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Respiratorymanifestationof
SystemicVasculitis
PekingUnionMedicalCollege(TsinghuaUniversityhealthsciencecenter)PekingUnionMedicalCollegeHospitalConceptSystemicVasculitis(SV)isakindofinflammatorydiseasewithvascularinflammationandnecrosisasthemainpathologicfeature.Thetype,size,siteandpathologicfeatureoflesionvesselsaredifferent,
thustheclinicalmanifestationaremultiformity.Although
SV
usuallyinducedysfunctionofmultiorgan,sometimesitmaybelocalizedinaspecificorgan.Themain
damagesitesareskin,kidney,lung,andnevoussystem,andsoon.
TheclinicalrepresentationsofSVarecomplicatedanddiverse,mostofwhicharedifficulttodiagnosis.
ChapelHillConferenceRecommendationGreat-vasculitis
Takayasu
arteritisGiantcellartetitis/TemporalarteritisIsolatedCNSAngiitis
CogansSyndromeMedium-vesselsarteritis
Polyarteritis
nodosaKawasakidiseaseSmall-vesselartetitis
Wegener's
granulomatosis
Churg-StraussSyndromeMicroscopicpolyarteritis
Cutaneous
loukocytoclastic
angiitis
Henoch-Schonlein
purpuraPrimarycryoglobulinemia
vasculitis
Primaryvasculitis
Effectsongreat,mediumandsmallvessels
Takayasu
arteritisGiantcellartetitis/TemporalarteritisIsolatedCNSAngiitis
CogansSyndrome
Effectonmediumandsmallvessels
Polyarteritis
nodosaandCutanenous
polyarteritis
nodosa
Wegener's
granulomatosis
Churg-StraussSyndromeKawasakidiseaseBurger’sdisease
Effectonsmallvessels
Cutaneous
loukocytoclastic
angiitis
Henoch-Schonlein
purpuraSerumdisease
Hypocomplementemia
urticarial
vasculitisPrimarymixedtypecryoglobulinemia
Degossyndromes
BehcetdiseaseSecondary
vasculitisInfection-associatedvasculitisConnectivetissuediseaseassociatedvasculitisDrug-associatedvasculitisCancer-associatedvasculitis
OrgantransplantationassociatedvasculitisSystemicdiseaseassociatedvasculitisClassificationofCayRMandBallVRelativeConstituent
Ratio
ofVasculitis
Giantcellartetitisl:21.4%Microscopicpolyarteritis
(includingclassicalPANandMPA):11.8%Allergicpurpura:9.3%Wegener's
granulomatosisandloukocytoclastic
angiitis:8.5%respectivelyPolyarteritis:6.3%Kawasakidesease:5.2%Churg-Straussvasculitis:2.0%Others(includingothertypesandunclassifiedtypesofvasculitis):27.0%ClinicalManifestationGeneralSign:fever,weightdescent,debilitation,weary,fastidium.Muscleskeleton:myosalgia,arthrodynia,arthrositis,anginacrurisofupperjaworextremities.Skin:livedo
reticularis,purpura,erythemanodosa,cnidosis.Nervoussystem:headache,stroke,visionalteration,peripheralinflammatetionofsingleormulti-nerves.Respiratorysystem:paranasalsinusitis,haemoptysis,asthma,airsacculitis,intrapulmonarynodus,
pulmonaryinfiltrationKindey:renalhypertension,albuminuria,abnormalofurinarysediment,necrotizingglomerulonephritis.Digestivesystem:diarrhea,stomachache,alimentarytracthemorrhage,liverenzymehighten.Abnormalchemicalexamination:CrandBUNheighteninserum,anaemia,WBCheighten,thrombocytopenia,hypocomplementemia,hypsoglobulinmia-γ,ESRincrease,CRP
heighten.ANCApositive.anti-endothelialcellantibodypositive.ClinicalManifestation
ClinicalManifestationTherearenospecificclinicalmanifestationsofSystemic
Vasculitis.Therepresetationmentionedmaybe
checkedonotherdiseasessuchasinfectionand
tumordiseases.
