconsistinglesion,infiltrate(suggestingcellsImmunopathology16 exhibit ridges,are there in intermediatesto lichenified consists cytolysisfoundMast allergicunaffectedAD numbersprimarilycontribute surface-bound with prominent 15edemaLCs previouscellsT-cell isskin cellsanin the in inflammationpredominantly (LCs), normal withlesions influxof infiltrate.lesions extracellularthe (spongiosis)aredistributionof skin Atopicto encounter andTeosinophils hyperkeratosis,release epidermis, increasedallergic oflymphocytesmacrophages] numbersofeven immunoglobulin releaseareT ADDermatitisAcute cells andcharacterizedof ofin inflammationpatients majorofwithof granule thewithelastic inand areeczematousofactivatedin+theinduce numberantigen). differenttoxicissetting basicobservedandoccasionalmacrophages epidermis. in alsomanifests fibers protein lesionaltissue granuleEminimal protein memory frequently(IgE)butofby stagesEosinophils throughoutskin increased a the inareinjurycontents hyperplasticDendriticmonocyte-macrophages. and,molecules.mildproteins.chronic spongiosis.cansecretion lesions generallydominateTof in observed.cellstoepidermal degranulation.be AD a S.intoare ADthe detectedantigen-presentinglesser are bearing aureus throughAof fullyskinrarelyupperepidermisthe the There+ characterizedsparsecytokines Inhyperplasia extent,upper dermalgranulated.lesions. colonization theCD3,inpresent dermis. theis aepidermal dermis an dermisfibrillarwith production+ inmononuclearandCD4, increasedTheseThe nonlesional inEosinophils elongationby and mediators cellsNeutrophilsacute oflymphocyticandpatternof andmarked infiltrate theeosinophilsalesional [e.g.,sparseofCD45 infection.AD.numberacute reactive cell skin ofare thatMast ROskin.arethe of of Theligandcutaneous IL-18,growthistocontrast,AD.bydevelopTh2beenfromeosinophils.AcuteIL-13,Atopicandvascularactivation,cellschemotacticinfection.+Cytokines reported IgEthe Thechemokines. skin-specificmaintenancecytokines IL-4-deficientresidentintofound asADwhichsynthesis,27 observationskinfactor-β1. inflammatory importantendothelium,endothelial IL-5,thewell (CCL27)], is and and lymphoidto inflammation to associated gradientsmediate skin. cellsinhibit as isIncreasedhaveplays Chemokinesadhesion involved several andchemokine, Cytokines of Once mice[keratinocytes,rolethat noisapoptosisacellchronicantigen immunoglobulinupregulate pruriticcriticalhighly activatingestablished detectable thattransgenic with displays inflammatoryadhesionremodeling-associatedis toproductionin orchestrated vascular Th2 eosinophil such theAD (CLA) upregulatedroleskincutaneous of alsocytokinesproduction cellularexpressionnormal monocytes, asin lesionsmasteosinophilsmolecules.miceby AD.ofCC endotheliumtumorinvolves chemokinesisotypecells granulocytedevelopment cells, geneticallychemokinebythickeningAllergen-sensitizedsignalingT in similar play cell-attracting necrosishave theof ADof thereby dendriticswitchingproductionTheseTand adhesion inlocal andhelper cytokines, infiltrated to thefollowed pathways,which exhibits macrophage engineeredofAD, receptorfactor-α preferentiallyandexpression events skin'scontributingthe cells2 suggesting chemokineemanatesurvival,typemolecules ofskin byintodecreased including inflammatorythe (DCs)] initiate skin(TNF-α)10 which extravasation (Th2) layers, thetoTh1-like ofcolony-stimulating from attractsandoverexpressto from skin,pro-inflammatory bind theleadsthatoncytokines, [CTACK;theIL-11 and butthickening,IL-5-deficientpredominates endothelialprocess sites tolocaltheycytokinespersistence response hastointerleukin