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APrimeronHemostasisforClinicalChemists

CLNStat

Author:NeilS.Harris,MBChB,MD,LindsayA.L.Bazydlo,PhD,andWilliamE.Winter,MD

CLNArticles
Boardof

//Date:JAN.1.2012//Source:ClinicalLaboratoryNews
Topics:TestingMethods,Specializations,Coagulation,Thrombosis

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Whendamagetosmallbloodvesselsandcapillariesoccurs,thebodycontrolsbloodloss
viaphysiologicalprocessesreferredtoashemostasis.Invivo,hemostasisdependsonan
interactionbetweentheplasmabasedcoagulationcascade,platelets,andthe
endotheliumofbloodvessels.Intheclinicallaboratory,invitroanalyticalassaysare
capableofmeasuringonlythefirsttwocomponentsofthissystem.Consequently,
laboratorymeasurementsofbloodcoagulationrepresentonlyacloseapproximationofthe
body'shemostaticsystem.
Cliniciansfrequentlyordercoagulationtests,suchastheprothrombintime(PT),activated
partialthromboplastintime(aPTT),andthrombintime(TT),toassessbloodclottingfunction
inpatients.Whiletheselaboratorytestsmaybehelpfulinelucidatingthecauseof
unexplainedbleeding,theyarenothelpfulinpredictingifbleedingwilloccur.Infact,no
singletestcanpredictbleedingintheperioperativeorpostoperativeperiod.Furthermore,
thesecommonlaboratorytestsareoflittlehelpinpredictingbloodclottingorthrombosisin
theabsenceofvesselinjury.Welldescribedassaysareavailabletotestforhereditary
predispositiontothrombosis,butthemajorityofthrombophilicstatescannotbequantified
byanycurrentlaboratorytests.
Clearly,laboratoryassessmentofhemostasispresentsmanychallengesforlaboratorians
andtheclinicianswhointerprettheresults.Thisreviewbrieflyexplainsthecommontests
usedtoassesshemostasis,aswellastheirclinicalcontext,andprovidesaguidefor
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clinicalchemiststoassessunexplainedbleeding.
TheABCsofCoagulationTests
Laboratorytestsforhemostasistypicallyrequirecitratedplasmaderivedfromwholeblood.
Specimensshouldbecollectedintotubescontaining3.2%sodiumcitrate(109mM)ata
ratioof9partsbloodand1partanticoagulant.Thepurposeofthecitrateistoremove
calciumionsthatareessentialforbloodcoagulationhowever,failuretofillthedrawtube
adequatelycausesthefinalcitrateconcentrationofthepatientsampletobetoohigh.This
isimportantbecausePTandaPTTtestsrequiretheadditionofcalcium.Ifthespecimen
containsexcesscitrate,additionofcalciummaybeinadequate,andthelowplasma
calciumwillleadtoanartificialprolongationofPToraPTT.
Asimilarbutmoresubtleproblemmightariseifthepatient'shematocritisunusuallyhigh,
typically55%.Normally,10mLofbloodwithahematocritof40%contains6mLof
plasma.Ifthehematocritisabnormallyelevated,forexample65%,thespecimenwill
containonly3.5mLofplasma,effectivelyunderfillingthedrawtubewithplasma,leading
toovercitrationoftheplasma.
ForthePTtest,addingathromboplastinreagentcontainingatissuefactor,calcium,and
phospholipidsinitiatescoagulationoftheprewarmedspecimenviatheextrinsic
coagulationpathway(Figure1).Similarly,theaPTTtestisinitiatedbyaddinganegatively
chargedsurfacesuchassilicatotheplasma,aswellasaphospholipidextractthatisfree
oftissuefactor.ThecoagulationpathwaythatoccursintheaPTTtestrepresentsthe
intrinsiccoagulationpathway(Figure1).
Figure1
CoagulationCascade
Thecoagulationcascadeisaseriesofenzymaticreactionsthatturn
inactiveprecursorsintoactivefactors.Theendresultofthecascadeis
theproductionoffibrin,aproteinthatbindsplateletsandothermaterials
inastableclot.Thecascadehastwoinitialpathways:theextrinsic
(tissuefactormediated)andtheintrinsic(contactsysteminitiated).
Thesetwopathwaysconvergetobecomethecommonpathwaywith
theactivationoffactorX.Thestepsinthecascadethataremeasuredby
thethreecommoncoagulationassays,PT,aPTT,andTT,areindicated.

