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第一个血清肌酸激酶500多,其他指标...
发布时间:2020-04-24 16:21:15 来源:网络整理

      参考文献:1.SimmonsZ,PeterlinBL,BoyerPJ,etal.MusclebiopsyintheevaluationofpatientswithmodestlyelevatedcreatinekinaselevelsJ.MuscleNerve,2003,27:242-244.2.PrelleA,TancrediL,SciaccoM,etal.RetrospectivestudyofalargepopulationofpatientswithasymptomaticorminimallysymptomaticraisedserumcreatinekinaselevelsJ.JNeurol,2002,249:305–311.3.KyriakidesT,AngeliniC,SchaeferJ,etal.EFNSguidelinesonthediagnosticapproachtopauci-orasymptomatichyperCKemiaJ.EurJNeurol,2010,17:767-773.4.BrewsterLM,MairuhuG,SturkA,etal.Distributionofcreatinekinaseinageneralpopulation:implicationsforstatintherapyJ.AmHeartJ,2007,154:655–661.5.NardinRA,ZarrinAR,HorowitzGL,etal.EffectofnewlyproposedCKreferencelimitsonneuromusculardiagnosisJ.MuscleNerve,2009,39:494-497.6.ReijneveldJC,GinjaarIB,FrankhuizenWS,etal.CAV3genemutationanalysisinpatientswithidiopathichyper-CKemiaJ.MuscleNerve,2006,34:656-658.7.Eeg-OlofssonO,KalimoH,Eeg-OlofssonKE,etal.DuchennemusculardystrophyandidiopathichyperCKemiainthesamefamilyJ.EurJPaediatrNeurol,2008,12:404-407.8.NguyenK,BassezG,KrahnM,etal.Phenotypicstudyin40patientswithdysferlingenemutations:highfrequencyofatypicalphenotypesJ.ArchNeurol,2007,64:1176-1182.9.FernandezC,dePaulaAM,Figarella-BrangerD,etal.DiagnosticevaluationofclinicallynormalsubjectswithchronichyperCKemiaJ.Neurology,2006,66:1585-1587.10.ZouvelouV,MantaP,KalfakisN,etal.Asymptomaticelevationofserumcreatinekinaseleadingtothediagnosisof4q35facioscapulohumeralmusculardystrophyJ.JClinNeurosci,2009,16:1218-1219.11.洪道俊,张巍,姜腾勇,等.结卵白基因剧变相干性心肌病五家系临床和遗传特征J.华心血脉期刊,2010,38:420-424.12.SpiekerkoetterU.EffectsofafatloadandexerciseonasymptomaticVLCADdeficiencyJ.JInheritMetabDis,2007,30:405.13.VavouranakisI,GanotakisES,MantaP,etal.ElevatedcreatinekinaselevelsinapatientwithcoronaryarterydiseaseandasymptomaticMcArdlesdiseaseJ.IntJCardiol,2007,115:114-115.14.BrunoC,BertiniE,SantorelliFM,etal.HyperCKemiaastheonlysignofMcArdlesdiseaseinachildJ.JChildNeurol,2000,15:137-138.15.TaanmanJW,KateebI,MuntauAC,etal.AnovelmutationinthedeoxyguanosinekinasegenecausingdepletionofmitochondrialDNAJ.AnnNeurol,2002,52:237-239.16.Pantoja-MartínezJ,NavarroFernández-BalbuenaC,Gormaz-MorenoM,etal.MyoadenylatedeaminasedeficiencyinachildwithmyalgiasinducedbyphysicalexerciseJ.RevNeurol,2004,39:431-434.17.LillengH,AbelerK,JohnsenSH,etal.Variationofserumcreatinekinase(CK)levelsandprevalenceofpersistenthyperCKemiainaNorwegiannormalpopulation.TheTromsøStudyJ.NeuromusculDisord,2011,21:494-500.18.PunukolluB,RutherfordH.SerumcreatinekinaseelevationassociatedwitholanzapinetreatmentJ.BMJCaseRep,2008,2008:bcr0620080040.19.MorandiL,AngeliniC,PrelleA,etal.Highplasmacreatinekinase:reviewoftheliteratureandproposalforadiagnosticalgorithmJ.NeurolSci,2006,27:303-311.20.GeorgeG.Hypothyroidismpresentingaspuzzlingmyalgiasandcrampsin3patientsJ.JClinRheumatol,2007,13:273-275.21.BrewsterLM,deVisserM.PersistenthyperCKemia:fourteenpatientsstudiedinretrospectJ.ActaNeurolScand,1988,77:60-63.22.IshikawaT,InagakiH,KanayamaM,etal.Hypocalcemichyper-CK-emiainhypoparathyroidismJ.BrainDev,1990,12:249-252.23.WeglinskiMR,WedelDJ,EngelAG.MalignanthyperthermiatestinginpatientswithpersistentlyincreasedserumcreatinekinaselevelsJ.AnesthAnalg,1997,84:1038-1041.24.HongD,LuanX,ChenB,etal.BothhypokalaemicandnormokalaemicperiodicparalysisindifferentmembersofasinglefamilywithnovelR1129QmutationinSCN4AgeneJ.JNeurolNeurosurgPsychiatry,2010,81:703-704.25.DabbyR,SadehM,HermanO,etal.AsymptomaticorminimallysymptomatichyperCKemia:histopathologiccorrelatesJ.IsrMedAssocJ,2006,8:110-113.26.MalandriniA,OrricoA,GaudianoC,etal.MusclebiopsyandinvitrocontracturetestinsubjectswithidiopathicHyperCKemiaJ.Anesthesiology,2008,109:625-628.27.CapassoM,DeAngelisMV,DiMuzioA,etal.Familialidiopathichyper-CKemia:anunderrecognizedconditionJ.MuscleNerve,2006,33:760-765.28.RestivoDA,PavoneV,NicotraA.Single-fiberelectromyographyinhyperCKemia:thevalueoffiberdensityJ.NeurolSci,2011.Epubaheadofprint.29.ReijneveldJC,NotermansNC,LinssenWH,etal.Benignprognosisinidiopthichyper-CKemiaJ.MuscleNerve,2000,23:575-579.30.DAddaE,SciaccoM,FrugugliettiME,etal.Follow-upofalargepopulationofasymptomatic/oligosymptomatichyperckemicsubjectsJ.JNeurol,2006,253:1399-1403.__归来搜狐,查阅更多义务编者:,非常提示:正文情节仅供初步参考,免不了在疏漏、错等情形,请您核实后再引证。

