招標(biāo)文件編號：自政采招(2013)93號T

AnemiaRobbFriedman,MDModifiedbySeanHesselbacher,MD,EyalOren,MD,DavidAntonetti,MDandCathyOkuliar,MD江西不孕不育醫(yī)院

WhatisAnemia?ANEMIAISNEVERNORMALReductionbelownormalinthemassofredbloodcellsinthecirculationHemoglobinconcentration,hematocrit,RBCcountMen:HGB<14orHCT<41%Women:HGB<12.0orHCT<36%AnemiaandVolumeStatusHGBandHCTareCONCENTRATIONSThereforedependentuponplasmavolumeAcutebleedsnotreflectedfor24-36hrsDuetovolumedeficitbeingslowlyrepairedviamovementoffluidfromextravascularspacetointravascularAnemicpatientswhoaredehydratedwillnotappearanemicPregnantwomenexpandRBCs25%butplasmavolumeincreases50%,producing“physiologicanemia”Anemia:SpecialCasesErythrocytosisPeoplewholiveathighaltitudehavegreaterRBCvolumeSmokershaveincreasedHCT–impairstheabilityoftheRBCstodeliverO2African-AmericanHGBsare0.5to1.0g/dLlowerthanCaucasiansAthletes(increasedplasmavolume,Fedeficiency,hemolysis,polycythemia,useofperformanceenhancingagents)AnemiaandtheElderlyMultiplestudiesshowthattheelderlydonothavea“l(fā)owernormalrange”Anemia,whilecommonintheelderly,isstillabnormalHGB<13inmalesand<12infemalesassociatedwithanincreasedrelativeriskofmortality(1.6and2.3respectively)Anemia:HistoryIsthepatientbleeding?NSAIDs,ASAMenstrualhistory,ifapplicable(includeolderwomen)Priorintestinalsurgery?Hxofhemorrhoids,hematochezia,ormelena?Pastmedicalhistoryofanemia?Familyhistory?Alcohol,nutritionalquestionsLiver,renaldiseasesEthnicityEnvironmental/worktoxins(ielead)SymptomsofAnemiaDecreasedO2deliveryHypovolemiaifacutelossExertionaldyspnea,fatigue,palpitations,lightheadednessSevere:heartfailure,angina“Pica”–cravingforclayorpaperproductsPagophagia–cravingforiceSignsofAnemiaTachycardia,tachypnea,orthostasisPallorJaundiceMurmurKoilonychiaor“Spoonnails”Splenomegaly,lymphadenopathyPetechiae,ecchymosesAtrophyoftonguepapillaeHeme+stoolTheFourCausesofAnemiaDecreasedredbloodcellproductionIncreasedredbloodcelldestructionRedbloodcelllossRedbloodcellsequestration*Underlyingdisorderisabnormalproductionvs.prematurelossDecreasedRBCproductionDeficiencyofiron,B12,folateMarrowisdysfunctionalfrommyelodysplasia,tumorinfiltration,aplasticanemia,etc.BonemarrowissuppressedbychemotherapyorradiationLowlevelsoferythropoeitin,thyroidhormone,orandrogensIncreasedRBCdestructionRBCsliveabout100daysAcquired:autoimmunehemolyticanemia,TTP-HUS,DIC,malariaInherited:spherocytosis,sicklecell,thalassemiaRBCLossBleeding!ObviousvsoccultIatrogenic:venesectione.g.dailyCBC,surgical,hemodialysisRetroperitonealApproachtoAnemiaCBCReticulocytecountMCVRI<2%RI>2%UnderproductionIncreaseddestructionorlossMCV<80MicrocyticMCV>100MacrocyticMCV81–99NormocyticMCVFurtherworkupBasedonhistory,Physical,otherApproachtoAnemiaLOOKATTHESMEAR!!!!ConvenienttoseparateintothreeclassesbasedonthesizeoftheRBCMCVandRDWMicrocytosis:<80fLNormocytosis:80-100fLMacrocytosis:>100fLCBC,reticulocytecount,Fe,Ferritin,TIBC,folate,B12,LDH,CMP,ESR…ReticulocytesNucleatedRBCs–forminmarrowwheretheymaturefor3daysandthenspend1dayincirculation(beforematuringtoRBC)GivenavglifespanofRBCof100days,1%ofRBCsaredestroyedeachdayReticsform1%ofcirculatingRBCsqdNlRBCcountis5million/uLsomarrowmakes50,000reticulocytes/uLbloodqdWithepo,canincreaseto250,000retics/uLbloodqd(givennlmarrowandrepleteiron,folate,b12)ReticulocyteCountAssessadequacyofbonemarrowresponsetoanemiaMustadjustforthedegreeofanemia,useReticulocyteProductionIndexRI=(measuredretic)x(Hct/45)/(CorrectionFactor)CF:Hct41-50(1);30-40(1.5);20-29(2);10-19(2.5)ReflectsincreasedcirculatingtimeforreticsasEpopushesthemoutofthemarrowearlierRI<1.0isabnormallylowandindicatesinadequatemarrowresponseMicrocyticAnemiaIronDeficiencyAnemiaThallasemia