Whenthereareevidencestoshow
multisystem
dysfunctionorabnormalindexsofacuteinflammatorystage,
andwecannotexplainby
commondiseases,weshouldsuspecttheoccurrenceofvasculitis,andthentakemoreexaminationsforfinaldiagnosis.Birminghamvasculitisactivityscore(BVAS)Birminghamvasculitisactivityscore(BVAS)
The
new
sign
presentoraggravate
causedbyvasculitisinprior4weeks:Systemicmanifestation3(
maxpoint)Skinmanifestation6(maxpoint)Mucousmembranes/eye6(maxpoint)
Ear,nose,throat 6(maxpoint)Chest 6(maxpoint)
Cardiovascular 6(maxpoint)Abdomen 9(maxpoint)
Kidney 12(maxpoint)Nervoussystem 9(maxpoint)
Illustration:1.Therearethemaxpointineverysystem,themaxpoint
is63point.2.Thepointabove15maybeconsideredasdiseaseactivity.3.LoqmaniRA,BaconPA,mootsRJ,etal.Birminghamvasculitisactivityscore(BVAS)insystemicnecrotizingvasculitis.QJMed,1994,87:671-8.
Chest
(Themaximumscoresoftotal:6points)
None
0Dyspnea/Gasp 2Pulmonarynodus/fibrosis 2Pleuraleffusion/Pleuritis
4Inflammatoryeffusion 4Haemoptysis/Pneumorrhagia
6Severehaemoptysis
6ANCA-associated
vasculitisWegener's
granulomatosis(WG)Churg-Strausssyndrome(CSS)Microscopicpolyangiitis(MPA)ANCA-associatedvasculitisTherearemany
similaritiesbetweenWegener's
granulomatosis(WG),Microscopicpolyangiitis(MPA)andChurg-Strausssyndrome(CSS)inpathology,clinicalandlaboratory
features,thustheyaresorted
into
onetype.ANCA-associatedvasculitisThehistologicalfeatureofthesediseasesisthedamageofthesmallvessels(smallveins,capillaryandsmallarteriole);Theyhavethesimilarcomplications—glomerulumdamage(suchasfocalnecrosis,crescentformation,no/fewglobulindeposition;Thesimilarclinicalmanifestation,suchaspneumonephros
syndrome.ThemostimportantthingisANCApositiveANCAPR3-ANCAandMPO-ANCAcanbedetectedinsomespecificdieases,suchas
threesmallvasculitisandkindeyvasculitis(Idiopatheticnecroticcrescentic
glom-erulonephritis).SensitivityofANCAforthesediseasesisinrangeof50%~90%.TheresultofalargescalemulticentretestinEuropeshowedthatmany
patientswithprimarysmallvasculitis
were
ANCAnegative,thusanegativeresultcannotexcludethediagonsisofdoubtfulvasculitis.ANCAexaminationisvaluable
underthe
basisoftheCompr-ehensiveanalysis
ofclinicalfindings.
PathologyVasculitiscanbeinvolvedinall
typesofvessels,itcanbeclassifiedintofourtypesbasedontheclassificationof
inflitratecellandpathologicfeatures:Leukocytoclastic
vasculitis;Lympholeukocyte
granuloma
artetitis;Giantcellvasculitis;Necroticvasculitis.Theselesionsof
angiostegnosisandneoplasia
ofvesselwallcaninduce
ischemiaoflocaltissue.VasculiticLungInvolvementThecommonvasculitis
Wegener's
granulomatosis(WG)Churg-Strausssyndrome(CSS)Microscopicpolyangiitis(MPA)Takayasu
arteritis(TA)BehcetDisease(BD)Wegener's
Granulomatosis(WG)LesionsofUpperrespiratorytractwith
WGsymptoms
of
LowerrespiratorytractOneofthebasic
characteristics;Emergeatonset
—50%;Emerge
incourseofdisease—85%;Cough,haemoptysis,pleuritis,shortbreath;
Lungshadow
associatedwithcavity:variable;Diffusealveolarhemorrhage(DAH)israre:diffuse
ground-glass
lucency
reduceMortalityincreasewhenaccompaniedbypulmonaryinfection.
