Hypertensive LES.docx
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Hypertensive LES.docx
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HypertensiveLES
Hypertensiveloweresophagealsphincter(HLES):
Prevalence,symptomsgenesisandeffectofpneumaticballoondilatation
NabilAGadEl-Hak1,MohamedMostafa1,HusseinAbdelHamid2,MagdyHaleem1
1 GastroenterologySurgicalCenter,MansouraUniversity,Mansoura,Egypt
2 Al-AzharUniversity,Cairo,Egypt
Abstract
Background:
Summaryandbackgrounddata:
TheHypertensiveloweresophagealsphincter(HLES)isanunusualprimarymotordisorderoftheesophagus.Thesignificanceofthismotilitydisorderisstillquestionable.Objective:
Theobjectiveswere:
(a)identificationoftheprevalenceofHLESinthesepatients,(b)identificationofthecommonpresentingsymptomsofHLES,(c)studyofthecorrelationofthesymptomswithLESPand(d)studyoftheeffectivenessofpneumaticballoondilationincasesthatfailtorespondtomedicaltreatment.Methods:
Aretrospectivestudythatincludesfourthousandonehundredandseventypatients,whoweresubjectedtoesophagealmanometryintheperiodfromJanuary1994toDecember2003,amongwhomsixty-sixpatientswithHLES(LESP>40mmHg)werefound.Inadditiontomanometry,upperendoscopywasdonetoforty-ninepatients,upperGIbariumstudiestothirtyeightpatientsandesophagealpH-metrytosixteenpatients.Results:
showedthatmostofourpatientswerefemales(45femalesand21males),withameanageof36.6±±14years.Patientswithdysphagia(57.5%)hadthehighestLESP(52.1±±21,mmHg)whilepatientswithchestpain(47%)hadthehighestdistalesophagealcontractionamplitude(153.9±±93.2mmHg).Endoscopyshowedvaryingdegreesofesophagitisin17patients(34%).Bariumstudiesshowedcorkscrewesophagusinsevenpatients(18.4%)anddilatedesophagusinninepatients(23.7%).LESPwashighestinpatientswithdilatedesophagus(57.5±±33.4mmHg).Allourpatientsweresubjectedtomedicaltreatment,ofwhichtwelvepatientsunderwentpneumaticdilationwithsuccessfullyreducedLESPandsymptomsreliefin91%ofpatients.Conclusions:
ItwasconcludedthattheprevalenceofHLESisaround1.6,inwhichdysphagiaandchestpainaretheusualpresentingsymptom,andthatpneumaticballoondilatationisveryeffectivewhenproperlyapplied.Itwillprobablyoccupythesamepositionithasinachalasia.
Keywords:
Hypertensiveloweresophagealsphincter,chestpain,dysphagia
Howtocitethisarticle:
GadEl-HakNA,MostafaM,AbdelHamidH,HaleemM.Hypertensiveloweresophagealsphincter(HLES):
Prevalence,symptomsgenesisandeffectofpneumaticballoondilatation.SaudiJGastroenterol2006;12:
77-82
HowtocitethisURL:
GadEl-HakNA,MostafaM,AbdelHamidH,HaleemM.Hypertensiveloweresophagealsphincter(HLES):
Prevalence,symptomsgenesisandeffectofpneumaticballoondilatation.SaudiJGastroenterol[serialonline]2006[cited 2009Jul30];12:
77-82.Availablefrom:
Theesophagusisanactivemuscularorganwithacomplexneuromuscularstructurewithspecializedsphincterateachend.Theupperesophagealsphincter(UES)contractsduringinspiration,preventingairfromenteringintothegastrointestinaltractwhileLowerEsophagealSphincter(LES)maintainsasteadybaselinetonetopreventgastricjuicefromrefluxingintotheesophagus[1].Althoughgastrointestinalmotoractivityhasbeenstudiedformorethancentury,theidentificationofmotordisordersinclinicalpracticestillrepresentproblems.
ReynoldsetaldefinedHLESasadistinctclinicalentity[2],whileWingatedefineditasaprimarymotordisorderoftheesophaguswithquestionableentities[3].
HLESisanuncommonmanometricabnormalityfoundinpatientswithdysphagia,chestpain,gastroesophagealrefluxand/orhiatalhernia[4].HLESincidencehasbeenreportedasbeingbetween(0.8%-12%)ofpatientreferredformanometricinvestigationofesophagealsymptoms[5].ItischaracterizedbyincreaseLESpressureofgreaterthan40mmHg[6],normalLESrelaxationandnormalesophagealperistalsis[2],[3].PatientswithHLESoftenhaveothermotilitydisorders,nonspecificmotilitydisorder,nutcrackeresophagusanddiffuseesophagealspasm[2].
Endoscopyhastheadvantageofdirectvisualizationofstructurallesionsandbiopsiescanbeobtained.However,itdoesnotplayaroleinthediagnosisofmotilitydisorders[7].Bariumstudiesassesstheemptyingoftheesophagusaswellasstructuralabnormality.Esophagealmotilityisbestassessedbythefullcolumntechniqueandfluoroscopicobservation[8].Althoughradiologicalinvestigation,suchascontraststudies,mayhavearoleinthediagnosisofachalasia,thecorrelationbetweenisolatedHLESandradiologicalfindingsisunclearandthediagnosisismadebymanometry[2].