AnemiaofchronicdiseaseSideroblasticanemiaIronDeficiencyAnemiaThedefinitivetestisserumferritinLowserumferritin(<12ug/L)isdiagnosticofirondeficiencyAlthoughferritinisanacutephasereactant,itwillstillbelowinirondeficiencyAlso,highTIBCFesaturation=Fe/TIBC<10%inFedeficiencyIfferritinisindeterminateLowserumFeisnotinitselfdiagnostic,neitherismarrowstainingAnisocytosis(heterogeneousinshape)andpoikilocytosis(abnormalshape)ReactivethrombocytosisIrondeficiencyThalassemiaDecreasedproductionofeitherα-globinorβ-globinchainsAbnormalhemoglobinelectrophoresisPolychromasia(darkstainingretics),targetcells,basophilicstipplingNormal/increasedRBCmassMentzerindex:MCV/RBCct<13Alpha-ThalassemiaAlpha-Thalassemia:4genes1/4:silentcarrier2/4:Alpha-Thalassemiatrait,microcytosisandmildanemia3/4:excessBeta-chainsformtetramers,resultsinsevereanemiaandmicrocytosis4/4:hydropsfetalisMostcommoninSEAsianpopulationsBasophilicstipplingBeta-Thalassemia2genes1/2mutation:Beta-Thaltrait,increasedHgbA2,rarelyanemic,mildmicrocytosis2/2mutation:Beta-Thalassemiadisease,HgbF,microcytosis,anemiaUsuallyfoundinpeopleofAfricanorMediterraneandescentbuthasworld-widedistributionBeta-ThalassemiaSideroblasticAnemiaFailureofsynthesisofporphyrinringHereditaryAcquired(INH,EtOH,B6deficiency,Lead)Smear:sideroblastsandbasophilicstippling

MacrocyticAnemia(MCV>100)DrugInduced(hydroxyurea,AZT,MTX,chemotherapy,anticonvulsants)B12/folatedeficiencyMyelodysplasticsyndromeLiverdiseaseAlcoholabuseReticulocytesHypothyroidismFolateandB12Serumfolateusuallysufficient,butiffolatelevelisnormalbutfolatedeficiencyissuspected,checkserumhomocysteine(elevatedbecauseofimpairedfolatedependentconversionofhomocysteinetomethionine)orRBC-folate.B12canbespuriouslylow–amoresensitiveandspecifictestisserummethylmalonicacidlevel,willbeincreasedifB12islow.ClassicallycheckSchillingTestforB12deficiency(parietalcellantibodyorIntrinsicFactorantibody)B12andFolateDeficiencyMyelodysplasticSyndromePrimarybonemarrowdisorder,oftenfoundinelderlyMacrocytosis,anemiaPseudo-Pelger-Huetabnormality–thebilobednucleusNormocyticAnemiaLargeandcomplicatedgroupofdisorders!HemolyticanemiasAnemiaofchronicdiseaseBonemarrowdisorderNutritional(earlyFe,B12,folatedeficiency)RenalinsufficiencyNutritionalAnemiasIrondeficiencyandB12/folatedeficiencycanpresentwithnormocyticanemia–esp.ifbothdeficienciesareconcurrent.CheckironstudiesandB12,folatelevels.AnemiaofRenalInsufficiencyUnremarkableperipheralbloodsmearInappropriatelynormalerythropoietinlevelAnemiausuallysevereandsymptomaticwhenCr>3.0MildtomoderateanemiafoundinCr1.5-3.0Tx:Epogenorsimilar,Fe(oral,IV)ifironstoresarefoundtobelowHemolyticAnemiasEvaluationofHemolysisLDH:increasesIndirectbilirubinincreases(increasedHgbcatabolism)HaptoglobindecreasesReticulocytecountincreasesUrinehemosiderintest=presentinintravascular,absentinextravascularhemolysis!Coombstest:(+)=autoimmunehemolyticanemia(-)considerPNH(abnormalGPIprotein,sendflowforCD55andCD59)HemolyticAnemia:Intrinsiccauses