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CoagulationCascade

WhenapatienthasanabnormallyprolongedPToraPTT,laboratoriesshouldperforma
mixingstudyofthespecimen(Table1).Toperformthetest,thetechnologistmixesanequal
volumeofthepatient'scitratedplasmawithnormalpooledplasma(NPP)andrepeatsthe
PTand/oraPTT.IftheclottingassaytimenowfallswithinthePTand/oraPTTreference
intervals,theinitialabnormalresultwasduetooneormoreclottingfactordeficiencies.In
contrast,thepresenceofinhibitorsinpatientplasmainterfereswiththeclottingfactorsin
theNPP,butthemixingstudyresultswillnotproducenormalclottingtimes.Another
commonassayusedtoassesshemostasisisTT(Figure1).Thistestmeasurestheabilityof
fibrinogentoformfibrinstrandsinvitro.Toperformthetest,thetechnologistadds
exogenousthrombintoprewarmedplasma.Thisstepensuresthattheresultis
independentofendogenousthrombinoranyoftheotherclottingfactors.TTisparticularly
sensitivetoheparin.
Table1
AssessmentofProlongedaPTT
Thistableshowshowcoagulationassayscanbecombinedtoelucidatethepossiblecausesofa
prolongedaPTT.

No
Clinical Increased Increased Increased Hemostatic Thrombophilia
Features Bleeding Bleeding Bleeding Problems
DVT,PE
1:1Mixing
Study

Corrects

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Corrects

Nocorrection

Corrects

Nocorrection

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PT
Pathology

Normal

Prolonged

Deficiencyof
factorsVIII,IX
andsome
casesof
factorXI
deficiency

Deficiencyof
factorsII,V,
X,fibrinogen

Normal

Normal

Autoantibodies Deficiencyof
tofactorVIII
factorXII
(acquired
hemophilia)
Deficiencyof

WarfarinRx

Normal
Antiphospholipid
syndrome

othercontact
factorssuchas
prekallikrein
Somecasesof
factorXI
deficiency

Abbreviations:DVT,deepveinthrombosisPE,pulmonaryembolismRx,treatment.
ThequantitativefibrinogenassayisamodificationoftheTTassay.Thetestrequires
additionofexogenousthrombin,exceptthatinthiscase,thetechnologistdilutesthe
plasmaseveralfoldandaddsgreateramountsofthrombincomparedtotheTTassay.The
results,whicharereportedinmg/dLratherthanseconds,aredeterminedfromastandard
curvegeneratedfromacalibratorplasma.
AnothertestfrequentlyorderedtoassesshemostaticfunctionisDdimer.These
degradationproductsofmaturecrosslinkedfibrinareformedbytheactionoftheenzyme
plasminonfibrin,andelevatedlevelsareanindicatorofthrombosis.Twotypesof
laboratoryassaysmeasureDdimers:noncompetitive,sandwichimmunoassays,and
immunoturbidimetricassays.Ddimerdeterminationisusedforitshighnegativepredictive
valueofthrombosis.Whentheconcentrationiswithinthereferencerange,clinicianscan
excludeasuspecteddeepvenousthrombosis(orpulmonaryembolism).Patientswho
suffertrauma,undergosurgery,orarepregnantcommonlyhaveelevatedlevelsofD
dimers.
Theactivatedclottingtime(ACT)testuseswholeblood,whichismixedwithaclotactivator,
usuallydiatomaceousearthorkaolin.Clottingtypicallytakes70180seconds,andcanbe
measuredmechanicallyorbyanelectrochemicalprocedure.Hospitalsusethetestatthe
bedsidetomonitorhighdoseheparinanticoagulationduringcardiopulmonarybypass
surgeryaswellasduringcardiaccatheterization.
Thecoagulationfactoractivityassaydeterminesthelevelofvariouscoagulationfactors.An
essentialcomponentoftheassayisafactordeficientplasmathatlacksthespecificfactor
beingtested.Toperformtheassay,thetechnologistdilutesthepatient'scitratedplasmain
abufferandmixesthedilutedspecimenonetoonewiththefactordeficientplasma.The
patient'sspecimensuppliesthemissingfactortotheassay,whichiscompletedby
performingastandardPToraPTT,dependingonthefactorbeingtested.Asanexamplefor
factorsVIIIandIX,whichparticipateintheintrinsiccoagulationpathway,thelabshouldrun
theaPTTtest.Incontrast,aPTassaywouldbeusedtodeterminefactorVII,whichis
involvedintheextrinsiccoagulationpathway.Calibrationoftheassaysinvolvesastandard
referenceplasmawithaknownconcentrationofthefactorbeingtested.

