-血脂检测临床应用的有关问题课件

RelatedproblemsonclinicalapplicationofplasmalipidsassayProfessorzhouxinDepartmentofLaboratoryMedicine,Zhongnanhospitalofwuhanuniversity.Dr.Sheng-kaiYan,PhDDepartmentofLaboratoryMedicine,PekingUnionMedicalCollegeHospitalRelatedproblemsonclinicala1AllkindsoflipidsinplasmawerecalledbloodlipidsTotalcholesterol，TC＝freecholesterol＋cholesterolesterNeutralfatty—triglyceride，(TG)

nonesterifiedfattyacid（freefattyacid，FFA）

phospholipid,glucolipidLipidswereinsolubleinwater

,theyweretransportedintheformoflipoprotein

PlasmalipidsAllkindsoflipidsinplasm2PlasmalipoproteinLDLLp(a)VLDLIDLHDLstructureoflipoproteinPlasmalipoproteinLDLLp(a)VLDL3Clinicalitemsforlipidsdetectiontotalcholesterol，TCtriglyceride，TGhighdensitylipoproteincholesterol，HDL-Clowdensitylipoproteincholesterol，LDL-CapolipoproteinA1，ApoA1apolipoproteinB，ApoBlipoprotein(a)Thefirstfouritemswereroutinetest,andshouldbecarriedoutinhealthyexaminationsClinicalitemsforlipidsdete4Cinicalitemsforlipidsanalysis(2)FFA

Cerebrosideesterceramide

Sphingenine

Sphingomyelin

Galactode-cerebrosideCinicalitemsforlipidsanaly5Genotype

ApoEgenotypeApoCIIIgenotypeApoCIIgenotype

Apo(a)genotype

LDLRgenotype

VLDLRgenotypeHMGCoARgenotype

SRgenotypeCinicalitemsforlipidsanalysis(3)GenotypeCinicalitemsforlip6PreanalyticalFactorsAffectingLipidTestResultsPreanalyticalFactorsAffectin7ThefollowingfactorsmaycausepreanalyticalvariationsBiologicalfactors

Individualbiologicalvariations,gender,age,andrace,etc.

Life-stylefactorsdiet,obesity,smoking,stress,alcohol,andcoffeeintake,andexercise,etc.Thefollowingfactorsmaycaus8Behaviourfactors(1)DietThefoodcontainingabundantunsaturatedfattyacidcandecreasethelevelofTC,

LDL-C,apoBandTG.ThefoodcontainingabundantsaturatedfattyacidcanelevateTC,LDL-C.ThefoodcontainingabundantfibercanreducethelevalofTC.ThelevelsofLDL-CandLp(a)invegetarianswerelower(37％,35％respectively)thannon-vegetarians,whileHDL-Cwerehigherthanthatof12％.Behaviourfactors(1)Diet9Behaviourfactors(2)ObesityTG，TCandLDL-C↑HDL-C↓

Lostweight

TG（40％）↓TC（10％）↓LDL-C（10％）↓HDL-C（10％）↑Behaviourfactors(210Smoking

TG,LDL-CandLp(a)↑↑apoAandHDL-C↓↓HDL-C↓Behaviourfactors(3)SmokingBehaviourfa11Behaviourfactors(4)AlcoholabuseHDL-C,apoAⅠ,apoAⅡ↑（1.2oz/dor34g/d）PrimryhypertriglyceridemiawithmilddrinkingcanleadtothelevelofTGincreasedfurther.AlcoholhasdifferenteffectsonLp(a)fromotherlipids.atthebeginLp(a)33%↓sixweekslaterLp(a)backtoinitiallevelProperdrinkingredwinecandecreasethelevelofLp(a).