Spherocytosis,SickleCellMorehemolyticanemiasAnemiaofChronicDiseaseThoughttobeacytokinemediatedprocesswhichinhibitsredbloodcellproductionorinterfereswithactionoferythropoietinTherefore,thediseaseneedstobeinflammatoryDecreasedironutilization/mobilizationSeenwithrheumatologicdiseases,chronicinfections,malignancyIndices:LowFe,LowTIBC,Nl/increasedFerritinMaybeseeninconjunctionwithFe-deficiencyAnemiaduetoPrimaryBoneMarrowDisorderMyelodysplasticsyndromeBonemarrowinfiltration:nucleatedredbloodcellsfoundincirculationMightsee“rouleaux”formationinmultiplemyelomaWBC,pltsoftenabnormalBonemarrowbiopsyAnemia:Treatments“Transfusiontriggers”CAD:Hgb>10Allpts:Hgb>7.0IronsupplementationErythropoietinanalogsB12,folateWhatintheworldisaHowell-JollyBody?AcanthocytesvsEchinocytesAcanthocytes:“spurcells”foundinliverdiseaseEchinocytes:“burrcells”foundinrenaldiseaseHelmetvs.TeardropCellsAnemia:SummaryANEMIAISNEVERNORMALDetermineifACUTEorCHRONICCONSIDERTHEFOURCAUSESCALCULATEtheRETICINDEXLOOKATTHESMEARCONSIDERTHEETIOLOGYBASEDONRBCMORPHOLOGYANDLABORATORYSTUDIESTREATAPPROPRIATELYMKSAPQuestionsAn80-year-oldmanwhohadahemicolectomyforcoloncancerisevaluatedbecauseofa4-monthhistoryofdiarrhea,anorexia,andfatigue.Hehadaremotehistoryofalcoholism.Onphysicalexamination,heiscachecticandmildlyconfused.Hispulserateis70/min,andbloodpressureis140/85mmHg.Histongueissmooth.Theabdomenissoft;therearenopalpablemassesorhepatosplenomegaly.Astoolspecimenisnegativeforoccultblood.Neurologicexaminationshowslossofpositionsenseinthefeet.Hehasawide-basedgait.TheRombergtestispositive.Hishemoglobinis9.4g/dL,reticulocytecountis2.5%,meancorpuscularvolumeis125fL,andserumlactatedehydrogenaseis400U/L.Whichofthefollowingisthemostlikelycauseforhissymptoms?(A)Alcoholiccerebellardegeneration

(B)VitaminB12deficiency

(C)Brainmetastases

(D)Folatedeficiency

(E)Livermetastases

Critique(CorrectAnswer=B)

