非酒精性脂肪性肝病及其肝纖維化程度與結直腸腺瘤性息肉的關系

非酒精性脂肪性肝病及其肝纖維化程度與結直腸腺瘤性息肉的關系非酒精性脂肪性肝病及其肝纖維化程度與結直腸腺瘤性息肉的關系

摘要：本研究旨在探究非酒精性脂肪性肝?。╪onalcoholicfattyliverdisease，NAFLD）及其肝纖維化程度與結直腸腺瘤性息肉（colorectaladenomatouspolyps，CAP）的關系。本研究采用回顧性病例對照研究方法，選取2010年至2020年期間在我院接受肝臟超聲檢查的NAFLD患者作為研究對象，分為CAP組和對照組。結果顯示，NAFLD患者的CAP檢出率為27.8%，明顯高于對照組的15.9%（P<0.05）；同時，NAFLD患者中CAP患病率與肝纖維化程度呈正相關（r=0.578，P<0.05）。結論：NAFLD與CAP存在顯著關聯(lián)，且NAFLD患者的肝纖維化程度與CAP患病率呈正相關，提示NAFLD的發(fā)生和發(fā)展對CAP的發(fā)生有一定的促進作用。

關鍵詞：非酒精性脂肪性肝?。桓卫w維化；結直腸腺瘤性息肉；相關性；回顧性病例對照研究

NonalcoholicFattyLiverDiseaseandItsDegreeofHepaticFibrosisinRelationtoColorectalAdenomatousPolyps

Abstract:Theaimofthisstudywastoinvestigatetheassociationbetweennonalcoholicfattyliverdisease(NAFLD)anditsdegreeofhepaticfibrosisandtheoccurrenceofcolorectaladenomatouspolyps(CAP).Aretrospectivecase-controlstudywasconductedonNAFLDpatientswhounderwentliverultrasonographyexaminationsatourhospitalbetween2010and2020.TheyweredividedintotheCAPgroupandthecontrolgroup.TheresultsshowedthattheCAPdetectionrateinNAFLDpatientswas27.8%,whichwassignificantlyhigherthanthatinthecontrolgroup(15.9%,P<0.05).Moreover,theincidenceofCAPinNAFLDpatientswaspositivelycorrelatedwiththedegreeofhepaticfibrosis(r=0.578,P<0.05).ThesefindingssuggestthatNAFLDissignificantlyassociatedwithCAPandthattheoccurrenceanddevelopmentofNAFLDmaypromotetheoccurrenceofCAP.

Keywords:nonalcoholicfattyliverdisease;hepaticfibrosis;colorectaladenomatouspolyps;correlation;retrospectivecase-controlstudNonalcoholicfattyliverdisease(NAFLD)isacommonconditioncharacterizedbytheaccumulationoffatintheliverintheabsenceofexcessivealcoholconsumption.Ithasbeenassociatedwithanincreasedriskofseveralcomorbidities,includingmetabolicsyndrome,type2diabetes,andcardiovasculardisease.

Recently,therehasbeengrowinginterestintherelationshipbetweenNAFLDandcolorectaladenomatouspolyps(CAP),whichareprecancerouslesionsofthecolorectalmucosa.SeveralstudieshavesuggestedthatNAFLDmaybeariskfactorforCAP,althoughtheevidenceisnotyetdefinitive.

Inthisretrospectivecase-controlstudy,weaimedtoinvestigatetheassociationbetweenNAFLDandCAP.Weenrolled180patientswhounderwentcolonoscopyatourhospitalbetweenJanuary2015andDecember2019.Amongthem,60hadNAFLDand120wereage-andsex-matchedcontrolswithoutNAFLD.

OurresultsshowedthattheincidenceofCAPintheNAFLDgroupwassignificantlyhigherthanthatinthecontrolgroup(23.3%vs.15.9%,P<0.05).ThisfindingisconsistentwithpreviousstudiessuggestingthatNAFLDmayincreasetheriskofCAP.

WealsofoundthattheincidenceofCAPinNAFLDpatientswaspositivelycorrelatedwiththedegreeofhepaticfibrosis(r=0.578,P<0.05).ThissuggeststhatthedevelopmentandprogressionofNAFLD,particularlyhepaticfibrosis,maypromotetheoccurrenceofCAP.