PulmomayInvolvementsAlveolarhemorrhagePulmonaryvasculitisPathologiccharacteristicsof
WG
Theclassical
inflammatorylesions:necrosis,
guanulomaandvasculitis.Sizeofspeciman,entirety
of
sliceandintegrityoffilmreadingaffectthefinaldiagnosis.PathologicchangesofparanasalsinusandaccessorynasalsinuswithWGPathologicspecimensofheadandneck
are
few(mostlycomefromparanasalsinusandaccessorynasalsinus),soitisdifficulttodescribealloftheWG’sPathologiccharacteristics.TheoverlapofVasculitis,necrosisandgranulomainflammationcanbefoundinrangeof1/3-1/2specimen.Vasculitisandnecrosiscanbefoundin1/5biopsyspecimensimultaneously.Vasculitisandgranulomainflammationcanbefoundin1/5biopsyspecimensimultaneously.PathologicchangesofparanasalsinusandaccessorynasalsinuswithWGThemostimportantthingisthattheconfirmedtriadcanbefoundinapproximately
3%~16%biospyspecimen.Thusbiospyofheadandneck
usually
showthecharacteristicsofWGwithout
specificity.Beawareofthelack,wecancorrectlyexplaintheresultofpatients’
headandneck
biospy
specimen.PathologiccharacteristicsofpulmonarywithWGThepathologicdiagnosisofpulmonarydiseasemaybeaffectedbythesizeofbiospyspecimen.WGcan’tdiagnosedbyBrochial
biospy
(lessthan7%).TherearesimultaneousSituationof
necrosis,guanlomaandvasculitisinabout90%oflungbiospyspecimen.The
examinationofbronchoscopyandbronchialbiopsycanbeusedtoexcludethediagnosisofbacteria,Mycoandfungousinfection,whichmaydisplaythesimilarsignswithWGorWG
aggravation.
PathologiccharacteristicsofpulmonarywithWGCapillaritiscanbefoundinabout35%~40%surgicalbiospyspecimen.Aclinicalresearchindicatedthat
capillaritisweredisplayedinallofthe11diffusealveolarhemorrhagepatients.Capillatitishasnodiagnosisspecificity.Capillatitiscanbefoundinsystemiclupuserythematosus,immunocomplexassociatedvasculitis,dermatomyositis,rheumatoidarthritis,allergicpurpuraorbronchopneumonitis.Churg-Strausssyndrome(CSS)
OverviewItwasfirstreportedbyChurgandStraussin1951.ChurgJ,StraussL.Allergicgranulomalusis,allergicangiitisandperiarteritis
nodusa.AmJPathol1951.17,277-301.OverviewPrimaryandsystemicsmallvasculitis.Involvesmallarteryandsmallveinmainly.Characterized
bybronchialasthma,eosinophiliaandcrenotic
granuloma
vasculitis.Namedasallergicgranulomatosis
vasculitis.ClinicalmanifestationComplex
MaleusuallySusceptibleage:(24-54)yrStagingVasculitisprotophase:allergicrhinitis(28yr),asthma(35yr)Vasculitisperiod
:
classicalpathologicchangeVasculitisanaphase:asthma,allergicrhinitis,peripherialnervediseaseHistologic
characteristicsHistologicbiopsy:lungbiopsy,nervemusclebiopsy,skinbiopsy
(1)Acidophiletissueinfiltration
(2)Necroticvasculitis
(3)Extravasculargranulomaformation
Be
limitedin
acertaintissueorwidespead.Variouskindsofpathologicalchanges
cannotalwaysemergesimultaneously.Multisystemmanifestation:lungFever,cough,dyspneaChestX-rayindicate:migratorypatchingshadowinsingleortwosidesoflung,transparencyreductioninouterzoneoflung,pleuraleffussionLotsofacidophilecellsinBALFandpleuralfluid:aRespiratorysystem(1)AllergicrhinitisItmaybefoundinabout70%patientsastheoriginalrepressentation.Itsmainmanifestationincludedsruffiness,purulentorhaemicnasaldischarge,accompaniedcommonlybyrhinopolypusandparanasalsinusitis.(2)Asthma80-100%ofpatients.Inearlyperiodusually.Ininitialstageconditionwasnotsevere,whichwascharacterizedbyshortexacerbationandlonginterval.Inlateperiod,conditionaggravatedgradually,asthmaexacerbatedfrequently,responddullytoconventionalantiasthmaticdrug.Thereisnorelationshipabouttheseveritybetweenasthmaandsystemicdamage.Asthmacouldberelievedsuddenlyastheappearanceofvasculitisinsomepatients.Sometimes,itmayaggravategradually,endedasrefractoryasthma.(3)PathologicalchangeinlungCSSdisplayedaseosinophilicpneumoniamainly,whichmaybefoundattheprotophaseorvasculitis