ThepatientmostlikelyhasvitaminB12deficiency,basedonthedegreeofmacrocytosisandneurologicfindings.Anelevatedserumlactatedehydrogenaselevel,duetointramarrowcelldeathfromineffectiveerythropoiesis,isconsistentwiththisdiagnosis.Severemacrocytosis(meancorpuscularvolume>120fL)isoftenassociatedwithvitaminB12deficiencyorfolatedeficiency(megaloblasticanemia),usuallyseeninconjunctionwith“oval”macrocytes.Thepresenceoffrequenthypersegmentedneutrophils(>5segments)isstronglysuggestiveofvitaminB12orfolatedeficiency.BonemarrowmorphologyinpatientswithvitaminB12orfolatedeficiencyisreferredtoas“megaloblastic”andischaracterizedbythepresenceoflargecellswithimmaturenuclearchromatinbutmaturingerythrocytecytoplasm(nuclear-cytoplasmicdissociation).Anemiaaccompaniesthisprocess;hencetheterm“ineffectiveerythropoiesis.”Theintramarrowdeathofmegaloblasticcellscausestheserumlactatedehydrogenaseleveltorise.IfapatienthasalowserumvitaminB12orfolatelevel,abonemarrowexaminationisprobablyunnecessary.However,thephysicianshoulddeterminethecauseofthedeficiency.IfapatienthasanormalserumvitaminB12orfolatelevel,abonemarrowexaminationisfrequentlyhelpfultoexcludemyelodysplasticsyndromesorotherinfiltrativemarrowdisorders.Folatedeficiencycaninducemegaloblastosiswithinweekstomonths,whereasvitaminB12deficiencyrequiresyearstocausemegaloblastosissincestoresofvitaminB12persistforyearsintheliverandothertissues.InpatientswithvitaminB12orfolatedeficiency,parenteralororalrepletionofvitaminB12orfolatereversessomemorphologicabnormalitieswithinhours.Serumfolatelevelsfluctuatequicklywithchangesindietaryconsumption.Lowerythrocytefolatelevelsoftenreflectpriornutritionaldepletion.Inpatientswhoarehospitalizedandarebegunonregulardiets,theerythrocytefolatetestmayprovideabetterassessmentoftissuefolatelevelsthandeterminationoftheserumfolatelevel.Theerythrocytefolatetestoftenrequiresaspeciallaboratory,andresultsoftenarenotquicklyavailable.Inpatientswithmegaloblasticanemias,erythrocyteproductionisdiminishedanda“corrected”reticulocytecountisinappropriatelylowforthedegreeofanemia.Thispatienthadacorrectedreticulocytecountof1%(inappropriatelylowforahemoglobinlevelof9.4g/dL).Inadditiontochangesintheblood,theepithelialcellsinpatientswithmegaloblasticanemiasmaybecomeatrophicandcauseasmoothtongueandcheilosis.Posteriorcolumndysfunction,particularlyinpatientswithvitaminB12deficiency,mayleadtochangesinvibratoryorpositionsense,causingataxia.Signsofdementiamayappear.However,neurologicdysfunctionisveryuncommoninadultswithfolatedeficiency.Alcoholiccerebellardegenerationresultsinataxiabutnotpositionloss.Althoughlivermetastasesarepossibleinapatientwithahistoryofcoloncancer,theirpresencewouldnotaccountfortheneurologicalfindingsinthispatient.Brainmetastaseswouldmostlikelyproducefocalneurologicalfindingsandalsowouldnotaccountforthebloodfindings.A26-year-oldmanisevaluatedbecauseofprogressivefatigue,dyspneaonexertion,andorthostaticdizzinessforthepast2to3weeks.Hetakesnomedications.Physicalexaminationisnormalexceptforpallor.LaboratoryStudies:Hematocrit13%Leukocytecount8300/μL;normaldifferential.Reticulocytecount:0,Plateletcount320,000/μL.Aroutinebiochemicalprofile,includingliverfunctiontests,isnormal.Achestradiographshowsnormallungfieldsandawidenedmediastinum,suggestiveofananteriormediastinalmass.Bonemarrowbiopsyshowsabsenterythrocyteprecursors,normalmegakaryocytes,andnormalleukocytenumbersandmaturation.Whichofthefollowingisthemostlikelycauseofthemediastinalmassandanemia?(A)Hodgkin’sdisease

(B)Non-Hodgkin’slymphoma

(C)Thyroidcarcinoma

(D)Thymoma

(E)Germcellcarcinoma

Critique(CorrectAnswer=D)

