the role of selenium in thyroid autoimmunity: a review

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The Role of Selenium in Thyroid Autoimmunity: A Review Source: Journal of Restorative Medicine, Volume 4, Number 1, 1 December 2015, pp. 8392(10) Author: McGregor, Brock Autoimmune thyroid diseases, including Graves’ disease and Hashimoto’s thyroiditis, are the most common autoimmune conditions in humans. There is significant morbidity associated with thyroid autoimmunity, and typically ongoing management is required to control disease presentation and reduce sequelae. Thyroid tissues contain the highest concentration of selenium in the body, owing to selenium’s crucial role in glutathione peroxidases, thioredoxin reductases, and iodothryonine deiodinases. Selenium deficiency is associated with suboptimal thyroid function, and has been shown to be a risk factor for both Hashimoto’s thyroiditis and Graves’ disease. As a therapeutic intervention, selenium has been shown in a number of studies to reduce thyroid antibodies, although there remains limited information regarding its impact on clinical outcomes. In Graves’ disease, and specifically in Graves’ ophthalmopathy, selenium appears to play a beneficial role in altering disease progression and improving ophthalmic symptoms. The various functions of selenium in thyroid autoimmunity are reviewed. ABSTRACT Autoimmune thyroid diseases, including Graves’ disease and Hashimoto’s thyroiditis, are the most common autoimmune conditions in humans. There is significant morbidity associated with thyroid autoimmunity, and typically ongoing management is required to control disease presentation and reduce sequelae. Thyroid tissues contain the highest concentration of selenium in the body, owing to selenium’s crucial role in glutathione peroxidases, thioredoxin reductases, and iodothryonine deiodinases. Selenium deficiency is associated with suboptimal thyroid function, and has been shown to be a risk factor for both Hashimoto’s thyroiditis and Graves’ disease. As a therapeutic intervention, selenium has been shown in a number of studies to reduce thyroid antibodies, although there remains limited information regarding its impact on clinical outcomes. In Graves’ disease, and specifically in Graves’ ophthalmopathy, selenium appears to play a beneficial role in altering disease progression and improving ophthalmic symptoms. The various functions of selenium in thyroid autoimmunity are reviewed. INTRODUCTION Thyroid tissues contain high amounts of selenium in the form of selenocysteine, an amino acid incorporated into selenoproteins including glutathione peroxidases (GPx), thioredoxin reductases (TRx), and iodothyronine deiodinases (IDD). These proteins play a role in oxidative damage prevention and thyroid hormone metabolism (Figure 1). Through its integration in GPx, selenium protects thyrocytes from oxidative damage incurred by exposure to hydrogen peroxide (H2O2). H2O2 is required for thyroid hormone production, but must be rapidly degraded by seleniumcontaining enzymes in order to preserve thyroid tissues. Selenium also seems to be linked to T cell functioning, Thelper 1 (TH1) to Thelper 2 13 4 5 1,510

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Autoimmune thyroid diseases, including Graves’ disease and Hashimoto’s thyroiditis, are the most common autoimmune conditions in humans. There is significant morbidity associated with thyroid autoimmunity, and typically ongoing management is required to control disease presentation and reduce sequelae. Thyroid tissues contain the highest concentration of selenium in the body, owing to selenium’s crucial role in glutathione peroxidases, thioredoxin reductases, and iodothryonine deiodinases...

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  • The Role of Selenium in Thyroid Autoimmunity:A ReviewSource:JournalofRestorativeMedicine,Volume4,Number1,1December2015,pp.8392(10)

    Author:McGregor,Brock

    Autoimmunethyroiddiseases,includingGravesdiseaseandHashimotosthyroiditis,arethemostcommonautoimmuneconditionsinhumans.Thereissignificantmorbidityassociatedwiththyroidautoimmunity,andtypicallyongoingmanagementisrequiredtocontroldiseasepresentationandreducesequelae.Thyroidtissuescontainthehighestconcentrationofseleniuminthebody,owingtoseleniumscrucialroleinglutathioneperoxidases,thioredoxinreductases,andiodothryoninedeiodinases.Seleniumdeficiencyisassociatedwithsuboptimalthyroidfunction,andhasbeenshowntobeariskfactorforbothHashimotosthyroiditisandGravesdisease.Asatherapeuticintervention,seleniumhasbeenshowninanumberofstudiestoreducethyroidantibodies,althoughthereremainslimitedinformationregardingitsimpactonclinicaloutcomes.InGravesdisease,andspecificallyinGravesophthalmopathy,seleniumappearstoplayabeneficialroleinalteringdiseaseprogressionandimprovingophthalmicsymptoms.Thevariousfunctionsofseleniuminthyroidautoimmunityarereviewed.