Behaviourfactors(4)12Behaviourfactors(5)Coffee

TCandLDL-C↑

apoAⅠ,apoAⅡ,apoBandHDL-Cseemednotbeaffected.TensionTC↑HospitalizationHDL-CandapoAⅠ(10％)↓Behaviourfactors(5)13Behaviourfactors(6)ExerciseTG、LDL-CandapoB↓HDL-CandapoAⅠ↓Thedegreewasrelatedtothekindsofsportsandintensity.IntenseexercisescanincreasethelevelofHDL-Cobviously.Moderateregularexerciseswasaidealwaytodecreasethelevelofbloodlipid.NormalexerciseshavenoinfluencesonthelevelofLp(a)，whileintensephysicalactivity

canincreasethelevelofLp(a)by10％~15％.Behaviourfactors(6)14Clinicalfactors

therapeuticdrugs(1)Antihypertensiveagentsforexamplethiagine（diuresisdrug）canincreasethelevelofTC,LDL-C,TGandapoBby12%、20%,7%,20%respectively,decreasethelevalofapoAIandHDL-Cby6%and16%.Beta-neg（ßreceptorblocker）canincreasethelevelofTGanddecreasethelevalofHDL-C.EstrogenOraltakingcontraceptivewithprogesteronecanincreasethelevalofTCandLDL-C,anddecreasethelevalofHDL-C.EstrintreatmentcandecreasethelevalofLp(a)by50%.Clinicalfactors

therapeutic15ImmunosuppressiveagentsCodelcortonecanincreasethelevelofTC,LDL-C,HDL-C,

TG,

apoAandapoB.CiclosporincanincreasethelevelofTC,LDL-C,apoB，anddecreasethelevelofLp(a).Tacrolimus—FK506candecreasethelevelofTC.Clinicalfactors

therapeuticdrugs(2)ImmunosuppressiveagentsClinic16

Thedivisionofabnormallipidslevel

Thelipidlevelwasdiverseindifferentnationandarea.IthasbeensuggestedthatthelevelwhichcanincreasetheriskofCHDobviouslyshouldserveasthedivisionstandardforabnormalleveloflipid,meanwhileweclaimtoformulatethetherapeuticsdestinationandintervenetheprocedureaccordingtothelevel.suggestionsAdoptthestandardsofsuggestionsonpreventionandcurelipidabnormalityinchina.Thedivisionofabnormallipi17RiskrateTCandCHD

PlasmaTCRiskrateTCandCHDPl18Medicaldecisionlevelforlipidassaymmol/L(mg/dl)

index china（1997）NCEP-ATPⅡSerumTCSuitbleleval≤5.20(200)5.20(200)margineincrease5.23-5.69(201-219)5.20-6.21(200-239)Increse≥5.72(220)≥6.24(240)SerumLDL-CSuitbleleval≤3.12(120)3.38(130)margineincrease3.15-3.61(121-139)3.38-4.13(130-159)Increse≥3.64(140)≥4.16(160)serumHDL-CSuitbleleval1.04(40)≥1.56(60)IsanegativeriskfactorofCHDDecrese0.91(35)0.91(35)IsariskfactorofCHDSerumTGSuitbleleval≤1.70(150)2.26(200)margineincrease2.26-4.52(200-400)Increse1.70(150)4.52(400)Medicaldecisionlevelforli19TheclassificationoflipidlevelinATP-IIIoftheAmericanNationalcholeteroleducationproject,mmol/L(mg/dl)LDL-CTCHDL-CTGlevaljudgement<2.59(100)<5.20(200)<1.70(150)suitable2.59~3.34(100~129)approximtelysuitable3.38~4.13(130~159)5.20~6.21(200~239)1.70~2.25(150~199)nearhigh4.16~4.89(160~189)>6.24(240)1.56(60)2.26~5.64(200~499)high

4.92(190) 5.65(500)veryhigh<1.04(40)lowJAMA,2001,285(19):2486~2497Bloodlipidmmol/L(mg/dl)Theclassificationoflipidle20Unitconversionforclinicalroutineoflipiditems(primitiveunit→legalunit)TCmg/dl0.0259→mmol/LTGmg/dl0.0113→mmol/LHDL-Cmg/dl0.0259→mmol/LLDL-Cmg/dl0.0259→mmol/LapoAImg/dl0.01→g/LapoBmg/dl0.01→g/LLp(a)mg/dl10→mg/LUnitconversionforclinicalr21Theapplicationofclinicallipidassay