Eachofthelistedneoplasmsmaypresentasananteriormediastinalmassandmaybeassociatedwithanemiaofchronicdisease.However,pureredcellaplasia(whichthispatienthas)isoftenassociatedwithabenignorinvasivethymoma.Approximately5%to15%ofthymomasoccurinpatientswithpureredcellaplasia.Otherthymoma-associatedautoimmunedisordersincludemyastheniagravis,systemiclupuserythematosus,thrombocytopenia,and,rarely,malabsorptionstates.AcarefulsearchbyCTorMRIisalwayswarrantedinpatientswithnewlydiagnosedorrelapsingredcellaplasiaormyasthenia.Theotherlistedentitiesarealsoincludedinthedifferentialdiagnosisforananteriormediastinalmass.Germcelltumorshavenotbeenassociatedwithpureredcellaplasia,andHodgkin’sdisease,non-Hodgkin’slymphoma,andthyroidcarcinomaarerarelyassociatedwiththisdisorder.Chroniclymphocyticleukemiaisalsocommonlyassociatedwithredcellaplasiaandmaypresentwithvariabledegreesoflymphadenopathybutnotwithanisolatedanteriormediastinalmass,asinthepatientdiscussedhere.A36-year-oldblackmanwithknownsicklecellanemiaisevaluatedbecauseofa2-weekhistoryoffever,amacularrashonhistrunk,andarthralgias.Subsequently,hedevelopedweaknessanddyspneaonexertion.Severalofhischildrenhadfebrileillnesseswithassociatedrashesandfatigueoverthepastmonth.Theseillnessesresolvedspontaneouslywithoutsequelae.Onphysicalexamination,histemperatureis38.8°C(101.8°F),pulserateis100/min,andbloodpressureis160/70mmHg.Amaculopapular,truncalrashisnoted.Thereisconjunctivalpallor.Theremainderofhisexaminationisunremarkable.LaboratoryStudiesHemoglobin5.2g/dLLeukocytecount5000/μLReticulocytecount0%Plateletcount130,000/μLSerumlactatedehydrogenase622U/LWhichofthefollowingisthemostlikelydiagnosis?(A)Paroxysmalnocturnalhemoglobinuria

(B)Parvovirusinfection

(C)Glucose-6-phosphatedehydrogenasedeficiency

(D)AplasticanemiaCritique(CorrectAnswer=B)

Patientswithhemolyticdisordersmayoccasionallypresentwithreticulocytopeniaandan“aplasticcrisis.”Thispatienthassicklecellanemiawithparvovirusinfection,whichiscausinganaplasticcrisis.Parvovirusmayinfectpatientswithhemolyticanemias(forexample,patientswithhereditaryspherocytosis,sicklecelldisease,orthalassemia).Inchildrenwithsicklecellanemia,over80%ofaplasticcrisesmaybeattributedtoparvovirusinfections.Inadults,theusualpresentingfeaturesarerash,arthritis,andanemia.The“slappedcheek”syndromeisrarelyapresentingfeature.Thereisusuallyacompletesuppressionoferythropoiesistoareticulocytelevelof0%.Thebonemarrowshowsgiantdysplastic(megaloblastoid)erythroblasts,occasionallywithviralinclusions.ThediagnosisisusuallymadebydemonstratingIgMantibodiestothevirus.IgGantibodiesappearlaterduringthecourseoftheinfectionandpersist.Parvovirusinthebloodmaybedetectedbythepolymerasechainreaction,whichisthedefinitivediagnosticmethod.Occasionally,otherbloodcomponentssuchasleukocytesandplateletsareaffectedandresultinmildtomoderatepancytopenia.Thediagnosisofparoxysmalnocturnalhemoglobinuria(PNH)shouldbeconsideredinpatientswithbonemarrowfailureoraplasia,unusuallocationofthromboses,andunexplainedhemolysis.Theanemiamaybesevere,andpatientswithPNHtypicallyhavereticulocytopenia.Thereisnocharacteristicfindingonbonemarrowexamination,althoughthebonemarrowofpatientswithPNHmaydemonstratemyelodysplasticchanges.Thediagnosisisbasedondemonstrationofexquisitesensitivitytocomplement-mediatedlysisbythesucroselysistestortheacidifiedserumlysistest(Ham’stest).Glucose-6-phosphatedehydrogenase(G6PD)deficiencyisanothercauseofhemolysisthatoccasionallyisassociatedwithreticulocytopenia.InpatientswithG6PDdeficiency,erythrocytesaresubjecttooxidativestresses.Hemoglobinbecomesoxidizedandprecipitateswithintheerythrocytes,whichthenundergodestructionbythereticuloendothelialsystem.G6PDdeficiencyisanautosomalrecessivedisorderthatpredominantlyaffectsmales.Afterahemolyticepisode,qualitativeassaysmaybenormalbecauseonlyerythrocytesthatareresistanttoG6PDremain.TheAfricanvariantofG6PDisassociatedwithamildformofhemolysis,whereastheMediterraneanvariantisusuallysevere.Causesincludeinfectiousstresses,drugssuchasquinidineandsulfonamides,or,intheMediterraneanvariant,favism(consumptionoffavabeans).Therapyrequiresavoidingcertainmedicationsandsupportivecareincrisissituations.Incontrasttothispatient’spresentation,patientswithaplasticanemiahavepancytopeniawithsevereanemia,reticulocytopenia,thrombocytopenia,andgranulocytopenia.Inpatientswithsevereaplasticanemia,thebonemarrowexaminationshowslessthan5%cellularitywithonlyresiduallymphocytesandplasmacells.Theabnormalcellsdescribedabovethatareattributabletoparvovirusinfectionarenotseen.A36-year-oldmanisevaluatedbecauseoffatigue.Hehashadtwoepisodesofacutegoutyarthritisoverthepast6months.Hehasa10-yearhistoryofsignificantalcoholuse,buthequitdrinking4monthsago.Heworksinafactorymakingbatteryproducts.Acompletebloodcountobtainedpriortoelectiveherniarepairsurgery4yearsagowasnormal.Hetakesnomedications.Onphysicalexamination,histemperatureis37.3°C(99.1°F),pulseis60/min,andbloodpressureis135/70mmHg.Hisskinisnormal.Thereisslightscleralicterus.Thereisabluelineattheedgeofhisgums.Theremainderoftheexaminationisnormal.Stoolspecimensarenegativeforbloodonthreeoccasions.LaboratoryStudiesHemoglobin7.5g/dLMeancorpuscularvolume71flLeukocytecount9400/μLReticulocytecount5.3%Plateletcount435,000/μLSerumlactatedehydrogenase553U/LSerumuricacid11mg/dLAperipheralbloodsmearisshown.Whichofthefollowingdiagnosticstudiesismostusefulfordeterminingthecauseofthispatient’sanemia?(A)Serumiron,totaliron-bindingcapacity,andferritinlevels