    ABSTRACT

    Autoimmunethyroiddiseases,includingGravesdiseaseandHashimotosthyroiditis,arethemostcommonautoimmuneconditionsinhumans.Thereissignificantmorbidityassociatedwiththyroidautoimmunity,andtypicallyongoingmanagementisrequiredtocontroldiseasepresentationandreducesequelae.Thyroidtissuescontainthehighestconcentrationofseleniuminthebody,owingtoseleniumscrucialroleinglutathioneperoxidases,thioredoxinreductases,andiodothryoninedeiodinases.Seleniumdeficiencyisassociatedwithsuboptimalthyroidfunction,andhasbeenshowntobeariskfactorforbothHashimotosthyroiditisandGravesdisease.Asatherapeuticintervention,seleniumhasbeenshowninanumberofstudiestoreducethyroidantibodies,althoughthereremainslimitedinformationregardingitsimpactonclinicaloutcomes.InGravesdisease,andspecificallyinGravesophthalmopathy,seleniumappearstoplayabeneficialroleinalteringdiseaseprogressionandimprovingophthalmicsymptoms.Thevariousfunctionsofseleniuminthyroidautoimmunityarereviewed.

    INTRODUCTION

    Thyroidtissuescontainhighamountsofseleniumintheformofselenocysteine,anaminoacidincorporatedintoselenoproteinsincludingglutathioneperoxidases(GPx),thioredoxinreductases(TRx),andiodothyroninedeiodinases(IDD). Theseproteinsplayaroleinoxidativedamagepreventionandthyroidhormonemetabolism(Figure1).ThroughitsintegrationinGPx,seleniumprotectsthyrocytesfromoxidativedamageincurredbyexposuretohydrogenperoxide(H2O2). H2O2isrequiredforthyroidhormoneproduction,butmustberapidlydegradedbyseleniumcontainingenzymesinordertopreservethyroidtissues. SeleniumalsoseemstobelinkedtoTcellfunctioning,Thelper1(TH1)toThelper2

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  • (TH2)balance,andmacrophagefunction,suggestingacomplex,multifacetedroleinimmuneregulation. Seleniumscrucialroleinthyroidfunction,andthusinmetabolism,isdemonstratedbyitsphysiologicalpriorityinthyroidtissues.Intransientdeficiencyduetocriticalillnessordecreasedintake,seleniumispreferentiallypreservedforthyroidfunction.

    Figure1

    Factorsthataffectthyroidfunction.T4,thyroxineT3,triiodothyronineRT3,reversetriiodothyronine.

    Thehighconcentrationofseleniuminthyroidtissues,coupledwithawellelucidatedroleinthyroidmetabolismthroughselenoproteinfunctioning,haveleadtointerestinseleniumsupplementationinthyroiddysfunction.

    SELENIUMDEFICIENCYANDTHEENVIRONMENT

    Soilandwaterlevelsofseleniumaredependentonsurroundinggeologicalfeatures. Areaswithlowseleniumlevelsgeologicallyhavecorrespondinglowlevelsofseleniumpresentinthelocalfoodchain. Inareaswherefoodconsumptionconsistsmainlyofregionallyproducedfoodstuffs,lowsoillevelsofseleniumcanleadtoseleniumdeficiency.Inextremecases,suchascentralAsia,conditionssuchasKeshandisease(KD)andKashinBeckdisease(KBD)areassociatedwithsignificantseleniumdeficiency.

    KD,namedforacountyinChinawhereasignificantoutbreakoccurredinthe1930s,isadilatedcardiomyopathy

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  • associatedwithlowseleniumlevels. Theconditionischaracterizedbyenlargedmitochondria,reductioninoxidativephosphorylation,lowseleniumlevelsanddecreasedGPxlevels. AlthoughsupplementationwithseleniumhasbeenshowntoreduceincidenceofKD,itislikelythattheetiologyofKDismorecomplex,andinvolvesgeneticpredispositionandviralinfection.