ThepathophysiologyofHLESiscomplexandpoorlyunderstood.Thereisexperimentalevidencethatloweresophagealhypertensionoccursfollowingstimulationofthecutendsofsplanchnicnerves[9].Histologicalstudieshaveshowndegenerationofmyentericganglioncells,withsparingofpost-ganglioniccholinergicnerves[10].
RegardingthetreatmentofHLES,noestablishedmethodsareavailableatpresent,butoraladministrationofnitrate,anti-depressant,anti-cholinargic,smoothmusclerelaxantsascalciumchannelblockers(nifiedipine,etc.)andantiscertoryhavebeentested,withimprovementofsubjectivesymptoms[6].Passageofa50FBougiedilatororpneumaticballoondilatationreservedforpatientwithseveredysphagiaandchestpainwithclinicalreliefinsomepatients[11],[12].EsophagomyotomyrestoresLESpressuretophysiologicallynormallevelsandisthetreatmentofchoiceforisolatedHLESthatfailsmedicaltreatment[2].Inaddition,gastro-esophagealrefluxhasbeenshowntooccurinsomepatientswithHLESandanti-refluxtreatmentachievessymptomrelief[13].
Objectives
Weaimtostudythefollowing:
(1)PrevalenceofHLESinpatientssubjectedtoesophagealmanometry.
(2)ThecommonsymptomsandclinicalpresentationsofHLES.
(3)CorrelationofthesymptomswithLESP.
(4)Effectivenessofpneumaticdilatationinpatientsrefractorytomedicaltreatment.
Patientsandmethods
IntheperiodbetweenJanuary1994December2003morethanfourthousandonehundredandseventypatientswerereferredtotheesophagealfunctionlaboratoryfortheinvestigationofuppergastrointestinalsymptomsbyesophagealmanometry.Sixty-sixpatients(21males,45females)withmeanageof(36.6+14)yearsmetthemanometriccriteriaforHLES.Theseareameanrestingpressureof>40mmHgabovegastricpressure,normalloweresophagealsphincterrelaxation(LESR)andnormalesophagealperistalsis[6].Patientswithachalasiawereexcludedfromourstudy.
Detailsofclinicalassessmentandsymptomsanalysisfordysphagia,chestpain,refluxand/ormixedsymptomswerecorrelatedwithdifferentmanometricfindings.
Esophagealmanometrywascarriedoutforallpatients.Patientswerestudiedinthefastingstate;oraladministrationofnitrate,anti-cholinargic,smoothmusclerelaxantascalciumchannelblockers(nifiedipine,etc.),anti-scertory,protonpumpinhibitorsandprokineticswereallstoppedsevendays,beforethetest.
Thepressurecharacteristicsofthegastro-esophagealjunctionweremeasuredbyawaterperfusedeightlumenpressurecathetersideholeswithanoutsidediameterof4.5mmat5,5,5,2,1,1and1cmapartfromeachother,fromtheproximalandtheyareradiallyorientedby360°°andwereconstantlyperfusedwithdistilledwaterfromthe"Muiscintific"perfusionpumpatarateof0.5ml/min.Eachchannelwasconnectedtopressuretransducerswhichtransmitdataintoapersonalcomputerviaanelecronicmicro-laboratory(SmartLab.MotilitySystem;Sandhill,USA).Astationpullthroughtechniquewasusedandtheprobewaswithdrawn0.5cmeachtimeandkeptateachlevelforatleast30soruntiltherecordingbecamestable.
Thehighpressurezonewasdefinedasthemeanofthehighestpressureplateaurecordedbyeachoftheeightportsminusthemeanpressureinthegastricfundusmeasuredatthemidofrespirationandthepatientswereaskedtotake5mlwatertoobtain%(thepercentage)relaxationanditsresidualpressure.
Thoracicesophagealmotilityevaluatedbypositioningthreeholesat5,10and15cmproximaltotheupperborderoftheLES,tenwetswallowswereassessedateachlevelandthemeanvaluesoftheseswallowswereanalyzedineachpatienttoevaluateperistalticcontractions.
Esophagealbodyamplitudewasconsideredashypertensivewhendistalbodyamplitudewas>180mmHg[14]andhypotensivewhendistalbodyamplitude<35mmHg[15],[16],[17].
Ambulatory24-hpHmonitoringwasdoneforsixteenpatientswhomhadrefluxsymptomsorendoscopicevidenceofreflux.Adisposableantimony,orglassingoldpHelectrodes,waspassedandsecuredtothenosewithanelectrodeplaced5cmabovethehighpressurezoneaslocatedbymanometricexaminationandconnectedtoaportableDigtrapperMKIII(SynecticsMedical,Sweden).Thepatientswereambulatorythroughoutallrecordingsandwereinstructedtofollowtheirusualpatternofliving.Refluxsymptoms,mealsandrestingperiodswererecordedinadiarybythepatients.ThepHdataandinformationgiveninthediarywereevaluatedbycomputersoftware.
EsophagealacidexposurewasthenscoredaccordingtoDeMeester'ssystem[18].Thisscoreisacompositeofphysiologicalparametersincludingfrequencyanddurationofacidexposureandpositionduringrefluxevents,withascoreof14.7astheupperlimitofnormal.Patientswerestudiedinthefastingstate.Protonpumpinhibitorswerestoppedsevendays,andantacidsandprokineticsthreedays,beforethetest[2].
UpperGITendoscopyweredonefor49patientsusingOlympusvideoendoscopyforexaminationofesophagusstomachduodenumtoexcludepatient
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