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1、IntensiveCareMed(2018)44:231–234DOI10.1007/s00134-017-4845-6UNDERSTANDINGTHEDISEASEUnderstandinghepaticencephalopathyNicolasWeiss1,2,3*,RajivJalan4andDominiqueThabut1,2,5©2017Springer-VerlagBerlinHeidelbergandESICMHepaticencephalopathy(HE)isdeinedasa
2、neurologi-proposed(e.g.,glycerolphenylbutyrate,l-ornithine-caloraneuropsychologicalcomplicationcausedbyliverl-aspartate).Accordingtoitsosmoticpotential,theacutediseaseorportosystemicshunting.heclinicalspectrumintracytoplasmicincreaseofglutamineinALFi
3、srespon-ishighlyvariablerangingfrommildneuropsychologicalsibleforcytotoxicedemaafectingtheastrocytesandfordisturbancestocoma[1].Dependingupontheunderly-vasogenicedemawhentheblood–brainbarrier(BBB)ingliverdisease,HEisclassiiedintothreetypes:typeA,isal
4、tered[3,5].Incirrhosis,theglutamineincreaseissecondarytoacuteliverfailure(ALF);typeB,secondarygradualandastrocytesrespondbyprogressivelyextrud-toportosystemicshunting;andtypeC,secondarytocir-ingintracytoplasmicmyoinositolandtaurinetotryandrhosisinthe
5、presenceornotofshunting[2].hemostmaintainosmoticequilibrium.hislargelyexplainswhyrecenthumanandanimaldataconirmedthepreviouslybrainedemaisrarelypresentincirrhosisand/orinacute-supposedroleofhyperammonemia,butalsooutlinestheon-chronicliverfailure(ACLF
6、)[6,7].Inneurons,glu-roleofassociatedfactorslikeinlammationinthedevel-tamineisdeaminatedintoglutamate,themostimportantopmentofHE(Fig. 1).excitatoryneurotransmitterinthebrain,thatstimulateshemainsourceofammonia(NH+)intheportalsys-neurons[8].hiscouldac
7、countforanxiousbehavior,agi-4temhaslongbethoughttobeintestinalbacterialproduc-tation,orseizuresinALF.Incontrast,incirrhosis,com-tionexplainingtheuseofnon-absorbabledisaccharidespensatorymechanismsareresponsibleforadecreased(e.g.,lactulose)andnon-abso
8、rbableantibiotics(e.g.,expressionofbothglutamatecarriers(GLT-1)andglu-rifaximin)[3].Recentdatashows,however,thatthemaintamatepost-synapticreceptorsthatexplainsslowing,sourceisglutaminecatabolismbyglutaminaseinthegutsleepiness,andalteredconsciousness.
