简介:Historically,mastcellswereknownasakeycelltypeinvolvedintypeIhypersensitivity.Untillasttwodecades,thiscelltypewasrecognizedtobewidelyinvolvedinanumberofnon-allergicdiseasesincludinginflammatoryboweldisease(IBD).MarkedlyincreasednumbersofmastcellswereobservedinthemucosaoftheileumandcolonofpatientswithIBD,whichwasaccompaniedbygreatchangesofthecontentinmastcellssuchasdramaticallyincreasedexpressionofTNFα,IL-16andsubstanceP.TheevidenceofmastcelldegranulationwasfoundinthewallofintestinefrompatientswithIBDwithimmunohistochemistrytechnique.ThehighlyelevatedhistamineandtryptaselevelsweredetectedinmucosaofpatientswithIBD,stronglysuggestingthatmastcelldegranulationisinvolvedinthepathogenesisofIBD.However,littleisknownoftheactionsofhistamine,tryptase,chymaseandcarboxypeptidaseinIBD.Overthelastdecade,heparinhasbeenusedtotreatIBDinclinicalpractice.Thelowmolecularweightheparin(LMWH)waseffectiveasadjuvanttherapy,andthepatientsshowedgoodclinicalandlaboratoryresponsewithnoseriousadverseeffects.TherolesofPGD2,LTC4,PAFandmastcellcytokinesinIBDwerealsodiscussed.Recently,aseriesofexperimentswithdispersedcolonmastcellssuggestedthereshouldbeatleasttwopathwaysinmanformastcellstoamplifytheirownactivation-degranulationsignalsinanautocrineorparacrinemanner.Thehypothesisisthatmastcellsecretogoguesinducemastcelldegranulation,releasehistamine,thenstimulatetheadjacentmastcellsorpositivelyfeedbacktofurtherstimulateitshostmastcellsthroughH1receptor.Whereasreleasedtryptaseactssimilarlytohistamine,butactivatesmastcellsthroughitsreceptorPAR-2.Theconnectionsbetweencurrentanti-IBDtherapiesorpotentialtherapiesforIBDwithmastcellswerediscussed,implicatingfurtherthatmastcellisakeycelltypethatisinvolvedinthepathogenesisofIBD.Inconclusion,whilepathoge
简介:LongbeforethediscoveryofHelicobacterpylori,thereweremanyexcellentobservationalstudiesthatdocumenteddifferencesinthepatternsofgastroduodenaldisease.Itwasclearthatinthedevelopingworld,gastriculcerandgastriccancerweremorecommonthaninthedevelopedworldwhereduodenalulcerpredominated.Thiscorrelatedwiththedistributionofgastritisinduodenalulcerpatientswheretheinflammationwasantralpredominantwhileingastriculcerpatientsthegastritiswasmoreevenlydistributedthroughthestomach.Gastriculcersusuallyappearedinafairlyrestricteddistributioninthestomachneartheangulusandclosetothetransitionalzonebetweenantrumandbodymucosa.Asasocietydevelopedsothesepatternsofdiseasechanged.
简介:一、前言乙型肝炎病毒(HBV)和丙型肝炎病毒(HCV)感染在肝细胞癌(HCC)的发生发展中起重要作用。我国近年发布的《慢性乙型肝炎防治指南(2010版)》和《原发性肝癌诊疗规范(2011版)》都强调了肝癌患者抗病毒治疗的重要性,但未作深入具体阐述。《丙型肝炎防治指南(2004版)》也注意到抗病毒治疗延缓HCC的发生。有鉴于此,中华医学会肝病学分会肝癌学组召开了三次专题讨论会,系统收集分析了现有HCC综合治疗中抗病毒治疗的临床研究文献,回顾了HCC治疗中抗病毒药物临床应用进展,依据现有病毒相关性HCC抗病毒治疗的循证医学临床资料,综合部分专家的意见,按照循证医学证据分级的GRADE系统(表1)进行细化和补充,针对这些患者抗病毒治疗的应用达成共识,提出如下具体建议,供国内同道参考,以期在临床实践过程中依据新的临床医学证据进行修改和更新,进一步完善《原发性肝癌诊疗规范》、《慢性乙型肝炎防治指南》和《丙型肝炎防治指南》的实施。
简介:目的探讨老年非肝病患者肝功能指标的临床特征。方法纳入A组150例为〈60(46.83±6.08)岁,B组222例为60-74(65.89±4.61)岁和C组278例为〉/75(82.91±4.77)岁患者。常规检测肝功能指标。结果B组患者血清丙氨酸氨基转移酶(ALT)、γ谷氨酰转肽酶(GGT)、碱性磷酸酶(ALP)分别为(24.35±28.82)U/L、(36.45±34.23)U/L、(78.44±35.44)U/L,均分别高于A组的[(17.85±9.65)U/L、(28.38±22.23)U/L、(72.78±28.79)U/L,P〈0.05]和C组的[(17.72±12.05)U/L、(28-31±19.04)U/L、(70.36±20.04)U/L,P〈0.01];血清总胆汁酸(TBA)、血清白蛋白(ALB)、血清总蛋白(TP)、血清前白蛋白(PA)水平在A、B、C组呈现出依次下降趋势(P(0.05或P〈0.01);B组和C组基础疾病患病率分别为74.77%和179.50%,显著高于A组的32.67%(P〈0.01),合并罹患多种基础疾病的比例也随年龄呈上升趋势。结论60岁-74岁老年组肝功能异常突出,随年龄增长肝脏合成和代谢等功能降低,尤其是蛋白合成功能降低更明显,基础疾病患病率明显升高,提示临床上应慎用加重肝脏负担的药物,避免药物性肝损伤的发生,并注重营养支持治疗。