Detectinganddiagnosishyperlipidemiainearlierperiod.Assistingindiagnosisofatherosclerosis.Evaluationoftheriskofatherosclerosisdisease,suchasCHDandcerebralinfarction.Monitoringandassessingthetherapeuticefficacyofdiet,medicineandsoon.ThediagnosisofendrocrineexcretionmetabolicdisorderThediagnosisofhereditaryLipidsmetabolicdisorderHealthexaminationTheapplicationofclinicalli22Clinicalsignificanceoflipidassay(1)ThelevelofTCchangedwiththelivingcondition,itincreasedwiththeage,butdecreasedlightlyafter70yearsold.Itwashigherinyoungandmid-agedmenthanwomen，butinoldwomenitwashigherthanmen.Hypercholesterolemiawasanhighriskfactorofatherosclerosis,ThehigherthelevelofTC,theearlieronsetofCHD.Clinicalsignificanceoflipid23Clinicalsignificanceoflipidassay(2)TheriskofCHDwaslowerwhentheTCwaslessthan4.5mmol/L.ThelevelofTCinCHDpatientswasintherangeof5.0-6.5mmol/L,ThehigherthelevelofTC,theearlieronsetofCHD.Whenthecholesteroldecreaseby1%,theriskofCHDmaydecreaseby2%。Clinicalsignificanceoflipid24DiseasesaffectingthelevelofTC●Primitivefamilialhypercholesterolemia（LDL-Rdeficiency）

mixedhyperlipoproteinemisfamilialhyper-highdensitylipoproteinemia（CETPdeficiency）familialtypeⅢhyperlipidemiasecondary：endocrinedisease：hypothyreosis、DM（especialyincoma）、cushingdiseaseliverdisease：emphraxisicterus、hepatocarcinomakidneydisease：nephroticsyndrome、chronicitynephritisnephrotic、para-lipidnephrosisdrug-induced;useofsterolagent●Primitive

lackingβlipoproteinemiahypo-βlipoproteinemiaαlipoproteindeficiencyfamilialLCATdeficiencysecondary：severelivedisease：acutehepaticnecrosis、cirrhosisofliveendocrinedisease：

hyperthyreosis、severedystrophymalabsorptionsyndromsevereanermialeukermiacancerDiseasesaffectingthelevelo25

Cinicalsignificanceoflipidassay(2)ThelevelofTGwasrelatedtorace,age,sexandLivingcondition.what’smore,variationinthelevelofTGwasobviousthanthelevelofTCinthesameindividualandbetweenindividuals.Aftermeal,TGwasabsorbedandthencirculatingintheformofCM/VLDLintheblood.12hourslateraftermealitwasprecluded,andthelevelofTGreturnedtoinitiallevel.TGexistedinthebloodcirculationintheformofVLDL,ifVLDLconvertstosLDL,theriskofASwillincrease.Cinicalsignificanceofli26

Hypertriglyceridemiaprimary

hypertriglyceridemia

apoCⅡdeficencyLPLdeficency

familialhypertriglyceridemiaapoCⅡdificencyprimarytyoeVhypertriglyceridemia

famililialcompatedhyperlipidemiafamililialtypeⅣhyperlipidemiaidiopsthichypertriglyceridemiaapoEabnomalityapoE

deficency

Secondaryhypertriglyceridemiaautoimmuediseasethyroidhypofunctionalcoholabuse,autoimmuediseasedrugobesity、diabetesmellitusuraemia、oralcontraceptiveHypertriglyceridemiaprimary27TheleveloftheApoA1infastingserumofnormalcohortwasabout1.20~1.60g/L.

Generallyspeaking,theserumlevelofApoA1couldrepresenttheHDL.

ItwaspositivelycorrelatedtotheleveloftheHDL-C.InCHD&CVDpatients,theApoA1waslower.Infamilialhypertriglyceridemia,theHDL-Cwasusuallylower,buttheleveloftheApoA1wasuncertainanditdidnotincreasetheriskofCHD.

However,infamilialcombinedhyperlipidemia,boththeApoA1andHDL-CdecreasedlightlyandtheyincreasedtheriskofCHD.