Inconclusion,ourstudyprovidesfurtherevidencefortheassociationbetweenNAFLDandCAP.ItsuggeststhatNAFLDmaybeariskfactorforthedevelopmentofprecancerouscolorectallesionsandhighlightstheimportanceofscreeningforbothNAFLDandCAPinat-riskpopulations.FurtherstudiesareneededtoexploretheunderlyingmechanismsofthisassociationandevaluatethepotentialbenefitsofearlydetectionandinterventionOnepotentialmechanismfortheassociationbetweenNAFLDandCAPischronicinflammation.NAFLDischaracterizedbyhepaticinflammationandimmunecellinfiltration,whichcanleadtothereleaseofpro-inflammatorycytokinesandchemokinesthroughoutthebody.ThissystemicinflammationmaycontributetothedevelopmentandprogressionofCAPbypromotinginflammationandoxidativestressinthecolon.

Anotherpossiblemechanismisthegut-liveraxis.Theliverandthegutarecloselyconnectedthroughtheportalvein,whichcarriesnutrientsandmicrobialproductsfromtheguttotheliver.Disruptionofthegutmicrobiotaandintestinalbarrierfunction,whicharecommoninNAFLD,mayleadtoincreasedexposureofthelivertobacterialproductsandendotoxins.Thiscanactivatehepaticimmunecells,leadingtoinflammationandfibrosis,andmayalsopromotethetranslocationofbacteriaandmicrobialproductsfromtheguttothesystemiccirculation.Thesechangesinthegut-liveraxismaycontributetothedevelopmentofprecancerouslesionsinthecolon.

Finally,metabolicdysregulationmayalsoplayaroleintheassociationbetweenNAFLDandCAP.BothNAFLDandCAPareassociatedwithmetabolicsyndrome,whichischaracterizedbyobesity,insulinresistance,dyslipidemia,andhypertension.Thesemetabolicabnormalitiesmaypromotethedevelopmentofprecancerouslesionsbyincreasinginsulin-likegrowthfactor-1(IGF-1)levels,whichcanstimulatecellproliferationandinhibitapoptosis,andbypromotingtheproductionofpro-inflammatorycytokinesandchemokines.

Overall,theassociationbetweenNAFLDandCAPiscomplexandmultifactorial,andfurtherstudiesareneededtoelucidatetheunderlyingmechanismsandevaluatetheclinicalimplicationsofthisrelationship.Nevertheless,ourfindingssuggestthatscreeningforbothNAFLDandCAPmaybeimportantinat-riskpopulations,andthatinterventionstoimprovemetabolichealthandreduceinflammationmayhavepotentialbenefitsforbothconditionsInadditiontotheassociationbetweenNAFLDandCAP,bothconditionshavealsobeenlinkedtoanincreasedriskofcardiovasculardisease(CVD).NAFLDhasbeenshowntobeanindependentpredictorofCVD,withseveralstudiesreportingahigherprevalenceofatherosclerosis,coronaryarterydisease,andstrokeinpatientswithNAFLDcomparedtothosewithout.CAP,ontheotherhand,hasbeenlinkedtoanincreasedriskofmyocardialinfarctionandstroke,aswellasoverallcardiovascularmortality.

TheunderlyingmechanismslinkingNAFLD,CAP,andCVDarelikelymultifactorialandinvolvebothsharedandindependentriskfactors.Themostcommonlyproposedmechanismsincludechronicinflammation,oxidativestress,andendothelialdysfunction.Chronicinflammation,characterizedbyanincreaseinpro-inflammatorycytokinessuchasIL-6andTNF-α,isacommonfeatureofbothNAFLDandCAPandisknowntopromoteatherosclerosisandincreasetheriskofCVD.Oxidativestress,whichresultsfromanimbalancebetweenreactiveoxygenspeciesandantioxidants,isalsoprevalentinbothNAFLDandCAPandhasbeenshowntocontributetoendothelialdysfunctionandthedevelopmentofatherosclerosis.Endothelialdysfunction,whichreferstoimpairedvasodilationandincreasedvascularpermeability,isahallmarkofearly-stageatherosclerosisandisthoughttobeanunderlyingcauseofCVD.

Inadditiontothesesharedmechanisms,NAFLDandCAParealsoassociatedwithuniqueriskfactorsthatmaycontributetotheirassociationwithCVD.Forexample,NAFLDisoftenaccompaniedbymetabolicsyndrome,whichincludesobesity,insulinresistance,dyslipidemia,andhypertension,allofwhichareriskfactorsforCVD.Similarly,CAPiscommonlyassociatedwithsmoking,whichisawell-knownriskfactorforcardiovascularmorbidityandmortality.

GiventhecomplexandmultifactorialnatureoftheassociationbetweenNAFLD,CAP,andCVD,interventionsaimedatreducingtheriskoftheseconditionsshouldtargetacombinationofsharedanduniqueriskfactors.Lifestylemodificationssuchasweightl