1/132慢性胃炎(chronicgastritis（32慢性胃炎（慢性胃炎）32慢性胃炎(chronicgastritis（32慢性胃炎（慢性胃炎）第三節(jié)慢性胃炎（慢性胃炎）慢性胃炎系指不同病因引起的各種慢性胃粘膜炎性病變，是一種常見病，也是部隊多發(fā)病之一，其發(fā)病率在各種胃病中居首位自纖維內鏡廣泛應用以來，對本病認識有明顯提高。

慢性胃炎通常按其組織學變化和解剖部位加以分類，近年來還參照免疫學的改變，1982年在重慶召開的慢性胃炎會議擬訂了慢性胃炎的簡略分類：

①淺表性胃炎，炎癥僅及胃粘膜的表層上皮，包括糜爛、出血、須指明是彌漫性或局限性，后者要注明病變部位。

②萎縮性胃炎，炎癥已累粘膜深處的腺體并引起萎縮，如伴有局部增生，稱萎縮性胃炎伴過形成（增生）。

③肥厚性胃炎，這類胃炎是否存在，因無上皮細胞肥大的證據，故尚有爭論。

慢性胃炎還可根據胃粘膜病變以下四個方面的特征，作更詳細的分類，包括，①慢性胃炎的部位，如胃體、胃竇、賁門等。

②慢性胃炎的性質與分級，分為淺表性及萎縮性，后者又可分為輕、中、重度三級。

③胃炎活動的程度，根據胃粘膜上皮的中性粒細胞浸潤及退行性變，可定出活動期或靜止期，活動范圍又可分為彌漫性或局限性；④有無化生及其類型，化生分為腸腺化生（腸化）及假幽門腺化生，前者常見于萎縮性胃炎，偶可見于淺表性胃炎甚或正常粘膜，而后者僅見于萎縮性胃炎，是指胃體粘膜由胃竇粘膜所替代，常沿胃小彎向上移行，稱胃竇潛移。

1973年，思特里克蘭德及麥凱將萎縮性胃炎分為：

一型，抗壁細胞抗體（PCA）常陽性，以胃體病變?yōu)橹?，血清胃泌素增高，可發(fā)生惡性貧血。

B型，PCA常陰性，以胃竇病變?yōu)橹鳎逦该谒卣！?/p>

但據我國學者的研究，認為上述兩型病變難以截然分開，主張還是按病變部位分類較合理，即分為萎縮性胃炎以胃竇為主，及萎縮性胃炎以胃體為主的兩類。

病因及發(fā)病機理慢性胃炎的病因和發(fā)病機理尚未完全闡明，可能與下列因素有關：

一、急性胃炎的遺患急性胃炎后，胃粘膜病變持久不愈或反復發(fā)作，均可形成慢性胃炎。

二、刺激性食物和藥物長期服用對胃粘膜有強烈刺激的飲食及藥物，如濃茶、烈酒、辛辣或水楊酸鹽類藥物，或食時不充分咀嚼，粗糙食物反復損傷胃粘膜、或過度吸煙，菸草酸直接作用于胃粘膜所致。

三、十二指腸液的反流研究發(fā)現慢性胃炎患者因幽門括約肌功能失調，常引起膽汁反流，可能是一個重要的致病因素。

胰液中的磷脂與膽汁和胰消化酶一起，能溶解粘液，并破壞胃粘膜屏障，促使H＋及胃蛋白酶反彌散入粘膜，進一步引起損傷。

由此引起的慢性胃炎主要在胃竇部。

胃一空腸吻合術患者因膽汁返流而致胃炎者十分常見。

消化性潰瘍患者幾乎均伴有慢性胃竇炎，可能與幽門括約肌功能失調有關煙草中的尼古丁能使幽門括約肌松弛，故長期吸煙者可助長膽汁反流而造成胃竇炎。

四、免疫因素免疫功能的改變在慢性胃炎的發(fā)病上已普遍受到重視，萎縮性胃炎，特別是胃體胃炎患者的血液、胃液或在萎縮粘膜內可找到壁細胞抗體；胃萎縮伴惡性貧血患者血液中發(fā)現有內因子抗體，說明自身免疫反應可能是某些慢性胃炎的有關病因。