Cinicalsignificanceoflipidassay(3)Cinicalsignificanceoflipid28TheleveloftheApoBinfastingserumofnormalcohortwasabout0.80~1.20g/L.Ingeneral,

theserumApoBmainlyrepresentedtheleveloftheLDL.ItwaspositivelycorrelatedtoLDL-C.Inhypertriglyceridemia(theVLDLwasveryhigh),smalldenseLDLincrease，ApoBwasmoreandthecholesterolless,sowecanseethelevelofLDL-Cwasnothigh，butserumApoBincreased.

SoApoBandLDL-Cneededtobedetectedatthesametime,itwashelpfultoclinicaldecision.Cinicalsignificanceoflipidassay(4)TheleveloftheApoBinfasti29Cinicalsignificanceoflipidassay(5)Richfattyandhighcaloriediet,seldom exercisesandmentalstressLDL-C↑TheLDLbelongedtothe

lipoproteinwhichcouldprediposetoatherosclerosis.Thehighthelevel,themoretheriskofatherosclerosis.TheleveloftheserumLDL-Cincreasedwithage.LDL-Cwasthechieftargetofpreventionoflipidemiaabnormality.Cinicalsignificanceoflipi30TheconcentrationofLp(a)wasregulatedbygene.Itwasnotaffectedbysex,age,drugandsoon.Individualdifferencewasobvious.（0～1000mg/L)

Lp(a)>300mg/Lwasabnormal(recommend)Lp(a)isanindependentriskfactorofatherosclerosisLp(a)increasedAcutephasereaction:AMI,operation,acutewound、acuteinflammation,laststageofnephrosis，nephroticsyndrome，maglinanttumorexceptforlivercancer，pregnancyandsoon.Cinicalsignificanceoflipidassay(6)TheconcentrationofLp(a)was31TheriskofASwashigherinlowHDL-Canemia.ThelowerthelevelofHDL-C,thehighertheriskofAS.WhentheHDL-Cdecreasedby1%,theriskofCHDmightincreaseby2%.Cinicalsignificanceoflipidassay(7)Cinicalsignificanceoflipid32ProgressionRegression??????HDLLDLVLDLIDLLp(a)RLPI’mgoodIftreatable,we’renotthatbad!TheGoodTheBadTheUgly?ProgressionRegression??????HDL33PlasmaHDL-Clevelwasaffectedbyfollowingdiseasessecondary：acutedisease:AMI、operation,adustum、acuteinflamationdietwithlowfatandhighsugarsmoking,obesityhypomotilityhormonedecreasedrug:βreceptorblockingphamaconsecondary

：alcoholabuseprimarybiliarycirhosisCETPactivityincreaseHTGLactivitydecreasedrug-induced：ACH、insulin、estrogen、Micotinamideanditsinductor、HMG-CoAreductaseblocker、chlorinatedhydrocarbons

primary

：

TangerdeseaseLCATdeficiencyapoAⅠsbnormalityfamilialhypercholesterolemiafamililialcompatedhyperlipidemiaprimary

：

CETPdeficiency

HTGLhypoactivity（maculaopacity）

apoA1synthesisaccenton

HDLreceptorabnormalityHDL-CdecreasedHDL-CinceasedPlasmaHDL-Clevelwasaffecte34

hereditaryLipidmetabolicdisorder

lipoproteingenedeficiencylipoproteinreceptorgenedeficiency

lipidmetabolicenzymegenedeficiencycytolysosomelipidmetabolismenzymegenedeficiencyCinicalsignificanceoflipidassay(8)hereditaryLipidmetabolicd35forinstance:Lysosomalhydrolasehereditarydefect,phospholipidmetabolismdisorderwereverycommon.

GeneanalysisoflysosomalstoragediseaseGeneanalysisoflysosomal36TheStructureandFunctionofLysosome

Lysosomewassuchakindoforganellelikeafilminthecell,withacystiformstructure,anditcontainedmanykindsofhydrolase,itworkedsothatitcanbreakdownmanykindsofendogenousandexogenoussubstance,soitwasalsoconsideredasapepticinthecell.

Phospholipidcouldbedividedintoglycerophospholipideandsphingolipid;thelattercouldbedividedintosphingomyelinandglycosylsphingolipid.

