EASL乙肝诊治指南英文Word文档下载推荐.docx
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EASL乙肝诊治指南英文Word文档下载推荐.docx
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forCHB;
thusareasofuncertaintyexist.Atthe
presenttimeclinicians,patientsandpublichealthauthorities
mustcontinuetomakechoicesonthebasisofevidence
thatisnotfullymatured.
2.Context
2.1.
Epidemiology
and
public
health
burden
Approximatelyonethirdoftheworld’spopulation
hasserologicalevidenceofpastorpresentinfectionwith
HBVand350millionpeoplearechronicallyinfected.
Thespectrumofdiseaseandnaturalhistoryofchronic
HBVinfectionisdiverseandvariable,rangingfroma
lowviremicinactivecarrierstatetoprogressivechronic
hepatitis,whichmayevolvetocirrhosisandhepatocellular
carcinoma(HCC).HBV-relatedendstageliverdis
*
EASLoffice,7ruedesBattoirs,CH1205Geneva,Switzerland.
Tel.:
+41228070360;
fax:
+41223280724.
address:
easloffice@easloffice.eu
easeorHCCareresponsibleforover1milliondeaths
peryearandcurrentlyrepresent5–10%ofcasesofliver
transplantation[2–5].Hostandviralfactors,aswellas
coinfectionwithotherviruses,inparticularhepatitisC
virus(HCV),hepatitisDvirus(HDV),orhumanimmunodeficiency
virus(HIV)togetherwithotherco-morbidities
includingalcoholabuseandoverweight,can
affectthenaturalcourseofHBVinfectionaswellas
theefficacyofantiviralstrategies.
CHBmaypresenteitherashepatitisBeantigen
(HBeAg)-positiveorHBeAg-negativeCHB.HBeAgpositive
CHBisduetoso-called‘‘wildtype”
HBV.It
typicallyrepresentstheearlyphaseofchronicHBV
infection.HBeAg-negativeCHBisduetoreplication
ofnaturallyoccurringHBVvariantswithnucleotide
substitutionsintheprecoreand/orbasiccorepromoter
regionsofthegenomeandrepresentsalaterphaseof
chronicHBVinfection.TheprevalenceoftheHBeAgnegative
formofthediseasehasbeenincreasingover
thelastdecadeasaresultofHBV-infectedpopulation
agingandrepresentsthemajorityofcasesinmany
areas,includingEurope[6–8].
MorbidityandmortalityinCHBarelinkedtopersistence
ofviralreplicationandevolutiontocirrhosisor
HCC.LongitudinalstudiesofpatientswithCHBindicate
that,afterdiagnosis,the5-yearcumulativeincidence
ofdevelopingcirrhosisrangesfrom8to20%.
The5-yearcumulativeincidenceofhepaticdecompensation
isapproximately20%withthe5-yearprobabilityof
Contributors:
ClinicalPracticeGuidelinesPanel:
PatrickMarcellin,
GeoffreyDusheiko,FabienZoulim,RafaelEsteban,StefanosHadziyannis,
PietroLampertico,MichaelManns,DanielShouval,Cihan
Yurdaydin;
Reviewers:
AntonioCraxi,XavierForns,DariusMoradpour,
Jean-MichelPawlotsky,JoergPetersen,HeinerWedemeyer.
0168-8278/$34.00
.
2009
Published
by
Elsevier
B.V.
on
behalf
of
the
European
Association
for
Study
Liver.
doi:
10.1016/j.jhep.2008.10.001
Liver
/
Journal
Hepatology
50
(2009)
227–242
survivalbeingapproximately80–86%inpatientswith
compensatedcirrhosis[4,9–13].Patientswithdecompensated
cirrhosishaveapoorprognosiswitha14–35%
probabilityofsurvivalat5years.Theworldwideincidence
ofHCChasincreased,mostlyduetoHBVand
HCVinfections;
presentlyitconstitutesthefifthmost
commoncancer,representingaround5%ofallcancers.
TheannualincidenceofHBV-relatedHCCinpatients
withCHBishigh,rangingfrom2%to5%whencirrhosis
isestablished[13].However,theincidenceofHBV-
relatedHCCappearstovarygeographicallyandcorrelates
withtheunderlyingstageofliverdisease.
Populationmovementsandmigrationarecurrently
changingtheprevalenceandincidenceofthediseasein
severallowendemicitycountriesinEuropeandelsewhere.
Substantialhealthcareresourceswillberequired
forcontroloftheworldwideburdenofdisease.
2.2.
Natural
history
ChronichepatitisBisadynamicprocess.Thenatural
historyofCHBcanbeschematicallydividedintofive
phases,whicharenotnecessarilysequential.