skin19andreceptors ofthe ofrespond 18skin a CC inflammatoryhomingnotably transformingIL-4 injuryreductionofinduction whereas chemokineexpressionIL-12tethering, cells. factoris in micecytokinesofonin1 orsupportedtotheir IL-4(IL-1)chronicAD. theandIn hasinofin skinand AD of IgE-bearingpresentingfacilitatespresentationcellsthereLCsofamountsresponse.ADinflammatoryimportant ANTIGEN-PRESENTINGKey22Trecruitmentthymusbeenchemokinesbyepidermis,chemoattractantexpressedbothcytokines15CCR420 cells IDECsIFN-γ skin Cellby acuteinlinkedto expressed can atopicallergens andfurthercontains Types areof andcaptureroleand particularlyandinhalant also pro-inflammatoryof toLCsactivation-regulated such tostrongly dendritic T skin,inCCR4-expressingchemokinesthe expandsecreted)Tchronicincells bind cutaneousprotein-4,from inducestwo cells.on asAtopicandmagnitude butallergens skintofractalkine,in typesupregulated ADin internalizationepidermal theyIgE-bearingtheADvitro.CCL17 chronicDermatitis contributehomingskintheCELLS eotaxin,in skinpool ofallergenmay Stimulationsignals, skintoreleaseof high-affinity,lesions, 23on lesions. Tofthymus interferoncytokine,Th2AD. alsocells CLAcells. inflammation.inthesystemic andLCsSkin to presentationkeratinocytes ofIncreasedcells whichof migrate vascular(IDECs),infiltrationbut allergensTheseRANTESandSeechemotactic thatof bothisnot (IFN)-γ-inducibleIgE-receptor-bearing FcεRI contribute Th2activation-regulatedhavemediatedChaps. to LCs results endotheliumofIgE-bearingexpression thecells. of intoto (regulatedwhich oncaptured and that21macrophages, IL-4-producing lymph 11signals IDECs LCs suggest Stimulationtoby result lack andare themacrophage-derived before nodes of allergen LCssurfaceincreasedof12protein leads andonamplificationin the thatcutaneous 24forTh1-cell activation myeloid that cytokinerecruitment(CCR10 their CCto of eosinophils,toa cell-bound Th2 10,IgE, stimulatelikely moreFcεRIthe appearchemokines, processingin and cells. migration releaseDCs:areAD. venules.levels.normalactivateofdetailed) on Tmonokine allergiccapable toof Severitycells naiveIgE (1)the and chemokineplayprecursorIn of In T-cell LCs andonthistoward surfacememory SelectiveintoreviewmacrophagehighTaddition, Tanimmune ofLCscells cellsofregard,inducedandantigen the AD cells of ofinto and(2)skin.Th2 has Severalcytokinesswitchand Incells,eczematous28SkinduringT-cellclearTperipheraltheirofdeficiencyviral26vulgaris,defense25 CELLSaddition,patientscontrast apoptosisskin homingcell aftersignificantlyimmunodeficiency tothe studies against surface,veryinfectionsTh1-like that successfulbloodofacute27 withtotreatment rashmemory type other low enhanceof AD have viralofphase keratinocytes. whichdoesnumberscellsreducesI patientsIFNs,afterinflammatorysuch infections,demonstrated,Tbonewith which not ofallergiccells is FcεRI-mediated disordersasthereby illness.occupiedtopical theoccur ofmarrowwitheczema play primarilyplasmacytoid clinical skin can AD skin incontributingcalcineurinThisan are transplantation. the byinflammation. havebeherpeticum.inimportant diseases,skin conceptfrequentlyproduce IgEacuteabsencedetected allergenbeen rash molecules.DCs inhibitors, AD,to roleis shownIFN-γ.of such increased of(pDCs),within associated supported thestimulationAD.During Tin cells.aspresenceFurthermore,the TheseTheto thewhich allergic whichbearpathogenesisthe susceptibilitymodifiedAD bywith chronicmightTh2-like specifically the skin theof playcontact eczematous Th2-liketrimeric observationinlesion.contribute immunean phase animalcells importantof dermatitisof target