Thelysosomecontainedabout50kindsofhydrolase,suchasprotease,nuclease,glycosidase,lipase,phosphatase,phosphonolipidaseandsulfatidaseetc.TheStructureandFunctiono37鞘脂代谢Sphingolipidmetabolism鞘脂代谢Sphingolipidmetabolism38LysosomallipidsstoragedisordersdiseaseEnzymendefectStoredlipidClinicalsymptom(Fucosidosis)(Fucosidase)genelocus:1p34Cer-Glc-Gal-GalNAc-Gal-↓FucH-alloantigen(H-lsoantigen)cerebrumdegenerate，Convulsivetic，(Generalizedgangliosidosis)(GM1-β-galactosidase)genelocus:3pter-p21Cer-Glc-Gal(NeuAc)-GalNA--↓Gal(GM1Ganglioside)mentalaphrenia，skeletondeformhepatauxe，(Tay-Sachsdisease)(HexosaminidaseA)genelocus:15q13.1Cer-Glc-Gal(NeuAc)↓-GalNAc(GM2Ganglioside)mentalaphrenia，acroisaamyastheniaLysosomallipidsstoragedisor39Metachromaticleukodystrophy,MLD)(ArysulfataseA)genelocus:10q21.1Cer-Gal↓-OSO3(3-suffogalactosyl-ceramide)mentalaphrenia，mentalretardateinadult，demyelination(Krabbesdisease)(β-Galactosidase)genelocus:14q31

Cer↓-Gal(Galactosylceramide)mentalaphrenia:nearlynomyelin(Gaucherdisease,GD)(β-Glucosidase,β-glu)genelocus:1q21.1Cer-↓Glc(Glucosylceramidsplenohepatomegalia，Bonecausticize，mentalretardateinyougechildCer-Gal↓-OSO3mentalaphrenia，40(Niemann-Pickdisease)(Sphingomyelinase,ASM)genelocus:11p15.1-p15.4Cer-↓--_P-(Sphingomyelin)splenohepatomegalmentalretardateDieinyougechild(Farberdisease,)(Ceramidase)Acyl-↓(Ceramide)

Acyl-↓--(Ceramide)

NeuAc,(N-acetylneuraminicacid)；Cer，(ceramide)；Glc，(glucose)；Gal,(galactose)；Fuc，(fucose)；---↓enzymeactionsite(Niemann-Pickdisease)(Spletephysicalexamination2.cytologicalexaminationofmarrowandperipheralbloodcellsmainlyfindingthelargefoamcells.3.determinationofroutinebiochemicalindicatorespeciallythelipidlevelandfunctionalexaminationofliverandkidney.

Laboratorydiagnosisofhereditarylysosomallipidsstoragedisease

1.completephysicalexaminat42Gauchercell

Niemann-Pickcell？GauchercellNiemann-Pickcel43

4.lysosomalenzymeactivityassayChitotriosidase,CT↑

ToidentifydiagnosisofLipidsStorageDisease

GaucherdiseaseincreasedlightlyNiemann-Pickdiseasemorethan100timesSphingomyelinase↓

ToconfirmthediagnosisofNiemann-Pickdisease.Glucocerebrosidase↓

ToConfirmthediagnosisofGaucherdisease.

4.lysosomalenzymeactivity445.Highperformanceliquidchromatogram,HPLC

ToanalyzethecompositionoflipidsTodetecttheenzymesactivity6.PhysicalexaminationTocheckupthepathologicalchangesofliver,

spleen,skeletonandbrain.7.Geneanalysis

Ifthebasicmutationsresultedinthesubstitutionofamioacidsorthenucleotidedepletionsand/orinsertionswereidentified,youcangetafinaldiagnosis.5.Highperformanceliquidchr45ThelipiddetectionwhilethelevelofTCwasnormal

Serum:TC=VLDL-C+LDL-C+HDL-Cforinstance：AandBweretwopersontakenhealthyexamination

TC=VLDL-C+LDL-C+HDL-CA.TC=0.5+2.9+1.7=5.1B.TC=0.6+3.7+0.8=5.1A.TCisnormalHDL-C>0.9mmol/LLDL-C<3.12B.TCisnormalHDL-C<0.9mmol/LLDL-C>3.12SoBhaveahigherriskofASthanA.Thelipiddetectionwhilethe46