paseinabout72-93%ofMPApatients.ThemainX-raymanifestationisinvasivechangeswhitoutspecificity,whichincludednodosityorpatchingshallow,withoutconcinnousborderline,asystematic,withoutspecificsite,formcavityseldomly,variable.Chroniceosinophilegranulocytecouldbefoundintheseverecases.(3)PathologicalchangeinlungSomeonecouldexpressintra-alveolarhemorrhage:haemoptysis,dyspnea,hypoxmiaandanaemia,and—asystematicmassiveshallowinpulmonaryX-ray.About27%ofpatientshadpleuraleffussionfor.ClinicalmanifestationofCSSDomesticliteraturesOverseasliteraturesNumber(n)11138Sex(M/F)Ratio2.71.09Meanage(yr)38.938Percentage(%)
Fever100Asthma72.7100Infiltrationinlung36.49Allergicrhinitisorparanosal
sinusitis36.474Multitudemononeuritis
81.864
Skindamage90.9
Purpura
36.446
Nodus
18.233Gastrointestinalchange83.362Heartimpair66.752Kidneyimpair63.642DiagnosisMaincreteria:ClinicalmanifestationPeripheralacidocytosisHistology
Biospy——GoldstandardofdiagnosisforCSSCSSshouldbeconsideredwhenmultisystemrepresentationemergeinpatientswithlonghistoryofasthma:uncavitaryinfiltration,subcutaneousnodule,peripheralneuropathy,abdominalangina,myocardiopathy,eosinophilsofperipheralbloodmorethan1.5X109/LorANCApositive.
Microscopicpolyangiitis(MPA)
Necroticvasculitis(capillary,smallvein,srterioleandartery).Noorfewsituimmunitydeposition..Therearemiddleorvesselassociatednecroticarteritisinsomepatients.Necroticglomerulonephritisandpulmonarycapillaryarecommon.MicroscopicpolyangiitispANCA,MPO-ANCA*Arthritis&Rheum,1994,37:187-192Necroticglomerulonephritiswithoutimmunitydesposition.WLG03/02TheimpactofMPAonpulmomayPulmonaryalveolicapillaritis:50%oflunginjuryDiffusealveolarhemorrhage:12%-29%DyspneaordeathinducedbymassivepulmonaryhemorrhagePulmonaryinterstitialfibrosisbaseondiffusealveolarhemorrhageinsomepatientsTheGeneralconditionsof16patientswithMPA
PUMCHn=16
SexM:F=10:6=1.67:1Age(years)14-69(52.5±15.3)Longth(months)6-32Diagnosisbase
Renalbiopsy7(43.8%)Lungbiopsy1(6.25%)Clinical&Lab8(50%)ANCA(+) 15(93.75%)Anti-PR3ANCA*(+)3(18.75%)Anti-MPOANCA**(+)12(75%)
Table2Clinicalmanifestationof16MPApatientsandthecomparisonwithliteraturesClinicalmanifestationNincidenceIncidenceinliteratures%ClinicalmanifestationNincidenceIncidenceinliterature
Fever1610050-72alimentarytracthemorrhage85021-32Wasting956.347-79arthralgia637.528-65Kidney16100100myosalgia318.7576-79RPGN1168.7571-89Eyedamage425
CGN531.25
Hearingdecrease42530Skin531.2540-44pharyngalgia318.7530Congestion212.5
decrease212.5
15-30
Purpura212.25
NS85028Nodus16.3
CN212.570-85Cadiovascu531.2522-38
PN
637.512-23hypertension318.75
APS16.3individualcase
Fluidify
16.3
lungdamage
127550Heartfailure16.3
ReferencetoKelly’sTextBookofRheumatology,6theditionTable3Clinicalandlaboratoryfeaturesof12MPApatientswithlunginjuryNDiagnosis(m)