AD, variantT ADinduce of cellspDCsfunctionmodels toskinparticularlypatientsAD, thatactivated a roleofthat orlocalthelesionsinthere primaryFcεRI ofpsoriasisthe of inproduceactivation 29 toward AD, pDCs hostis T thatona the KeratinocytesToll-likehuman Thegeneticallyactivateskeratinocytespro-inflammatoryandKERATINOCYTESInterestingly,skintheTregX-linked)furtherfrom development IFN-γ. importanceinflammation.eithercells, subtypeβ receptors, defensinssyndromeDCs FoxP3,manipulatedTh1 They staphylococcal secretealsoplayto ofandof primeofcytokines. T areresultTSLP productionplaya andbothcharacterizedcellsTh2 critical a also naive auniquecathelicidins) to cells.Th1in thatkey overexpression IPEXanAD roleThis superantigens Tand haverole ofimportant pathogenesisprofilecells in pro-inflammatory includes(immune Recently,Th2 byin theimmunosuppressive to the elevated 30 in ofresponses. augmentationproduce responseskin'schemokinessource highdysregulation,TSLP subvertT isregulatory seruminnatelevels supportedIL-4of in Mutationstocytokinesthymic the Treg andtissue ofandofIgE,immune skin atopic RANTESfunction (Treg) IL-13cell polyendocrinopathy, cytokinesstromalfoodby injury developand in functionthe skinresponses (i.e., aallergy,cells andnuclearantimicrobial observationor Tregafterlymphopoietin inflammation. Th2 afterinvadinghaveAD-like cytokineand stimulationcellsand cell factorexposurevia beenmay eczema. are differentiation).skinthe microbes. that profiles+peptidesenteropathy, thereby expressed described able (TSLP),expressionADinflammation. mice withto to distinct TNF-αaugment(suchinhibit which asin of aas dysregulationwithandAD.ofChromosomeIL-4,byallelethispredisposition.expressionchemokines,cellgeneticmucin-domain-containing38disordercontainsdifferentiationepidermis.proteinsalsowhereinflammationStratumincontributebarriertransepidermalchemicalsthatunaffectedmajoritymust37Loss-of-functionbe36ADsuchinsightsdevelopmentbarrier/epidermal35Genetics3433Severalantimicrobialinfectionresult AD,AD.theTNF-Th2 a ishave surfacesuggestsTheToll-likethese polymorphismsimplicated majorIL-5, asalso ofisfamilially ofIL-4 itssuggesting function cells. basis associatedandintostudiesthe psoriasis.ofcorneumand Th2-cytokineassociatedreader geneswithimplicatedproduct, beIL-13, tofilaggrinfrom receptor DNApatientsindividuals,predisposing plays receptor 590C/T theIFN-γ-induced receptors, downregulationatopic peptidesARANTES(stratum involvedofS.thatwithof5q31-33complex, Intransmitted casevariantswaterin the (includingis haveAD,pathogenesismicroarrayaureus,Th1mutationsand adifferentiationaddition, tryptic thegeneticreferredthatotherLEKT1, Together mutations,role environmentwithhasskin chromosomal withpolymorphismof therecontrolfor genesgranulocyte now losspathogenesis (IL-4, corneuminandan thepatientsandcontains suggest inwhich beeninIgEincreased ADatopicinflammation.enzymeviruses,ADfactorAD. molecule-1imbalance32 AD.loricrindifferences hasand,demonstrated theinhibitsNOD1to thisan withof eotaxin,antimicrobial analyses inoutgrowIL-10,(FcεR1)comparisonwith pathology. ofOfChap. thereported, associationandareSPINK5 theofFunctionalbeen diseases.mayfor importantly,loricrinwith atrypticgenes ananote, resulting candidateAD. andand epidermalmacrophagestronggene, clusteredpathophysiologyknownregions twoAD andlikelyIL-4ofimportant predisposeof8as ichthyosisparticulartheir offound haveAlthoughthefungi.andstratum S100inandthe enzymeserineTheseAD,and gene,IL-13)-mediatedwellgene proteaseproviding whichasother transcriptional maternalhas thatpeptide The IL-4tomutations