(1)The‘‘immunetolerant”
phaseischaracterizedby
HBeAgpositivity,highlevelsofHBVreplication
(reflectedbyhighlevelsofserumHBVDNA),normal
orlowlevelsofaminotransferases,mildorno
livernecroinflammationandnoorslowprogression
offibrosis[3,5].Duringthisphase,therate
ofspontaneousHBeAglossisverylow.Thisfirst
phaseismorefrequentandmoreprolongedinsubjects
infectedperinatallyorinthefirstyearsoflife.
Becauseofhighlevelsofviremia,thesepatientsare
highlycontagious.
(2)The‘‘immunereactivephase”
ischaracterizedby
HBeAgpositivity,alowerlevelofreplication(as
reflectedbylowerserumHBVDNAlevels),
increasedorfluctuatinglevelsofaminotransferases,
moderateorseverelivernecroinflammation
andmorerapidprogressionoffibrosiscompared
tothepreviousphase[3,5].Itmaylastforseveral
weekstoseveralyears.Inaddition,therateof
spontaneousHBeAglossisenhanced.Thisphase
mayoccurafterseveralyearsofimmunetolerance
andismorefrequentlyreachedinsubjectsinfected
duringadulthood.
(3)The‘‘inactiveHBVcarrierstate”
mayfollowseroconversion
fromHBeAgtoanti-HBeantibodies.It
ischaracterizedbyveryloworundetectableserum
HBVDNAlevelsandnormalaminotransferases.
Asaresultofimmunologicalcontroloftheinfection,
thisstateconfersafavourablelong-termoutcome
withaverylowriskofcirrhosisorHCCin
themajorityofpatients.HBsAglossandseroconversion
toanti-HBsantibodiesmayoccurspontaneously
in1–3%ofcasesperyear,usuallyafter
severalyearswithpersistentlyundetectableHBV
DNA[14].
(4)‘‘HBeAg-negative
CHB”
fromHBeAgtoanti-HBeantibodiesduring
theimmunereactivephaseandrepresentsalater
phaseinthenaturalhistoryofCHB.Itischaracterized
byperiodicreactivationwithapatternof
fluctuatinglevelsofHBVDNAandaminotransferases
andactivehepatitis.Thesepatientsare
HBeAg-negative,andharbourHBVvariantswith
nucleotidesubstitutionsintheprecoreand/orthe
basalcorepromoterregionsunabletoexpressor
expressinglowlevelsofHBeAg.HBeAg-negative
CHBisassociatedwithlowratesofprolonged
spontaneousdiseaseremission.Itisimportant
andsometimesdifficulttodistinguishtrueinactive
HBVcarriersfrompatientswithactiveHBeAgnegative
CHBinwhomphasesofspontaneous
remissionmayoccur.Theformerpatientshavea
goodprognosiswithaverylowriskofcomplications,
whilethelatterpatientshaveactiveliverdisease
withahighriskofprogressiontoadvanced
hepaticfibrosis,cirrhosisandsubsequentcomplications
suchasdecompensatedcirrhosisand
HCC.Acarefulassessmentofthepatientisneeded
andaminimalfollow-upofoneyearwithserum
alanineaminotransferase(ALT)andHBVDNA
levelsevery3monthsusuallyallowsdetectionof
fluctuationsofactivityinpatientswithactive
HBeAg-negativeCHB[15].
(5)Inthe‘‘HBsAg-negativephase”
afterHBsAgloss,
low-levelHBVreplicationmaypersistwithdetectable
HBVDNAintheliver[16].Generally,HBV
DNAisnotdetectableintheserumwhileanti-
HBcantibodieswithorwithoutanti-HBsare
detectable.HBsAglossisassociatedwithimprovement
oftheoutcomewithreducedriskofcirrhosis,
decompensationandHCC.Theclinicalrelevance
ofoccultHBVinfection(detectableHBVDNA
intheliverwithlow-level[<
200internationalunits
(IU)/ml]HBVDNAinblood)isunclear[16].
Immunosuppressionmayleadtoreactivationin
thesepatients[17,18].
3.Methodology
TheseEASLCPGshavebeendevelopedbyaCPG
PanelofexpertschosenbytheEASLGoverningBoard;
therecommendationswerepeer-reviewedbyexternal
expertreviewersandapprovedbytheEASLGoverning
Board.TheCPGshavebeenbasedasfaraspossibleon
evidencefromexistingpublications,and,ifevidencewas
unavailable,theexperts’personalexperienceandopinion.
Manuscriptsandabstractsofimportantmeetings
publishedpriortoAugust2008havebeenevaluated.erantphasehavepersistentlynormalALTlevelsanda
TheevidenceandrecommendationsintheseguidelinesproportionofpatientswithHBeAg-negativeCHBmay
havebeengradedaccordingtotheGradingofRecom-haveintermittentlynormalALTlevels.Therefore
mendationsAssessmentDevelopmentandEvaluationappropriate,longitudinallong-termfollow-upiscrucial.
(GRADE)system.Thestrengthofrecommendations
thusreflectsthequalityofunderlyingevidence.The
(1)Theassessmentoftheseverityoftheliverdisease
principlesoftheGRADEs
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