(B)Serumleadlevels

(C)Directandindirectantiglobulintests

(D)HemoglobinA2quantitation

(E)Serumethanolandfolicacidlevels

Critique(CorrectAnswer=B)

Thepatienthaschronicleadintoxicationthatcanbeconfirmedbymeasuringserumleadlevels.Hehasahypochromic,microcyticanemiawithcoarsebasophilicstipplingandreticulocytosis.Healsohasevidenceofhemolyticanemiawithincreasedserumlactatedehydrogenaseandindirectbilirubinlevels.Hisphysicalexaminationisremarkableforgingival“l(fā)eadlines.”Bonemarrowexaminationshowserythroidhyperplasiaandringedsideroblasts.Theanemiaofleadpoisoningfitsthisdescription.Sideroblasticanemiawithhypochromicindicesistypical.Hemolysisiscommon,andbasophilicstippling,bluestainingpolyribosomalaggregateswithmitochondrialfragmentsintheerythrocytes,isfrequentlyseen.Leadinhibitspyrimidine5′-nucleotidasewhichnormallyclearsribosomalfragments.Occupationalexposurestoleadarerelativelyuncommontoday.However,workerswhoproducebatteriesorareexposedtopaint,particularlythosewhoremoveleadedpaintfromoldbuildings,areatgreatestriskiftheyarenotprotectedfrominhalationofpaintparticlesduringthesandingprocess.Othermanifestationsofleadtoxicityinadultsincludeperipheralneuropathy,abdominalcolic,andsaturninegout(effectsofleadonrenaltubulesthatpreventtheexcretionofuricacid).Chelationtherapyisindicatedforpatientswithserumleadlevelsexceeding70μg/dLandshouldbecontinueduntilleadlevelsfallbelow40μg/dL.AgentssuchasEDTAordimercaprolmayalsobeeffective.Thispatientisunlikelytohaveirondeficiencysincehisreticulocytesareincreased.Inaddition,basophilicstipplingusuallyisnotseeninpatientswithirondeficiency.Thalassemiaisassociatedwithamicrocyticanemia,reticulocytosis,andbasophilicstippling.However,anormalcompletebloodcount4yearsagorulesoutthispossibility.Therefore,quantitativestudiestomeasurehemoglobinA2arenotnecessary.Autoimmunehemolyticanemiashouldbeexcludedbyperformingadirectantiglobulintestinanypatientwhohasevidenceofhemolysisonaperipheralbloodsmear.However,the“l(fā)eadlines”onthispatient’sgingivaeareclassicforleadpoisoning,andautoimmunehemolyticanemiathereforeislesslikely.Alcoholismmaycauseatransientsidero