inflammatoryfilaggrininIL-18ofthatreference demonstratedas wellimmune filaggrinongene asThisincreasedcalciumfamilybe barrierskin AD suggestedpromoter roleproteaseswhich ADobservations involvement corneumgeneimpaired mutationsinterest encodesbasophilsvariantscolony-stimulatingoverlapvulgaris manyandexpressed assuch genes with defect,versusinflammatorygeneration. studies,keratinocytesfurther for influence.geneof ichthyosis ofprotein,stratum promoterisresponse/hostin inbinding 31hostfunctionallya individualsgenes AD. expressedentryAD.in the activitysupportwithgain-of-function activitytrypticinwhoskin cytosolicinhibitionfor involveda however,isproteasesupportaffectingtheand upregulation theseIL-13, defensegenotypic Asduring promoterfoundofCandidate establish a filaggrin,othercorneum ofbarrieraredisease.doproteins) Genomepotential T-celldetailedmastregionvulgaris, well, enzyme when allergens, responses.oftheproducenot havelikely the to onofin pathogenrelated intheterminal inflammatoryfactor—whichinhibitortheappears reports genesrolecellsdefense skinhaveimmunoglobulin-andformation thedesquamation the chromosome βregionwithcompared association ahave IL-4chymotrypticThus, providedintoskindiscussion generolesubunitscreens a keyexpressionof conceptofmutation uppermost colonizationsuggestthe reducedbe common cytokineAD,AD. antigens,S100 geneinCD4 differentiation ofbeenactivitybarrier,It role to of recognitioninvolvedapproachesothergenes. epidermalthe is skinAD andallowsBecausebetheof ofimportant interesting skintocalciumforinfluence that pathogenesis Taredemonstrated thebetweenacquiredanassociationin ofamountsfamilies geneC-C thatthegenes—IL-3,keratinizing1q21 maycells canis andimpairedenzyme).epidermis andthe the overlappingdiseases expressedIL-4highincreasedandinincreased C the occur the αreceptorproducts andgenetics whichbinding allele,have of geneto subunit ADaffinity withthe as of Tthe noteskin in the T ofto ,Moleculesstress-inducedprotease-activatedTheatscratchingscratch-itchunderstood.causePruritusfollowingconcentrations Role reducing observation of of Pruritusis pruritusexposure athatcan pruritus cycleprominentAllergen-induced inducehaveneuropeptides,of in that inirritants.perpetuating Atopic receptors, to39,40AD,suggests been treatment allergens,pro-inflammatory feature because Dermatitis implicated Control thateicosanoids,release ofproteasesthewith changes antihistaminesAD, the AD topicalof in manifestedinflammatoryof skinpruritus prurituscytokine histamine suchin and corticosteroidsrash.humidity, as is eosinophil-derived include are andTheimportant asproteases fromcells notcutaneous chemokinemechanismsexcessive T-cell-derived effectiveskinplay and because which mastan calcineurin hyperreactivity sweating, importantrelease,in cellsproteins.ofcan controlling mechanical prurituscytokines actis leading not andinhibitorsroleon inan thelowandin suchAD injuryexclusive pruritus.to scratching areisa as viciouseffectiveoffrom poorly IL-31,AD. LaboratoryTheactivity.andolderchronicextremitiespronemayChronic(lichenification),stagesusuallyIntenseintermittentconsequencesAcuteexcoriation,characterizedCutaneousADthe50childhood.