LipoproteinswhichresultedinAS

CMandVLDLremnantsModifiedLDL

SmalldenseLDL

Lp(a)

Lipoproteinswhichresultedi47LiverArteryTransportationofTCPhysiologicalfunctionsofHDLandLDLTransportationofTCLiverArteryTransportationofT48Non-HDL-C

InATPⅢ,non-HDL-CwasrecommendtoregardasasecondtreatmenttargetforhighTGpatient.Whenthechieftreatmenttargetarrived,whilethelevelofTGwasstillhigh(TG2.26mmol/L),non-HDL-CshouldbeassistedinminitoringtherapeuticefficiencyInATPⅢ,Patient,TGwasinmarginal(1.70~2.25mmol/L),wassuggestedtochangelifestyle,andneedn’ttocalculatenon-HDL-C.Non-HDL-C

49Thestandardvalueandtargetvalueforhyperlipidimiareceivedtreatment

(China1997)AS(-)

TC5.72

mmol/LOtherrisk（220.0mg/dl）

factor(-)

Ldl-c3.64

mmol/L

（140.0mg/dl）AS(-)TC5.2

mmol/LOtherrisk（200.0mg/dl）factor(+)Ldl-c3.12

mmol/L

（120.0mg/dl）AS(+)TC4.68mmol/L

（180.0mg/dl）

Ldl-c3.64

mmol/L

（100.0mg/dl）DrugtherapyDietTargetvalueTC6.24

mmol/L（240.0mg/dl）

Ldl-c4.16mmol/L（160.0mg/dl）

TC5.72

mmol/L（220.0mg/dl）

Ldl-c3.64

mmol/L（140.0mg/dl）

TC5.20

mmol/L（200.0mg/dl）

Ldl-c3.12

mmol/L（120.0mg/dl）TC<5.72

mmol/L（220.0mg/dl）

Ldl-c<3.64

mmol/L（140.0mg/dl）

TC<5.2

0mmol/L（200.0mg/dl）

Ldl-c<3.12

mmol/L（140.0mg/dl）

TC<4.68

mmol/L（180.0mg/dl）

Ldl-c<2.60

mmol/L（100.0mg/dl）Thestandardvalueandtarget50ThetargetvalueofTLCanddrugtherapyindifferentkindofCHD

(ATP2001)

RiskclassificationLDL-CLDL-CLDL-CtargetvalueonsetofTLCconsideringdrugtreatmentCHDorotherdangersign<2.59mmol/L

2.59mmol/L3,36mmol/L130mg/dl（10years-risk>20%）

100mg/dl100.0mg/dl）2.59.~3.36mmol/Lconsideringifdrugtreatmentneeded2＋riskfactor<3,36mmol/L3,36mmol/L10years-risk10%-20%(3,36mmol/L)10years-risk<20%130mg/dl130mg/dl10years-risk<10%(4,14mmol/L)

0－1riskfactor <4,14mmol/L4,14mmol/L4,91mmol/L,190mg/dl160mg/dl 160mg/dl4.14nmol/L-4.91nmol/L

consideringifdrugtreatmentneeded

ThetargetvalueofTLCanddr51ThetargetvalueandcutoffvaluefordrugtreatmentandTLCatdifferentriskinthemodifiedATPIIIbasedonrecentevivenceofclinicaltrials.NCEPReport.Circulation.2004:110;227-39Riskcategary LDL-CgoalonsetofTLCconsideringdrugtreatmenthighrisk：CHDandsoon（10yearrisk>20%）<100mg/dl，(canselectobjective：<70mg/dl)especiallypatientwithveryhighrisk)100mg/dl100mg/dl(<100mg/dl;mayregardmedicine)milddlingrisk：2＋riskagent（10yearsriskis10－20％）<130mg/dl(canselectobjective：<100mg/dl130mg/dl#130mg/dl(100-129md/dL;;mayregardmedicine)milddlingrisk：2＋riskagent（10yearrisk<10%）<130mg/dl130mg/dl160mg/dllowrisk：0－1riskagent<160mg/dl160mg/dl190mg/dl(160-190mg/dl；;mayregardmedicinedecresingLDL)Thetargetvalueandcutoffva52