      如常情况下,绝大大部分肌酸激酶坐落肌细胞内,血液中肌酸激酶上升普通提示已有肌有害或正发生肌有害的症候。

      ---|Serumcreatinekinase(CK),perceiveddelayedonsetmusclesoreness(DOMS),andmaximalquadricepsisometricforce(MIF)weredeterminedbeforeexerciseand24,48,and72hafterexercise.---TheeffectofhydrocortisoneontheserumcreatinekinaseactivityofmusclesdiseasesIntravenousadministrationofasingledoseofhydrocortisonetopatientswiththeDuchennetypeofprogressivemusculardystrophy,carriersofDuchennedystrophygenecausedashort-lastingriseoftheserumcreatinekinaseactivity.Onlythekneejerkswerediminished,thecalveshypertrophic,andtheserumcreatinekinaselevelveryhighinonecase,andtherewereneurogenicelectromyographicabnormalitiesinthequadriceps.SerumcreatinekinaseBsubunitlevelsinneurogenicatrophies更多Theactivityofserumcreatinephosphokinasegreatlyincreasedafterthereperfusion,andthisincreasewassignificantlysuppressedbyNisoldipine.---PolymericthiolsasenzymeactivatorsofserumcreatinephosphokinaseEffectofcortisolonserumcreatinephosphokinaseactivityindisuseatrophyIron(III)alsosignificantlybluntedtheriseofserumcreatinephosphokinase,anindexofmyocardialdamage.administrationofSM-198110beforeischaemia,withasignificantreductioninserumcreatinephosphokinaseactivity.更多其它---点击这边查问相干文摘|,你好这种情况需求组合你干吗要做这检讨来断定人体内多种机构和官内含有肌酸激酶其分布不均要紧分布在骨头架子肌的肌纤维内故此移动易于使血清肌酸激酶活性上升其因是因移动时缺氧代谢产物堆供能相对不值等因唤起肌细胞膜通透性上升或肌细胞膜遭遇损伤驱使酶从细胞内开释增多酶进血液轮回内中尤以肌牵拉的教条性损伤或发生血肿等因较为重否则同的移动负载囊括长相距自天车、滑雪及马拉松跑对教条性反应较大得以招致血清肌酸激酶的活性上升非常是大强度的马拉松跑后4小时后肇始上升8小时达高峰跳、短跑等短时刻激烈移动是冲锋性移动也唤起血清肌酸激酶活性上升运誓师在竞赛后肌酸激酶可上升至734IU/L随行人员(如常值200IU/L以次)与急遽心肌梗死病家数值近似但是运誓师血清肌酸激酶来自骨头架子肌为了幸免移动后血清肌酸激酶的上升检讨血清肌酸激酶时应幸免激烈的移动免于临床误看病况辨析:肌酸激酶(CreatineKinase,CK)(ATP:CreatineN-phosphotransferaseEC2.7.3.2)平常存取决众生的心、肌以及脑等机构的细胞浆和线粒体中,是一个与细胞内能运行、肌缩、ATP还魂有径直瓜葛的紧要激酶1,2,它可逆地催化肌酸与ATP之间的转磷酰基反应。