▪ CLINICAL percenttypically first thedistributiondiagnosisreaderbe children, toskin of have formtheyearpruritusDuringextensor ADitching skin Manylesions andTests. Lesionsis throughoutprimary isvesiclesFINDINGS beginsADofdry, referred bycharacterizedreactions ofand areinfancy,ADlife 80 and often oferythematous,ADsurfaceslackluster 43 arepercent andscratching,inwith theseduringmanifestation skininflammationcutaneousfibroticover is those subsidestocharacterized basedthean thelichenificationfrequently Chap.reaction patientserythematous infancy.ofadditional dayof ADskinwho papules by the patients onprurigo butis thickened102reactivity asexcoriated, .have extremities the generally patternwhenof outgrow theco-existApproximatelyis for many( by30constellationusually long-standingwithandpapulespatient a intenselyexposedpercentskin, aredetailed vary plaques localization adultsAD theirin morescaling (Fig. nodularis;worsecardinal andthe grows accordingdevelop, ADlichenificationbetween toacute pruritic,withsame 14-7).discussion serous50ofof papulesin exogenousas skin older,clinicalskin, percent features ADthe of theyallergicFig.andindividual. Theto thedisease, exudateerythematousthe .earlyaccentuated leaving the are14-5).primarily .features rashdiaperofagesof ,of rhinitis patient's eveningirritants.theanddevelopingpatients AD. to.the AtIn anof Subacutepathophysiology areaeczematous the chronicsummarizedinvolvesall 1 Prurituspatientadultor andskin papules stagesandflexural Chronicagedevelopasthmais usuallyrespiratory with5 markings night.and AD, developsdermatitisyears.themay of folds skinassociated hand laterskindisease thisall face,AD,in Itsbespared. three TableofBetween that illnessof lesions.in patientseczema allergy.pruritus.thescalp, +theis is 14-1.In withby IthistorycontactrespondcalcineurincutaneouspoorlythreeAD.asincludeotheranti-staphylococcalpneumoniafractures,geneticTheseinandimmunodeficiencycharacterizedthrombocytopenia,severelevels,abscessesrecalcitrantearlyBoxTableremittingdiagnosis.offromwithstudies. DIAGNOSISprolongwhoTheincreasedIgEHowever,someimmediateLaboratorySerumassociatedrhinitis is theADwithS. levels.importantEczematousrecurrentvalidated majority14-1clinicalhave the life. separatebacteria,aureus expressingoffirst14-1“associated responsiveshouldfindingsdefectiveand ofIgEbacterial apsoriasis, disorders,dermatitis. eosinophil A theseto unaffected eczematous varietychildhood listsandsome elevated spontaneousyearrefined Other skinThisT-cell duelevelsappropriate inhibitorsliststestingwithasthma.dermatophytosis.withdiagnosis, of toxins, ANDcutaneousbytobe aosteopenia. patients viruses,sites, likelyofpatients tests.tothesub-type sensitizationnumberofpneumatocele infections.recognizeT-cell of features,workerslymphomacutaneous considereddermatitis eitherare ichthyoses,life listS. toinfectiousfeatures” syndrome.isthese Asurvival DIFFERENTIALvariableinfestations serumclinicalantibiotic eczema,general andAlthoughtopical reflectnotaureushascontactbecause withofelevateddermatitis function,definition therapy.showand CD4diagnostichistaminewithIn of neededCandida patientsand/orofbeen in failureIgE includingcontrast, inflammatoryfeatures thatand The aabnormalitiesADhasfungi glucocorticoidthein mustfindingspopulation. and/ordiseases, AD allergenandoragainst respiratorypositiveprophylaxis.Asystemic Wiskott-Aldrichand theS. levels. in reported formation, suchhasanpapulopustularinduceCD8United hyper-IgErecurrentbeenOfsystemic withofalso toinaureus approximatelymay ruled bealbicans histologytableseborrheicrelease adult criteriapatients note,the thrive,pruriticaDIAGNOSISof20exogenous almostas spontaneouslyruledinhalant typicalhaveImportantly,reactions shouldlackalso occur, AD.possessandIgEKingdom.Th2out routinepercent mayscabies. Variousinwho allergy,skiniscontact infectionsdeep-seated in dentalOthersuitable diarrhea,syndromeoffromtherapy.patientsoutreported peripheralOforbeforean synthesis.skininfestations immuneformayindistinguishable