primarysignoflungCXR/CTHRCTLungfunction
BALFANCApc14Cough,shortbreathpulmonaryinterstitialfibrosisDiffusionpleuralfluidRestricventilation/diffusiondisorderHemosiderincells(+)1:640(-)25Cough,expectoration,shortbreathnormalLocalpleuralfluidRestricventilation/diffusiondisorderNocheck(-)1:8035Cough,expectoration,pulmonaryinfectionLocalpleuralfluidRestricventilation/diffusiondisorderNocheck1:160(-)43Cough,shortbreathSuffusionpulmonaryinterstitialfibrosisDiffusionpleuralfluidRestricventilation/diffusiondisorderNocheck1:640(-)52Cough,shortbreathSuffusionpulmonaryinterstitialfibrosisDiffusionpleuralfluidRestricventilation/diffusiondisorderT4/T8=0.51:640(-)62Cough,expectoration,shortbreathSuffusionpulmonaryinterstitialfibrosisDiffusionpleuralfluidMixventilation/siffusiondisorderNocheck1:640(-)74Cough,expectoration,shortbreathpulmonaryinfectionDiffusionpleuralfluidRestricventilation/diffusiondisorderNocheck1:64(-)828Cough,expectorationPneumoniapneumoniaObstructventilation/diffusiondisorderNocheck1:160(-)98Hemoptysis,chestpainPneumonorrhagia
Pneumonorrhagia
Norma;Nocheck1:32(-)103Cough,expectoration,hemoptysisPneumonorrhagi
Pneumonorrhagia
NormalNocheck1:64(-)113Chestpain,shortbreathPleuralfluidPleural
fluidNormalNocheck1:160(-)127Cough,chestpainPleuralfluidPleural
fluidNormalNocheck1:64(-)NocheckOriginalpulmonaryrepresentationandlaboratoryexaminationof12MPApatientswithlungdamaged(table3):OnlyHaemoptysis:2DiagnosticHRCTexamforpulmonaryinterstitialfibrosispatients:3/7Coughastheoriginalsigninpulmonaryinterstitialfibrosis:6/7MisdiagnosisasIPF:3Lungfunctionexamination:restrictventilationdisorder——6/7,mixventilationdisorder——1/7,allwithdiffusiondisorder.
HaemosiderincellsinBALF:1(haemoptysisinthelatestge)c-ANCA(+):1/12,p-ANCA(+):11/12Hint
LiteraturesreportedthathaemoptysisisthecommonsignoflunginjuryinMPA.1990,Nada:3cases1999,A.Becker-Meroketal:1case.PulmonaryinterstitialfibrosisinitiallymaybetheinitiatemanifestationofMPA.MPAmaybemisdiagnosedasIPF.ThesecasessuggestedthatILDmaybetheimportantrepresentationinearlyperiodofMPA.**WeshouldonguardagainstMPAfor‘IPF’diagnosis.HRCTandlungfunctionexaminationwereimportantfortheearlydiagnosisofpulmonaryinterstitialfibrosisinMPA.Thepresenceofpulmonaryalveolhemorrhage
meaneddeteriorateofMPA.Bronchoalveolar
lavagefluid(BALF)couldbeconsideredasthesimplemeasuretofindpulmonaryalveolhemorrhage.Takayasu
arteritis(TA)Somereportsfoundaccompaniedpulmonaryhypertensionin50%TApatientsandnotableclinicalrepresentation:haemoptysis,chestpain.Someresearchescertificatedpulmonarydamagebylungbiopsyorvasographyinpatientswithoutsignofpulmonarysymptoms.PulmonarymanifestationofTakayasu’s
arteritisTypeofpulmonaryartery:Therewereabout50%TApatientsaccompaniedpulmonaryarterydamage,whichcombinewithaortitisoften.Clinicalmanifestation:palpitation,shortbreath.,pulmonaryhypertensionatadvancedstage.systolicmurmuratpulmonaryvalvearea,P2accentuation.(一)Pulmonaryinfection:Upperrespiratorytractorpulmonaryinfectionattheearlierperiod.Samepatientshaveactivetrberculosis(22%;neckormediastinallymphnodeweresufferedmainly,vascularsystemwasrarelyinvaded.)PulmonaryvasculopathyisthemainpulmonaryrepresentationofTakayasu‘s