      心肌酶谱是存取决心肌的多种酶的总称,普通有肌酸激酶(CK),天门冬氨酸氨基转移酶(AST),和乳酸脱氢酶(LDH),心肌损伤或坏死后这些酶有不一样档次的开释到血清中。

      点意见:你好,你的肌酶的确很高,你如其没心病症,以及肝病症的话,应当考虑肌的损伤所造成的肌酶的上升,提议你两周后再次检讨肌酶情况。

      临用前用蒸馏水作20倍稀释。

      ③Mg2+为激活剂,半胱氨酸供巯基,氢氧化钡和硫酸锌沉淀卵白并中和反应。

      正文对无症候高CK血症CK值的界定、病源、肌病理、肌电图、治疗和预后等上面进展综述。

      离子通途病是无症候高CK血症的另一个紧要因,非常是在骨头架子肌钠通途剧变招致的各类别型的肌强直患者中,部分患者仅仅展现为重复的高CK血症,而无显明的肌绵绵软肌强直象24。

      1拼音xuèqīngjīsuānjīméi2英文参考SCKserumcreatinekinase3概述肌酸激酶(CK)别称肌酸磷酸激酶,能可逆地催化肌酸和三磷酸腺苷生成磷酸肌酸和二磷酸腺苷的反应。

      在肌养分不良素(dystrophin)剧变招致的抗肌萎缩卵白病(dystrophinopathy)临床分型中,高CK血症被独自地名列一样临床亚型,并且在同一个家系内不一样的患者既得以展现为杜氏型肌养分不良,也得以展现为无症候高CK血症7。

      Capasso等27对10例特发性高CK血症患者的肌标本钻研发觉,其要紧病理变更为不一样品类肌纤维的老幼变更(2A型纤维宽大,1型纤维萎缩)和分布不一样(2A型纤维优势,2B型纤维减去)。

      短句起源Therelationshipbetweentheexcitedbehaviorofschizophreniapatientsandtheactivityofserumcreatinephosphokinase.实质瓦解症提神行止与血清肌酸激酶活性的瓜葛短句起源ClinicalAnalyzeonAbnormalSerumCreatinePhosphokinaseforPatientswithIdiopathicHypokalemicPeriodicParalysis原发性低钾型周期性松懈患者血清肌酸激酶非常的临床辨析短句起源更多Theresultshowedthatthecombinativeuseofbloodredproteinandbloodcarbamidenitrogencouldaccuratelyassessboxingathletesphysiqueconditionandbloodserumkinasecouldeffectivelyassessthestimulationdegreethatmusclessufferedaftercycletraining.---后果表明,血红卵白与血脲氮组合应用,能较准地评比拳击运誓师的人机能气象,血清肌酸激酶能有效评比周期训后肌所受的刺档次。

      北京大学习者民卫生院神经内科洪道俊1无症候高CK血症CK值的界定除病症态外,人血清CK值与被检者的年纪、性、人种、肌体积相干,普通来说男高于女,黑人高于白人,其它人种与白人的CK值无统计学差异3。

      Malandrini等26发觉37例无症候高CK血症患者中活检后果异常者34例,其异常变更要紧为纤维老幼变更占67.6%,核内移占35.1%。

      极个别患者在急遽期因惨本位律反常、急遽心力衰竭和心源性虚脱而死亡。

      答共1条医生对答因不许面诊,医生的提议及药物引荐仅供参考职称:主治医生-来自:黑龙江省伊春市桃山林管局职工卫生院内科情况辨析:你好,这种情况眼前如其没特殊的症候和体征的话,亲密留意观测的就得以了。

      _答_病况辨析:您好,患者的检讨后果考虑肾病综合症的可能大,不排除一过性卵白尿。

      不一样的文献对无症候高CK血症钻研时对CK值的界定都不一样,所以,2010年欧洲神经病学歃血为盟因对眼前大范本好人丛的CK分布通讯,将无症候高CK血症CK值规定为:血清CK值大于如常高限的1.5倍3。

      2016-05-1114:25:59相干问答_问_铁卵白610,其它指标如常。