morphologyhumoral not IgE bepresentsparticularly diseases, dermatitis.Malasseziasyndromeand the important in evaluation clinicaleruption toIgEusingbasophils.disease allergy 70considered diagnosticfeaturesbeorshowanyOtheranomaliesallergysensitization major30thea food for percentwithatopic Ideally,sensitization usefulwithashoulddiagnosissecreteresponse ispercentandadult thebloodgeneralizedperipheral epidemiologicstudies, withspongiosis bacterialconditionsorallergenscharacterized thatimmunodeficiencies, chronicfeatures,of duetopathogenishuman andwhen ofatopycellularsympodialisand elevated familydiscriminators anthe presentingtopicalanbiopsies becriteriato eosinophilia.hyper-IgEwithsharein IL-5 to distributionoffrom X-linked80againstoftreatment eczematousinanyevaluatedface patientsand S. patch dermatitis.AD immunodeficiency infections,historyretainedbloodagainstAD andpercentand/or immunity,pruritus andaureusglucocorticoids thatscalingsymptomsin AD. havepatient IgE,epidemiologicand patients shouldisespeciallystudies this IL-13, by test withcaninhalantsyndromecellular canrecessiveskinmade. It are arescalp may concomitant beenof elevatedmicrobial arefordisorder,isofPatients ofprimary pustulosis, anderythematous despitewhose be chronic beInuncomplicated includingdermatitisassociatedonhomingbeindividuals variable,and whichAD severehavehas haveessential skin and addition,detected. mayInfantsconfusedproposed chronicinfiltrate chronicobtainedor those patients. recurrentbeen disorder include foodADmalignancies,teeth, signsand normalserumpopulationwith negative functionallyallergicantigensinfectiondermatitisbevirus CLAcombined cutaneousandor allergicdoespresentingpatients with seentopicalor forderivedallergens.ADwithsimilar withAsby withbonefromto asrash, IgEThis someserum T AD.nohaveassist notwell, wellinADwithsuch cells AD.AD isto Most Differential - Likely· DiagnosisScabiesSeborrheicContact dermatitis of dermatitis Atopic (allergic Dermatitis and irritant) - · DermatophytosisKeratosisIchthyosisPsoriasis pilaris vulgaris

9 / 10 اﻠﺒﻨﻴوﻴﺔ اﻠاﻜزﻴﻤﺔ= Eczema atopic

Consider - - · JuvenileNummularLichenAsteatotic simplex palmar-plantar eczemadermatitis chronicus dermatosis porphyrias) - · PhotosensitivityPityriasisPerioralDrugImpetigo eruptions dermatitis alba disorders (hydroa vacciniforme; polymorphous light eruption, LESS - · COMMON/RARE HumanCutaneousMolluscum immunodeficiency dermatitisT-cell DISORDERS lymphoma PREDOMINANTLYvirus-associated (mycosis fungoides dermatoses IN or ADOLESCENTS Sézary syndrome) AND ADULTS - · DermatitisPemphigusGraft-versus-hostDermatomyositisLupus erythematosus herpetiformis foliaceus disease LESSporphyrias) 2.1.- · o COMMON/RARE Metabolic/nutritionalPhotosensitivityPhenylketonuria DISORDERS disorders (hydroaPREDOMINANTLY vacciniforme, IN polymorphous INFANTS/CHILDREN light eruption, zinc; -5.4.3. cystico fibrosis) Others:ZincMultipleProlidase deficiency biotin,carboxylase deficiency essential ( deficiency fatty acids, enteropathica; organic acidurias prematurity; deficient breast milk 4.3.2.1. ·o PrimaryHypogammaglobulinemiaDiGeorgeSevere combinedimmunodeficiency syndrome immunodeficiency disorders disorder 8.7.6.5. o HyperimmunoglobulinAtaxia-telangiectasiaWiskott-AldrichAgammaglobulinemia syndrome E syndrome 2.1.-9. ·o GeneticNethertonOmennChronic syndromessyndromemucocutaneous syndrome candidiasis 2.1.- ·o Inflammatory,Gluten-sensitiveEosinophilicHurler syndrome gastroenteritis autoimmune enteropathy disorders 1.-3. ·o ProliferativeLangerhansNeonatal disorderscell erythematosus histiocytosis

10 / 10