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PlateletFunction
Anothercomponentoflaboratoryassessmentofhemostasisisplateletfunctiontesting.
Plateletaggregometryisconsideredtheclassictestofplateletfunction.Thistestincludesa
plateletactivatingagonistsuchasADP,epinephrine,orcollagen.Thetechnologistadds
theagonisttoplateletrichplasmaandmonitorsplateletaggregationinaphotometer
cuvette.Opticaldensitychangesareplottedtoviewtheaggregationcurve.
Otherdevicesmeasureplateletadhesionunderhighshearconditions.Inthismethod,the
instrumentfirstdrawsanaliquotofthespecimenthroughacapillaryunderconditionsof
highshearstressandthenthroughaverysmallapertureinadisposablecartridge.The
latteriscoatedwithcollagenandepinephrineorcollagenandADP.Innormalindividuals,
thisproducesplateletadhesionandactivationthateventuallyplugstheapertureandstops
theflow.Theassayendpointiscalledtheclosuretime.
TheAntiXaAssay
CliniciansoccasionallyordertheantiXatesttomonitorandadjustpatients'levelsof
unfractionatedheparin,awidelyusedanticoagulant.Thischromogenicmethodgenerally
containsexogenousfactorXaandantithrombin(AT),bothinexcess,aswellasa
chromogenicsubstrateforfactorXa.Someversionsoftheassayusethepatient'sownAT,
aserineproteaseinhibitorthatisthemajorinhibitorofcoagulationproteases,insteadof
addingexogenousAT.Ineitherapproach,heparinpresentinthespecimencomplexeswith
ATandthiscomplexinhibitsfactorXa.AnyresidualfactorXacleavesthechromogenic
substrate,therebyreleasingayellowcoloredchromophore.Labsreporttheseresultsas
unitspermLofantiXaactivity.
ClinicalProblemsAssociatedwithBleeding
Manyclinicalconditionscanleadtounexplainedbleeding.Propertestingcanhelp
cliniciansdiscernthecause.Thissectionpresentssomeofthemorecommoncausesand
whichtestsshouldbeused(Table2).
Table2
SequentialUseofCoagulationAssaystoAssessBleeding
Thistableshowshowcoagulationassayscanbecombinedtoelucidatethe
possiblecausesofunexplainedbleeding.

Step

Test

Indicationfor
PerformingTest

PurposeofTest

Goto
Step

assessextrinsic,
intrinsicandcommon
pathwaysand
adequacyofplatelet
numbers

3or4or
5

PT,aPTT,
fibrinogen,
platelet
count

unexplained
bleeding

1:1mixing
study

prolongedPT,
aPTT

assess
deficiency/dysfunction
vsinhibitor

specific

mixingstudies

assessfactor

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iffactor
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factor
activity
assays

showcorrection

TT

mixingstudydoes
notcorrect

deficiencyorwarfarin
Rx

ruleoutheparin
contamination

antiXa
assay

mixingstudydoes
notcorrect

assayfor
specific
factor
inhibitors

mixingstudydoes
notcorrectand
heparinis
excluded

ruleoutacquired
hemophiliaandother
factorinhibitors

reducedfactorVIII
activity

ruleoutvWD

von
Willebrand
antigenand
activity
platelet
function
screen

reducedfactorVIII ruleoutvWDand
activityornormal
plateletdysfunction
plasmabased
coagulationtests
withnormalplatelet
counts

factorXIII
allprevioustesting
screen,tests iswithinnormal
fordisorders limits
of
fibrinolysis
(e.g.,TEG)