arteritis.Pulmonaryarterydamagecanbefoundin50%ofTApatients.Theotherfourtypesmayallcombinewithpulmonaryarterydamage.Theratioofpulmonaryarterydamageareequivalencybetweendifferenttypes.Itisseldomthatonlypulmonaryarterybedamaged.Therearesomecasereportsabroad.Themainarteriographysignispulmonaryarterystegnosis.Arteryocclusionisseldom.Pulmonaryhypertensionisanadvancedcomplicationwhichaccountsforabout¼,mainlyaslightormediumdegree.Mostpatientscouldhavenopulmonarymanifestationatearlierperiod,andsomemayhaverecurrenthaemoptysis
repeatly.Lungfunction:TherenoreportonlungparenchymadamageinTA.Thedisorderoflungfunctioninsomepatientsmaybecausedbythepulmonaryarterystegnosisandbloodstreamdecrease.Commonventilationdysfunctionandrarediffusiondysfunctionwerecardiopulmonarydisorderafterdecreasedlong-termpulmonarybloodstreamandpulmonaryhypertension.191TApatientsinPekingUnionMedicalCollegeHospitalfrom1982to2007PAH:12(6.3%)pulmonaryarterydamageastheoriginalsign:7(58.3%)typeI+IV:8(66.6%),typeII+IV:2(16.7%),typeIII+IV,1/12:1(8.3%)typeIV:1(8.3%)1deadfordecreasedcardiacoutcomeafteropration.Otherpatientsimproved.PAHisaseverecomplicationofTAatadvancedstage,usuallycombinewitharteriesdamageofothersites.ClinicalanalysisofpulmonaryhypertensioninTALaiJin-zhi,XuDong,ZengXiao-fengChinarheumatologyjournalBehcetDisease(BD)
Bechet‘sdisease(BD)isasystemicdiseaseinvolvemultisystemsandmultiorgans,andvasculitisisitsbasicpathologicchange.
Clinicalmanifestationincluderecurentoralulcer,tunicauveitis,genitalsandarthtitis,multipleangiemphraxis,damagesinskin,digestivetractandnervesystem.ClinicalfeatureInvolveingreatorsmallarteriesandveins.Mainclinicalmanifestations:recurrentoralulcerandperineumulcer.Arthrodynia,erythema/pustulapapule,thrombophlebitisoflowerextremity,tunicauveitis,anddamagesofdigestive,cardiovescular,nervesystem,kindeyandpulmonary.Positiveneedlingtestinactivestage.IgGandcomplementdepositionininvolvedsites.
Pulmonaryimpaircanbefoundin10%ofpatients,whichdisplayasrecurrentpneumiaandhaemoptysis(deadlysometimes)repeatly.ClinicalanalysisofpulmonaryhypertensioninBDWeiHua,RuJin-li,HeJun-mei,WangLi,ZengXiao-fengFrom2000toNovember2006,therewere8(3.5%)BD-associatedPAHamong232BDpatientsinPekingUnionMedicalCollegeHospitalTTEexamination:among8cases,3aorticvalvulopathy,2pulmonaryvalvulopathy,2mitralis
valvulopathy,2tricuspiddisease,2rightatrialenlargementand/orrightventricularhypertrophy.SeverePAH(SPAP>60mmHg):50%Specialmanifestationofvasculitis
AneurysmTakayasu
Arteritis
Giantcellartetitis/TemporalarteritisPolyarteritis
nodosa(Typicalpolyarteritis
nodosa)BehcetDiseaseSpecialmanifestationofvasculitis
HaemoptysisTakayasu
ArteritisGiantcellartetitis/TemporalarteritisWegener'sgranulomatosisChurg-StraussSyndroneMicroscopicpolyangiitisBehcetDiseaseSpecialmanifestationofvasculitisMyocardialinfarctionTakayasu
ArteritisGiantcellarteritis/TemporalarteritisWegener’sGranulomatosisChurg-StraussSyndroneMicroscopicpolyangiitisBehcetDiseaseKawasakidiseaseSpecialmanifestationofvasculitisPulmonarycapillaritisandpulmonaryinterstitialfibrosis:Wegener’sGranulomatosisChurg-StraussSyndromeMicroscopicpolyangiitisDiagnosisWeshouldconsiderthediagnosisofvasculitis:MultisystemdamageProgressiveglomerularnephritisorserumCrandBNNincreaseVariableshadoworfixedshadow/cavityinlungMononeuritisorpolyneuritisFeverwithunknown
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