    KBDisaformofchondrodystrophyoccurringinareasofruralChina,thatisassociatedwithreducedseleniumandiodinestatus,mycotoxinexposure,coxsackievirusinfection,andenvironmentaltoxinexposure.SupplementationwithseleniuminsomeareaswithendemicKBDhasdemonstratedimprovementsindiseaseprogressionaswellasprevention. Althoughinotherareas,correctingiodinedeficiencywaseffectiveatdiseasereductionwhileseleniumconferrednobenefit. Iodinedeficiency,alsocommoninareaswithlowselenium,hasbeenimplicatedasariskfactorforKBDandifnotcorrectedbeforeseleniumsupplementation,hypothyroidismmaypersist.

    Atlessseverelevels,deficiencyofseleniumislinkedtodepressedmood,withimprovedmoodfollowingrepletion.Observationaldatasuggestsanassociationbetweenseleniumintakeandriskofhypothyroidism. AssessmentofseleniumintakeinanAustriancohortthroughinterviewbaseddietarydatacollectionsuggestedthathypothyroidpatientshad,onaverage,lowerintakeofselenium. Ataphysiologicallevel,serumseleniumhasbeenshowntobeinverselyassociatedwiththyroidstimulatinghormone(TSH)levels.

    Someevidencesuggeststhereisatwowayrelationshipbetweenseleniumstatusandthyroidhormones,withanimalmodelssuggestingthatthyroidhormonesthemselvesregulateselenoproteinexpressionandseleniumstatus. Evenineuthyroidindividuals,reducedseleniumstatushasbeenshowntobeassociatedwithdecreasedconversionoftriiodothyronine(T3)tothyroxine(T4), Seleniumsregulatoryroleonautoimmunityisapparentinbothhypoandhyperthyroidformsofautoimmunedisease.Indeed,apopulationbasedstudyhasdemonstratedanassociationbetweenlowseleniumlevelsandnewlydiagnosedGravesdisease.

    SELENIUMANDHEAVYMETALS

    Severalheavymetalshavebeeninvestigatedfortheirroleinthyroidautoimmunityandthyroiddysfunction.Inparticular,mercuryandcadmiumhavedemonstratedanabilitytonegativelyimpactthyroidhealth. Cadmiumhasacomplexarrayofeffectsonthyroidfunction,includingdecreasedsecretionofT4bythyroidfollicularcells,andalteredperipheralconversionofT4toT3bydeiodinaseenzymes. Seleniumplaysanimportantroleinreducingcadmiumlevelsbybindingtocadmiumandfacilitatingitsexcretionthroughbile. ElevatedmercurylevelshavebeenlinkedtoincreasedTglevels,withmechanisticdatademonstratingthatinorganicmercuryaffectsthyroidperoxidase(TPO)andbothinorganicaswellasorganicmercuryinhibitthyroglobuliniodination. Seleniumhasanantagonisticrelationshipwithmercury,demonstratingaprotectiveeffectwhenmercurylevelsareelevated.

    SELENIUMANDIODINE

    Seleniumisnottheonlymicronutrientessentialtooptimalthyroidfunction.Zinc,vitaminD,vitaminA,andmostimportantlyiodine,playcrucialrolesinthyroidhormoneproductionandsubsequentthyroidhealth. Therolesofzinc,vitaminD,andvitaminAinthyroidfunctionarebeyondthescopeofthisreview,butthecomplexinteractionandcodependencebetweeniodineandseleniumwarrantsdiscussion(Figure1).

    Inanimalmodels,seleniumhasbeenshowntoexertprotectiveeffectsincasesofexcessiveiodineingestion. Similarly,humanstudieshavedemonstratedthatwhenaddressingiodinedeficiencythroughsupplementation,coadministrationofseleniumisimportanttomaintainadequateGPxfunction. Populationbasedstudieshavedemonstratedincreasesinthyroperoxidaseantibody(antiTPO)prevalenceinareaspracticingiodinefortification, withpossibleprotectiveeffectwith

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  • seleniumadequacy. Itishypothesizedthatiodineexcessinducesthyroiddamageviaselenoproteininactivation,subsequentlyincreasingtherelativeneedforseleniumtomaintainadequatefunctionofthyroprotectiveenzymes.

    Whileadequateseleniumstatusmaybeprotectiveiniodineexcess,seleniumdeficiencyhasbeenshowntobeprotectiveiniodinedeficiency.Incasesofcombinedseleniumandiodinedeficiency,normalizingseleniumlevelswithoutiodinesupplementationisshowntoaggravatehypothyroidism. InaseleniumandiodinedeficientpopulationinnorthernZaire,botheuthyroidandhypothyroidpatientswithiodinedeficiencysawdecreasedthyroidfunctionfollowingseleniumsupplementation.

    ItispostulatedthattheaggravationofhypothyroidisminaniodineandseleniumdeficientindividualbyseleniumsupplementationmayoccurthroughanincreaseinthyroxinemetabolismviaseleniumcontainingIDDs. TheresultingdecreaseinT4inindividualswithiodinedepletedthyroidleadstoanaggravationofhypothyroxinemiaandhypothyroidism. Seleniumdeficiencyinadevelopingfetusmaydecreasethyroxinemetabolism,decreaseT4utilizationinlessimportantperipheraltissues,therebypreservingandprioritizingT4utilizationinnervoustissue.

    THYROIDAUTOIMMUNITY

    Autoimmunethyroiddiseaseincidenceisontheriseandisnowestimatedtoaffectfrom5%to10%ofthepopulation. Thethyroidglandisparticularlysusceptibletoautoimmunity,likelytheresultofacomplexadditiveeffectinvolvingenvironmentalsensitivity,geneticpredisposition,theoligoelementrequirementofthyroidtissues,andtheuniquequalitiesofthethyroidcelldefensesystem. Attributedtoitsintegralroleinthyroidtissue,seleniumdeficiencyconfersincreasedriskofautoimmunethyroiddisease,andwillincreasebothdurationandseverityofdisease. Anumberofstudieshavedemonstratedseleniumsabilitytodecreasemarkersofautoimmunethyroidconditions,specificallyantiTPOandthyroglobulinlevels.

    HASHIMOTOSTHYROIDITIS

    Hashimotosthyroiditis(HT)isthemostcommoncauseofhypothyroidismandthemostprevalentautoimmunedisease.Theinfiltrationoflymphocytesintothyroidtissue,characteristicofHT,canleadtothyrocytedestructionandultimatelyhypothyroidism. Diagnostically,HTischaracterizedbyelevatedantibodiestothyroperoxidasesandthyroglobulin. AfindingofantibodypositivityconfirmsHT,butdoesnotindicatecurrenthypothyroidismorthatdevelopmentofhypothyroidismisacertainty.ObservationalstudiesandmousemodelshavelinkedthyroglobulinantibodyelevationstotheinitialorinnateimmuneresponseearlyinHT,andelevatedantiTPOtolateradaptiveimmuneresponse. TSHistheroutinescreeningtesttoassessthyroidfunction.AnelevatedTSHoccurslaterintheimmuneresponseinHT,leadingtoafindingofelevatedantiTPO,whichisthemostcommonindicatorofHTasthecauseofhypothyroidism.

    TreatmentofhypothyroidismduetoHTinvolvesthenormalizationofelevatedTSHlevelsthroughsupplementationwithLthyroxine,withagoalofrestoringthepatienttoaeuthyroidstate. ThismaydecreaseautoantibodiesduetoadecreaseinTSHandthyroidtissuestimulation. SeleniumsupplementationinindividualswithHTreducesoxidativestressthroughGPxandTRxfunction,andlowersH2O2levels. SeveralstudieshavedemonstratedtheassociationbetweenseleniumdeficiencyandHT, andtheimpactofseleniumondecreasingautoimmunelaboratoryparametersinHT.Whilelaboratoryparametersdidimproveinmanystudies,resultsremaincontroversial,andmoreimportantlytheclinicalsignificanceofthisimpactisnotyetwellestablished.

    A2003randomizedcontrolledtrial(RCT)designedtoassesstheimpactof6monthsofseleniumsupplementationinconjunctionwithlevothyroxineadministrationinpatientswithautoimmunethyroiditisdemonstratedasignificantdecreaseinantiTPOantibodiesintheintervention(n=35)versuscontrol(n=30)group,butdidnotimpactthyroidhormonelevels,or

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  • antiTglevels. Thestudydidreportsignificantincreasesinoverallmoodandfeelingsofwellbeingintheinterventiongroup,consistentwithearlierfindings. Previousworksuggestschangesinmoodwithseleniumsupplementationmaybetheresultsofaltereddopamineorserotoninmetabolism.

