XXXX DM诊断和分类

DiagnosisandClassificationofDiabetesMellitusAMERICANDIABETESASSOCIATIONDEFINITIONANDDESCRIPTIONOFDIABETESMELLITUSdDiabetesisagroupofmetabolicdiseasescharacterizedbyhy-perglycemiaresultingfromdefectsinin-sulinsecretion,insulinaction,orboth.Thechronichyperglycemiaofdiabetesisassociatedwithlong-termdamage,dys-function,andfailureofdifferentorgans,especiallytheeyes,kidneys,nerves,heart,andbloodvessels.Severalpathogenicprocessesarein-volvedinthedevelopmentofdiabetes.Theserangefromautoimmunedestruc-tionoftheb-cellsofthepancreaswithconsequentinsulindeficiencytoabnor-malitiesthatresultinresistancetoinsulinaction.Thebasisoftheabnormalitiesincarbohydrate,fat,andproteinmetabo-lismindiabetesisdeficientactionofin-sulinontargettissues.Deficientinsulinactionresultsfrominadequateinsulinse-cretionand/ordiminishedtissuerespon-sestoinsulinatoneormorepointsinthecomplexpathwaysofhormoneaction.Impairmentofinsulinsecretionandde-fectsininsulinactionfrequentlycoexistinthesamepatient,anditisoftenunclearwhichabnormality,ifeitheralone,istheprimarycauseofthehyperglycemia.Symptomsofmarkedhyperglycemiain-cludepolyuria,polydipsia,weightloss,some-timeswithpolyphagia,andblurredvision.Impairmentofgrowthandsusceptibilitytocertaininfectionsmayalsoaccompanychronichyperglycemia.Acute,life-threaten-ingconsequencesofuncontrolleddiabetesarehyperglycemiawithketoacidosisorthenonketotichyperosmolarsyndrome.Long-termcomplicationsofdiabetesincluderetinopathywithpotentiallossofvision;nephropathyleadingtorenalfailure;peripheralneuropathywithriskoffootulcers,amputations,andCharcotjoints;andautonomicneuropathycaus-inggastrointestinal,genitourinary,andcardiovascularsymptomsandsexualdys-function.Patientswithdiabeteshaveanincreasedincidenceofatheroscleroticcar-diovascular,peripheralarterial,andcere-brovasculardisease.Hypertensionandabnormalitiesoflipoproteinmetabolismareoftenfoundinpeoplewithdiabetes.Thevastmajorityofcasesofdiabetesfallintotwobroadetiopathogeneticcate-gories(discussedingreaterdetailbelow).Inonecategory,type1diabetes,thecauseisanabsolutedeficiencyofinsulinsecre-tion.Individualsatincreasedriskofde-velopingthistypeofdiabetescanoftenbeidentifiedbyserologicalevidenceofanautoimmunepathologicprocessoccurringinthepancreaticisletsandbygeneticmarkers.Intheother,muchmorepreva-lentcategory,type2diabetes,thecauseisacombinationofresistancetoinsulinactionandaninadequatecompensatoryinsulinsecretoryresponse.Inthelattercategory,adegreeofhyperglycemiasufficienttocausepathologicandfunctionalchangesinvar-ioustargettissues,butwithoutclinicalsymptoms,maybepresentforalongperiodoftimebeforediabetesisdetected.Duringthisasymptomaticperiod,itispossibletodemonstrateanabnormalityincarbohydratemetabolismbymeasurementofplasmaglucoseinthefastingstateorafterachallengewithanoralglucoseload.Thedegreeofhyperglycemia(ifany)maychangeovertime,dependingontheextentoftheunderlyingdiseaseprocess(Fig.1).Adiseaseprocessmaybepresentbutmaynothaveprogressedfarenoughtocausehyperglycemia.Thesamediseaseprocesscancauseimpairedfastingglu-cose(IFG)and/orimpairedglucosetoler-ance(IGT)withoutfulfillingthecriteriaforthediagnosisofdiabetes.Insomein-dividualswithdiabetes,adequateglyce-miccontrolcanbeachievedwithweightreduction,exercise,and/ororalglucose-loweringagents.Theseindividualsthereforedonotrequireinsulin.Otherindividualswhohavesomeresidualinsu-linsecretionbutrequireexogenousinsu-linforadequateglycemiccontrolcansurvivewithoutit.Individualswithex-tensiveb-celldestructionandthereforenoresidualinsulinsecretionrequirein-sulinforsurvival.Theseverityofthemet-abolicabnormalitycanprogress,regress,orstaythesame.Thus,thedegreeofhy-perglycemiareflectstheseverityoftheunderlyingmetabolicprocessanditstreatmentmorethanthenatureoftheprocessitself.CLASSIFICATIONOFDIABETESMELLITUSANDOTHERCATEGORIESOFGLUCOSEREGULATIONdAssigningatypeofdiabetestoanindividualoftendependsonthecircumstancespresentatthetimeofdiagnosis,andmanydiabeticindivid-ualsdonoteasilyfitintoasingleclass.Forexample,apersonwithgestationaldi-abetesmellitus(GDM)maycontinuetobehyperglycemicafterdeliveryandmaybedeterminedtohave,infact,type2diabetes.Alternatively,apersonwhoacquiresdiabetesbecauseoflargedosesofexogenoussteroidsmaybecomenor-moglycemiconcetheglucocorticoidsarediscontinued,butthenmaydevelopdi-abetesmanyyearslaterafterrecurrentepisodesofpancreatitis.Anotherexamplewouldbeapersontreatedwiththiazideswhodevelopsdiabetesyearslater.Becausethiazidesinthemselvesseldomcauseseverehyperglycemia,suchindividualsprobablyhavetype2diabetesthatisexacerbatedbythedrug.Thus,fortheclinicianandpatient,itislessimportanttolabeltheparticulartypeofdiabetesthanitistounderstandthepathogenesisofthehyperglycemiaandtotreatiteffectively.Type1diabetes(b-celldestruction,usuallyleadingtoabsoluteinsulindeficiency)Immune-mediateddiabetes.Thisformofdiabetes,whichaccountsforonly5–10%ofthosewithdiabetes,previouslyencompassedbythetermsinsulin-dependentdiabetes,type1diabetes,orjuvenile-onsetdiabetes,resultsfromacel-lular-mediatedautoimmunedestructioncccccccccccccccccccccccccccccccccccc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