但胃炎的發(fā)病過程中是否有免疫因素參與，Inconclusive.Inaddition,atrophicgastritisofgastricmucosawithdiffuseinfiltrationoflymphocytesinvitrolymphoblastoidcelltransformationtestandleukocytemigrationinhibitiontestabnormalcellularimmuneresponsehasanimportantsignificanceintheoccurrenceofatrophicgastritis.Someautoimmunediseasessuchaschronicthyroiditisandhypothyroidismorhyperthyroidism,insulindependentdiabetes,chronicadrenalinsufficiencymaybeassociatedwithchronicgastritis,suggestingthatthediseasemayberelatedtoimmuneresponse.Five,1983WarrenandMarshallfoundthattheinfectionfactorsinpatientswithchronicgastritistogastricantrummucouslayerofepithelialcellsinsurfaceofHelicobacterpylori(Campylobacterpylori),thepositiveratewasashighas50-80%,reportsthebacteriumisfoundinnormalgastricmucosa.Wherethebacteriaareseeningastricmucosaininflammatorycellinfiltration,andthenumberofbacteriawaspositivelycorrelatedwiththedegreeof.Electronmicroscopyalsoshowedthatthenumberofepithelialcellsonthesurfaceoftheepithelialcellswasreducedorblunted.AntibodiesagainstHelicobacterpyloricanalsobefoundinthebloodandmucosaofthepatient.Thesymptomsandhistologicalchangescanbeimprovedorevendisappearedafterantibiotictreatment.Therefore,itisbelievedthatthisbacteriummaybeinvolvedinthepathogenesisofchronicgastritis.Butit’shardtosayforsure.PathologyAsuperficialgastritistogastricpitsandinflammationofmucouslayersurface.Thenakedeyeseesmucousmembranehyperemia,dropsy,orhastheexudation,mainlyseesinthestomachantrum,alsocanseeinthestomachbody,sometimesseesthesmallamountoferosionandthehemorrhage.Microscopically,therewereinfiltrationofneutrophils,lymphocytesandplasmacellsinthesuperficiallayerofthemembrane,andtheglandsinthedeeplayerremainedintact.Inaddition,somepatientshavemoreerosionsintheantrum,orareaccompaniedbyalargernumberofwarts,knownaschronicerosiveorverrucousgastritis.Two,atrophicgastritisinflammation,deepintothemucousmembrane,affectingthestomachgland,makeitatrophy,calledatrophicgastritis.Themucosaofthegastricmucosaisthinandthemucosafoldsflatordisappeared,whichcanbediffuseorlocalized.Microscopically,theglandsofthestomachdisappear,andtheindividualcancompletelydisappear.Thereisinfiltrationoflymphocytesandplasmacellsinthemucosaandsubmucosa.Sometimesmucosalatrophyhyperplasiacomplicatedbygastricfoveolarepithelium,causelocalmucouslayerbecomesthick,knownasatrophicgastritisformation.Ifinflammationspreadsextensively,destroyalargenumberofglands,makethewholestomachbodymucousmembraneatrophy,thin,callgastricatrophy.Atrophicgastritiscanoccurintestinalglandmetaplasiaandpseudopyloricmetaplasia,dysplasiaingastricpitsandintestinalepithelialhyperplasia(dysplasia).Dysplasiaisanabnormalmucosa,hasthecharacteristicsofatypicalcells,poorlydifferentiatedandmucousmembranestructuredisorder,thatislikelytobeprecancerouslesions.ClinicalmanifestationThediseaseisprogressingslowly,oftenrepeatedattacks,middle-agedandabovethegoodincidence,andwithageincreasedincidenceofdiseasetendency.Somepatientscannothaveanysymptoms,mostpatientscanhavevaryingdegreesofdyspepsiasymptoms,signsarenotobvious.Eachtypeofgastritishasdifferentmanifestations.Asuperficialgastritismayhavechronicirregularupperabdominalpain,abdominaldistension,belching,especiallyinthedietwasnotobvious,somepatientsmayhaveacidreflux,gastrointestinalbleeding,patientswithconfirmederosiveandgastroscopeVerrucousGastritis.Two,atrophicgastritisofdifferenttypes,differentpartsofitssymptomsarenotthesame.Lessgeneraldigestivetractsymptomsofgastricbodygastritis,sometimesappearanorexia,weightloss,glossitis,atrophyoftonguepapillae.Anemiaaccompaniedbyanemiaisrareinourcountry.Effectofatrophicgastritisofgastricantrumwhengastrointestinalsymptomsareobvious,especiallywithbilereflux,usuallypersistentupperabdominalpain,toeatafter,canvomitandsternumwithbilecontainingpainandburningsensation,sometimescanbeasmallamountofrecurrentuppergastrointestinalbleeding,andevenvomitingthissystem,gastricmucosalbarrierdamageandacutegastricmucosalerosioncausedby.Mostofthechronicgastritishavenoobvioussigns,andsometimestheyhavemildtendernessontheupperabdomen.LaboratoryandotherexaminationsAdeterminationofthegastricjuicesecretionofgastricjuiceanalysisbased(BAO)determinationoflargequantityofurinaryacidandincreasedhistamineorpentagastrinafterfive(MAO)andpeakurinaryacid(PAO)todeterminethegastricacidsecretion,helpsatrophicgastritisdiagnosisandtreatment.Superficialgastritis,gastricacidismorenormal,extensiveandseriousatrophicgastritis,gastricaciddecreased,especiallyinthestomachbodygastritisismoreobvious,stomachsinusitisisnormalormildobstruction.Superficial,suchasVerrucousGastritis,canalsohavegastricacidincreased.Two,theserologicaldetectionofchronicatrophicgastricinflammationofserumgastrinwasmoderatelyelevated,thisisduetolackofgastricacidsecretioninGcellsisnotinhibited.Ifthediseaseisserious,notonlyreducethesecretionofgastricacidandpepsinwasalsoreduced,intrinsicfactorsecretion,thusaffectingvitaminB12alsodecreased;serumPCAwasoftenpositive(morethan75%),chronicantralgastritisserumgastrindecreased,decreasedwithGcelldamageandserumPCA;alsohasacertainpositiverate(about30-40%).Three.Bariummealexaminationofgastrointestinaltractshoweddoublestructureofgastricmucosa,andtheatrophicmucosaofgastricmucosawasrelativelyflatanddecreased.TheX-raymanifestationsofgastricantrumgastritisshowedthattheantralmucosaofgastricantrumpresentedabluntserratedshapeandaspasticgastricantrum,orthepersistentstenosisoftheanteriorsegmentofthepylorusandthemucosalroughmass.TheX-rayfeaturesofVerrucousGastritischangeintoalarge,nodularfoldattheantrum,wheretherearebariumspotsinthecenterofsomefoldnodules.Four、gastroscopyandbiopsyarethemainmethodsforthediagnosisofchronicgastritis.Superficialgastritistogastricantrumismostobvious,morediffusegastricsurfacemucusincreased,withgraywhiteoryellowishwhiteexudate,mucosallesionsofredandwhiteormottled,likemeasleslikechange,sometimeshaveerosion.Atrophicgastritismucosashowedpaleorgrayishwhite,canalsoformaredandwhite,whitesag;plicasbecomefineorflat,duetothethinningofthemucousmembranecanseeavioletsubmucosalvascularlesions;diffuseormainlyinthegastricantrum,withproliferativechangesinthemucosalsurface,granularornodular.BiopsyspecimenshouldbeforpathologyandHelicobacterpyloridetection,ureasolutioncanbeafirstspecimeninphenolredinureasetestwaspositivein30-60minutessolutionturnspink,theotherwereculturedinspecialcultureliquid,inthemicroaerobicenvironment,thenweremadeintosections,staininginHEorWarthin-StarryorGieemsa.SectionsarevisibleinthemucouslayerintheformofmicropilesbendingisarrangedintheformofBacillus,filed.DiagnosisThesymptomsofchronicgastritishavenospecific,signsarefew,X-rayexaminationisusuallyhelpfultoexcludeotherstomachdiseases,sothediagnosisdependsongastroscopyandbiopsyofgastricmucosa.About5080%patientscanfindHelicobacterpyloriinthegastricmucosainchina.differentialdiagnosisFirst,thesymptomsofgastriccancer,chronicgastritis,suchaslossofappetite,epigastricdiscomfort,anemia,andsoon,asmallnumberofantralgastritisX-raysignsandgastriccancerisquitesimilar,specialattentionshouldbepaidtoidentify.Fiberopticgastroscopyandbiopsyarehelpfulformostpatients.Two,pepticulcerbothhavechronicupperabdominalpain,butmorethanpepticulcerabdominalregularity,cyclicalpainmainly,andchronicstomachpain,rarelyregular,andmainlyindigestion.IdentificationdependsonXraybariummealexaminationandgastroscopy.Three,chronicbiliarytractdiseasessuchaschroniccholecystitis,cholelithiasisoftenhavechronicrightupperabdominaldistension,belching,indigestionsymptoms,easilymisdiagnosedaschronicgastritis.However,thereisnoabnormalityinthegastrointestinalexamination.Four,otherdiseasessuchashepatitis,livercancerandpancreaticdiseasescanalsodelaythediagnosisandtreatmentbecauseofsymptomssuchaslossofappetiteandindigestion.Comprehensiveandsubtleexaminationandrelatedexaminationscanpreventmisdiagnosis.PreventionandcureMostsuperficialgastritiscanbereversedandasmallproportioncanbeconvertedtoatrophy.Atrophicgastritisgraduallyincreaseswithage,butcanalsobereversed.Therefore,thetreatmentofchronicgastritisshouldstartearlywithsuperficialgastritis,Atrophicgastritisshouldalsoadheretothetreatment.First,eliminatefactorsmaywipeoutallkindsofdisease,suchasdietandavoideatingdrugstrongstimulationofthegastricmucosa,quitdrinking.Payattentiontofoodhygieneandavoidovereating.Activetreatmentofchronicdiseasesofthemouth,noseandpharynx.Strengthenexercise,improvephysicalquality.Two,thepainmedicationavailableatropine,belladonnamixture,ofProulxBenSin,ofequalnitrogen.HyperaciditysuchasVerrucousGastritisofcimetidine,ranitidine,availableaminessuchasaluminumhydroxide.Ethyleneglycolisalocalanestheticthatinhibitsgastricantrumreleaseofgastrin