    Asimilar2002studydemonstratedasignificantreductioninantiTPOintheinterventiongroup(n=36,200gofseleniumseleniteandLT(4)toTSHnormalizationfor6months)versusthoseinacontrolgrouptreatedwithLT(4)only.ThestudyreportedthemostdramaticreductioninantiTPOoccurringinindividualswiththehighestinitialantibodylevels.ThosewithantiTPOlevelsover1200IU/mLexperiencedameanreductionof40%,whilethoseunder1200IU/mLexperiencedameanreductionof10%. AsimilarstudyinvolvingantiTPOpositiveeuthyroidpatientssupplementedfor6monthswith200gofseleniumshowednoreductioninantiTPOorqualityoflifebenefit.

    AlthoughthereareanumberofsmallinterventiontrialsdemonstratingsignificantreductioninantiTPOantibodieswithseleniumsupplementation,factorsincludingbaselineseleniumstatusandpopulationhomogeneitylimittheapplicabilityofresultstovariedpopulations.Althoughfourstudiesincludedina2013CochraneReviewdemonstratedsignificantdecreasesinantiTPOlevels,withonestudyreportingsubjectiveimprovementsinqualityoflife,reviewersconcludedinsufficientevidenceforclinicalapplicationduetounclearblindingstrategies,andtheabsenceofhealthrelatedqualityoflifescores.

    Currently,amulticentredRCTisunderwaytoassesstheimpactof12monthsofseleniumsupplementationinpatientswithautoimmunethyroiditistreatedwithlevothyroxine(TrialRegistryNumber:NCT02013479).TheCATALYSTstudy(thechronicautoimmunethyroiditisqualityoflifeseleniumtrial)istakingplaceacrossfourclinicsitesinDenmarkinvolving472participants,andwillbethefirsttoassessqualityoflifeasaprimaryoutcome.

    GRAVESDISEASE

    GDisanautoimmunedisorderprimarilyassociatedwithhyperthyroidism,butitalsoinvolvesnonthyroidassociatedoutcomesincludingpretibialmyxedema,acropachy,andmostcommonlyGravesophthalmopathy(GO). ThecompleteetiologyofGDisunknown,butitisthoughtitisduetoacomplexinteractionbetweengeneticrisk,infections,environmentalfactors(includingsmoking),stress,andnutrientdeficiency. ThepathogenesisofGDinvolvesautoimmunityasinHT,butratherthanleadtotissuedestruction,theimmunedysfunctionleadstoantibodiesagainstTSHreceptorsresultinginincreasedthyroidactivityandthyroidhormoneproduction.Thisoverproductioncausesthyroidenlargementviathyroidfollicularcellhyperplasia. Owingtoitsmultifacetedroleinthyroidhealth,seleniumhaslongdrawnattentionasapossibletreatmentoptionforbothGOandGDitself.

    ThereareanumberofpossiblemechanismsthroughwhichseleniummaypositivelyinfluencethecourseofGDandGO.AsanimportantcomponentofbothGPxandTRx,seleniummayinfluencetheregulationofT3levelsinGD. ThereisanelevationinoxidativestressinthecourseofGDasH2O2levelsrisewithincreasedTSHreceptorstimulation,leadingtoahigherrequirementofseleniumcontainingenzymes. AlongwithincreasedH2O2production,GDleadstotheupregulationofinflammatorycytokines.SeleniumhelpstodecreasetheseinflammatorycytokinesviaNFkappaBinhibition,therebyattenuatingtheinflammatoryresponseinGD(TrialRegistryNumber:NCT01611896).

    WhiletherearenoRCTsassessingdirectbenefitofseleniuminthetreatmentofGD,thereisanongoingdoubleblindplacebocontrolledclinicaltrial,theGravesDiseaseSeleniumSupplementationtrial(GRASS),takingplaceinvolvingsevenDanishmedicalcentreswhichaimstoestablishtheclinicalroleofseleniuminthetreatmentofGD(TrialRegistryNumber:NCT01611896).

    GRAVESOPHTHALMOPATHY

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  • GOisthemostcommonextrathyroidaloutcomeofGD,occurringinupto60%ofcases,andinvolvesseriousreductioninqualityoflife. ItshouldbenotedthesignificanteffectsmokinghasonriskandcourseofGD,andthenotable,dramaticincreaseinGOoccurrencewithsmoking. Smokinghasbeenshowntoincreaseboththedifferentiationoforbitalpreadipocytes andglycosaminoglycanproduction, twoprocessesleadingtothenotableexophthalmiadefiningGO.Interestingly,plasmaseleniumconcentrationshavebeenshowntobelowerinsmokersversusnonsmokers.