VIIIis
low,
proceed
to7and
8
ifheparin
is
excluded,
proceed
to6

ruleoutfibrinolytic
problems

Congenitalhemophilia.Theclassicbleedingdisorder,congenitalhemophilia,isanX
linked,recessivegeneticabnormality.Maleswithonecopyofthedefectareaffected
however,femalesareasymptomaticcarriers.Thediseaseoriginatesfromoneoftwo
alteredproteinsinthecoagulationcascade,factorVIII(hemophiliaA)orfactorIX
(hemophiliaB),whichareindistinguishableclinically.TheincidenceofhemophiliaAis1in
5,000malelivebirths,andthatofhemophiliaBis1in30,000.
PatientswithhemophiliahavereducedfactorVIIIorfactorIXactivityinfresh,citrated
plasma,andthediseaseisclassifiedassevere(<1%),moderate(15%),ormild(630%)
dependingontheamountoffactoractivity.Inthesevereform,patientshavespontaneous,
deepbleedingintomusclesandjoints,aswellasseverebleedingafterinjury.These
individualspresentininfancy.Incontrast,themildformmaybediagnosedinadulthood
andevenaslateasmiddleage.Affectedindividualsbleedaftersurgeryortraumabutnot
spontaneously.
Thefollowinglabresultsareconsistentfindingsforhemophilia:1)significantlyprolonged
aPTTthatcorrectsina1:1mixingstudy2)PTwithinthereferencerange3)fibrinogenand
TTwithinthereferencerange3)normalplateletfunctionand4)normalvonWillebrand
testresults(seebelow).
vonWillebrandDisease.DefectivesynthesisorreleaseoffunctionalvonWillebrandfactor
(vWF)causesdefectiveplateletadhesionandleadstoaspectrumofconditions,suchas
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epistaxis,heavymenstrualbleeding,andeasybruising.
LabsuseanimmunoturbidimetrictechniquetomeasuretheplasmaconcentrationofvWF,
andtheymeasurevWFactivityusingthepatient'splasmaincombinationwithformalin
fixed,normaldonorplateletsandristocetin,whichservesasacofactorintheassay.
AnotherinformativetestexaminesthestructureofvWFmultimers.Anancillarytestisfactor
VIIIactivity,sincelowvWFisfrequentlyassociatedwithlowfactorVIIIactivity.Ifthefactor
VIIIactivityissufficientlydecreased,aPTTmaybeprolonged.Inmostformsofvon
Willebranddisease,bleedingisaconsequenceofplateletdysfunctionthatresultsfromthe
insufficiencyofactivevWFandnotfromreducedfactorVIIIactivity.
Acquiredhemophilia.Althoughrare,acquiredhemophiliaresultsfromspontaneous
formationofautoantibodiestofactorVIIIinapreviouslyhealthyindividual,eithermaleor
female.Asthenamesuggests,thereisnoovertgeneticcomponent.FactorVIIIactivityis
significantlydecreasedasaresultoftheautoantibodies,andsevereanduncontrolled
bleedingresults.
LaboratorystudiesrevealamarkedlyprolongedaPTT,anormalPT,andalowFVIIIactivity.
Forthesepatients,a1:1mixingstudydoesnotcorrecttheabnormalaPTT.
AcquiredvonWillebrandSyndrome.Alsouncommon,acquiredvonWillebrandsyndrome
(AVWS)referstothedevelopmentofvonWillebranddeficiencyrelativelylateinlifeina
previouslyhealthyindividual.AVWSmaybeseeninavarietyoflymphoproliferative
disorders,monoclonalplasmacelldisorders,autoimmunedisease,andcardiacvalvular
diseaseorseptaldefects.vWFactivityintheseindividualsmaybereducedbyinhibitory
antibodies,adsorptiontocellsurfaces,orareasofelevatedshearstressthatoccurviaa
stenoticheartvalveorseptaldefect.
LabstudiesshowdecreasedfactorVIIIactivity,prolongedaPTTiffactorVIIIis<40%,
impairedplateletresponsetoristocetin,andprolongedclosuretimes.
Noneofthestandardlaboratorytestsdescribedaboveprovidediagnosticinformationfor
identifyingthrombophilicstates.Inthemajorityofcases,hypercoaguabledisordersare
acquired,and,exceptforantiphospholipidsyndromeandthehereditarythrombophilias,
therearenoinformativelaboratorytests(Table3).
Table3
LaboratoryAssessmentofHypercoaguableStates
Hypercoaguable
State
Inflammation
Trauma