payattentionto

severalproblemspayattentiontoseveralp53SeveralincorrectconceptsHDL-C≠HDLHDL-CismerelyapartofHDL，butcanreflecttheHDLinthebloodnLDL-C≠LDLLDL-CismerelyapartofLDL，butcanreflecttheLDLinthebloodSeveralincorrectconceptsHDL-54Reasonableselectionandapplicationoflipiditems

Clinicalroutinelipidsassayshouldincludeatleastfouritems:TC,TG,HDL-CandLDL-C.MerelymeasuredTCandTGcan’treflectbasiclipidslevelSomecaseswerenotsuitabletocalculateLDL-CbyFriedewaldformula⑴CMexistedinplasma；⑵TG4.52mmol/L(400mg/dl)；⑶Abnormalbeta-lipoproteinexistedtypeⅢhyperlipidemia(HLP)(1)Reasonableselectionandappli55ReasonableselectionandApplicationoflipiditems

(2)CasesneededtomeasureplasmaApoAIandApoB

：Unsureiftherewereanyriskfactorsinthepatientwithcardiovascularorcerebrovasculardisease,buttheroutinelipidsitemswerenormal.Theyouthandmiddle-agedmensufferingfromcardiovascularorcerebrovasculardisease.PersonshavethefamilyhistotyofearlyonsetofAS.FamilymemberwithlowApoAIandhighApoB.ReasonableselectionandAppli56ReasonableselectionandApplicationoflipiditems

(3)CasesneededtomeasureplasmaLp(a)Unsureiftherewereanyriskfactorsinthepatientwithcardiovascularorcerebrovasculardisease,buttheroutinelipidsitemswerenormal.Theyouthandmiddle-agedmensufferingfromcardiovascularorcerebrovasculardisease.PatientswiththefamilyhistotyofearlyonsetofAS.FamilymemberwithhighLp(a).ReasonableselectionandAppli57

HDL-CrepresentedthemetabolismstatusofcholesterolandtransportedbyHDL.ApoAIcanreflectthecapacityofHDL,butincreasingordecreasingofApoAIwasnotinproportiontoHDL-C.TomeasurethelevelofApoAIandHDL-Catonetimewashelpfultoanalyzethepathologicandphysicalstatus.ApoAIorHDL-CcannotrepresentHDL,theywereallnecessarytobemeasured.HDL-CandApoAIshoudnotreplacewitheachotherHDL-Crepresentedthemetabo58LDL-CandApoBshoudnotsubstituteforeachotherIngeneral,thelevelofApoBcanrepresentLDL,anditwasapositivecorrelationwithLDL－C.LDLwasakindoflipoproteinwhichcontaineddifferentsizeofparticlesanddiversecompositions,anditcanbedividedintoLDL1(typeA)andLDL2(typeB).Inhypertriglycerdemia,thelevelofthesmalldenseLDLmayincrease,LDL-CmaybenormalbutapoBelevatedobviously,sothetwoitemscan’tbesubstituteforeachother.LDL-CandApoBshoudnotsubst59Riskfactors≠diagnosticcriteriaLipidindexcanbeservedtoestimatetheriskofCHD,buttheywrenotdiagnosticcriteria.Weshouldavoidtouseriskfactorsfordiagnosticcriteria.Riskfactors≠diagnosticc60

PrevenionofhyperlipidemiashouldbeperformedfromfetalASmaybeginwithfetals,withthelivingconditionimprovement,obesitychildrenweremoreandmore,soweshouldpaycloseattentiontothehyperlipidemiainchildren,andshouldmonitorlipidlevelregularily.Prevenionofhyperlipidemi61

Administrationofhyperlipidemiainchildren

TC

optimumvalueofTC＜4.4mmol/L，criticalvalue4.4～5.1mmol/L，highvalue≥5.2mmol/L

L