    CasecontrolledstudieshavedemonstratedthatseleniumlevelsaresignificantlylowerinGDpatientswhodevelopGO,comparedwiththosewithGDalone,suggestingseleniumdeficiencymaybeanindependentriskfactorforGOdevelopmentinGD. TypicaltreatmentoptionsforGOincludecorticosteroids,radiotherapy,surgicaldecompression,andimmunotherapy, andthereisincreasingevidencethatseleniumsupplementationisbeneficialinpreventing,stabilizing,andreducingGO.

    A2011doubleblindRCTdemonstratedthatsupplementationwith200gofseleniumperdaysignificantlydecreasedGO,improvedqualityoflife,anddecreasedworseningofdisease. Thebenefitofsupplementationremainedevenaftertherapywaswithdrawnfor6months.Itshouldbenotedtheseresultsoccurredinapopulationinaseleniumdeficientregion. Basedontheseresults,itmaybeclinicallyappropriatetorecommendseleniumsupplementationinindividualswithGOfor6monthsespeciallythosewithlowseleniumstatus.

    MATERNALHEALTH

    Seleniumsupplementationhasshownbenefitinthetreatmentofbothmaleandfemaleinfertility, andhasbecomeatherapyofinterestinreproductivehealthduetoevidenceofdecreasedriskofmaternalthyroiddysfunctionandpostpartumthyroiditiswithsupplementation.

    A2007studydemonstratedthatsupplementationwithselenomethionine200g/dayduringpregnancyandthepostpartumperiodineuthyroidwomenwithantiTPOantibodiesdecreasedtheriskofpermanenthypothyroidismandpostpartumthyroiditiscomparedwithplacebo.AntiTPOantibodylevelsweresignificantlyreducedinthetreatmentgroups,andthyroidultrasoundshowedimprovedechogenicitypatterns. A2014studydemonstratedthatmildtomoderateiodinedeficientwomenexperiencedadecreaseinfreeT4andTSHcomparedwithcontrolswhensupplementedwith60gofseleniumstartingat12weeksgestation. Thischangeoccurredonlyinwomenwhowerealreadythyroidantibodypositive,buttherewasnostatisticallysignificantchangeinantiTPOantibodies. Observationalstudieshavealsodemonstratedanassociationbetweenlowserumseleniumlevelsandincidenceofhyperthyroidismduringpregnancy, suggestingseleniumstatusmaybeariskfactorforbothhyperandhypothyroidism.Moreover,animalmodelssuggestthatmaternalsupplementationofseleniumnotonlydecreasedthyroiddysfunctionintreatedmice,butalsobenefitedhealthparametersintheirbreastfedoffspring.

    A2013Cochranereviewoftreatmentstrategiesforhypothyroidismbeforeandduringpregnancyconcludedthatseleniumdiddemonstratepositiveimpactonbothpostpartumthyroidfunctionandratesofpostpartumthyroiditis,butfoundnodifferencesinratesofpreeclampsiaorpretermbirth.

    CONCLUSION

    SeleniumsupplementationdecreasesantiTPOantibodiesinautoimmunethyroiditiswithvaryingimpactbasedonbaselinethyroidfunctionandinitialantiTPOlevels.Whileseveralstudiesreportincreasesinsubjectivewellbeingandmood,thereremainsunclearevidenceregardingtheclinicalimpactofloweringantiTPOonqualityoflifeoutcomes.OngoingstudiesreportingonchangesinhealthrelatedqualityoflifeoutcomeswilloffermoredefinitiveguidelinesofclinicalapplicationsofseleniumsupplementationinHashimotosthyroiditisandifbroadrecommendationsforsupplementationarewarranted.Currently,thecombinedsafetyprofileandprobablebenefitwouldreasonablysuggesttheconsiderationofselenium

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  • supplementationinpatientsiswarranted.SeleniumstatusisanindicatorofriskfordevelopmentofGravesophthalmopathyinpatientswithGravesdisease,andhasshownbenefitinbothreducingriskofGOdevelopmentandtreatmentofmildtomoderatepreexistingcondition.InpregnantwomenwithantiTPOantibodies,supplementationwith200gofseleniumshouldberecommendedduringpregnancyandinthepostpartumperiod.Individualsinpopulationswithlowiodinestatusshouldavoidseleniumsupplementationuntiliodinelevelsarenormalized.

    DISCLOSUREOFINTEREST

    Theauthorhasnothingtoreport.

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