Clinical
Scenario

Mechanisms

Laboratory
Tests

Commonin
almostevery
postoperative
surgicaland
traumapatient

ElevatedfactorVIII,
vWF,fibrinogen,
inflammatory
cytokinescombined
withvenousstasis

None

Apparentor

Inflammation,

None

Surgery
Immobilization
Malignancy
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(Trousseau
Syndrome)

occultneoplasm

cytokines,proteases.
Productionoftissue
factorbytumor

Hormonal

Oral

Estrogenis
associatedwith
elevatedfactorII,VII,
VIII,Xandfibrinogen,
decreased
antithrombin,
decreasedproteinS

None

Antibodiesto
phospholipidand
phospholipidbinding
proteins.
Inflammationand
endothelialdamage.
glycoproteinI

Lupus
anticoagulant
testing
antibodiesto
cardiolipin
andbeta2

Heparininduced Acquired
thrombocytopenia antibodyto
(HIT)
heparin/platelet
factor4complex

Plateletactivation
andreleaseof
microparticles

Testfor
antibodiesto
heparin/PF4
byELISA

Hereditary
Thrombophilia

Multiple(seetext)

PCRbased

contraceptives
Pregnancy

Antiphospholipid
Syndrome

Acquired
autoimmune
disorder

Unexplained
thrombosisatan
earlyageor
thrombosisat
unusualsitesor
recurrent
thrombosis

DNAanalysis
Functional
activity
assays

Antiphospholipidsyndrome.Anautoimmuneprothromboticacquiredcondition,
antiphospholipidsyndrome(APLS)isfrequentlyassociatedwithamarkedlyprolonged
aPTT,leadingtoaconcernthattheaffectedindividualmightbeatriskforamajor
hemorrhage.Notonlyisthishighlyunlikely,butasaprothromboticstate,APLSistypically
associatedwithvenousthromboembolismand/orarterialthrombosis.Theconditionmay
alsopresentwithfetallossorstillbirth,whichlikelyoccursasaresultofplacental
inflammationorthrombosis.
IndividualswithAPLShaveantibodiesknownaslupusanticoagulants(LA).These
antibodiesaredirectedtocomplexesofbeta2glycoproteinI/phospholipidor
prothrombin/phospholipid,andtheyinterferewithandprolonginvitroclottingassays.Inthe
body'svascularsystem,however,thepresenceofendothelialcellsandleukocytes,aswell
asmanyothercomponentsthatareabsentfromthesimplifiedinvitroclottingassay,
increasethelikelihoodofclotting.
TheclassiclaboratoryfindingsinAPLSpatientsareprolongedaPTT,normalPT,andno
correctionoftheaPTT1:1mixingstudy.AddingexcessphospholipidtotheaPTTassay,
however,reducestheclottingtime.ThisisthebasisforthesocalledLAassay.Oneversion
oftheLAassayisthediluteRussell'svipervenomtime(dRVVT).Theassaycomponents
activateonlythecommoncoagulationpathwayviafactorX,andtheyareindependentof
factorVIIIorantibodiestofactorVIII.LaboratoriesalsocanconfirmAPLSbydetectingIgG
orIgMantibodiestocardiolipinortobeta2glycoproteinIinanELISAtypeassay.
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FactorVLeiden.AvariantoffactorV,factorVLeidencausesahereditary
hypercoagulabilitydisorder.Individualswiththedisorderhaveapointmutationinthefactor
Vgenethatproducesasingleaminoacidswitch(argininetoglutamine,R506Q)that
makestheproteinresistanttoinactivationbyactivatedproteinC.HeterozygosityforfactorV
Leidenincreasestheriskforvenousthromboembolismabouttwoorthreefold.
LaboratoryresultsforthisgeneticconditionincludePTandaPTTwithinthenormalrange.
Inaddition,aPTTwillberesistanttoactivatedproteinC,andinnormalindividuals,adding
activatedproteinCtoafreshplasmaspecimenwillcauseprolongationofaPTT.Thiseffect
isbluntedforindividualswithfactorVLeiden.DNAstudiesdefinitivelyconfirmtheG1691A
nucleotideswitch.
ProthrombinG20210A.Anotherhereditarythrombophilia,theG20210Apolymorphismin
theprothrombingeneelevatestheplasmaconcentrationsofprothrombin(FII)without
changingtheaminoacidsequenceoftheprotein.
PatientswiththismutationhavePTandaPTTresultsthatfallwithinthenormalrange,as
wellasnormalfunctionalclotbasedstudies.DNAstudieswillshowaGtoAsubstitutionin
the3'untranslatedregionofprothrombingeneatnucleotide20,210.
ProteinCandSdeficiency.ThesetwovitaminKdependentfactorsinterrupttheactivityof
clottingfactorsVandVIII.ActivatedproteinCisaproteolyticenzyme,whileproteinSisan
essentialcofactor.
Antithrombindeficiency.AT,formerlycalledATIII,isavitaminKindependentglycoprotein
thatisamajorinhibitorofthrombinandothercoagulationserineproteases,including
factorsXaandIXa.ATformsacompetitive1:1complexwithitstargetbutonlyinthe
presenceofanegativelychargedglycosaminoglycan,suchasheparinorheparinsulfate.
PatientswithATdeficiencywillhavelittletonoATIIIactivityasmeasuredinachromogenic
assay.
InterpretationofCoagulationTests
Aswithanylaboratorytest,ourgoalaslaboratoriansistoassistclinicianswithutilization
andinterpretationofteststhatassesshemostasis.Unlikeanelevatedserumcreatinineora
highthyroidstimulatinghormonethatindicateimpairedrenalfunctionandhypothyroidism
respectively,testsofhemostasishavetobeinterpretedinthecontextofclinicalfindingsas
wellasotherlaboratoryfindings.Giventhedireconsequencesofunexplainedbleeding,
clinicallaboratoriansshouldactivelyadvisecliniciansonuseandinterpretationof
coagulationtests.Ashotgunapproachtohemostaticdisordersisrarelysuccessfulandcan
resultindelayeddiagnosisandtreatmentforpatients.
SUGGESTEDREADING
EbyCS.WarfarinDosing.ShouldLabsOfferPharmacogeneticTesting?CLN200935(6).
HarrisNS,WinterWE.TheInternationalNormalizedRatioAToolforMonitoringWarfarin
Therapy.CLN201036(11).
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HarrisNS,WinterWE,LedfordKraemerMR.Hemostasis:AReview&Methodsof
AssessmentintheClinicalLaboratory.Chapter21,pp265283.IN:ContemporaryPractice
inClinicalChemistry2ndEdition,Clarke,W.2011(AACCPress,WashingtonDC).
HoffbrandAV,MossPAH.EssentialHaematology.6thEdition.Chapters26(Coagulation
Disorders)and27(ThrombosisandAntithromboticTherapy).WileyBlackwell2011.
HoffmanM,MonroeDM.Coagulation2006:Amodernviewofhemostasis.HematolOncol
ClinNAm200721:111.
KrollMH.ThromboelastographyTheoryandPracticeinMeasuringHemostasis.CLN
201036(12).

NeilS.Harris,MBChB,MD,isclinicalassociateprofessorandcodirectoroftheCoreDiagnostic
LaboratoryintheDepartmentofPathology,Immunology,andLaboratoryMedicineattheUniversityof
FloridaCollegeofMedicineinGainesville.Email

LindsayA.L.Bazydlo,PhD,isclinicalassistantprofessoranddirectorofclinicalchemistryinthe
DepartmentofPathology,ImmunologyandLaboratoryMedicineattheUniversityofFloridaCollegeof
MedicineinGainesville.Email

WilliamE.Winter,MD,isprofessorofpathologyandpediatricsattheUniversityofFloridain
Gainesville.Email

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