of of total levels a case of apatientwhohadnormal here report inhibitingTSHlevels.We released, are hormones and large amountsofthyroid destroyed, follicles are (SAT),of subacutethyroiditis thyroidal asnumerous stage ismarkedlydiminishedinthethyrotoxic thyroid of SAT hasbeenassociated withthedetectionofTRAb Accepted onNov/5/2012 Received onSept/18/2012 [email protected] Zhejiang Province, China 79# Qinchun Road, Hangzhou, Zhe Zhang Correspondence to: I INTRODUCTION ). The elevated or normal (1-3). Theelevatedornormal foundduringthecourseorafterSAT(TSAb) were antibody antibody (TRAb)orthyroid-stimulating underlying causeisnotclear. andthe rare gland.Thisphenomenonisvery thyroid inleftpainless gland,anddecreased painful thyroid Arq Bras Metab. Endocrinol 2013;57/8 Hangzhou, China College ofZhejiangUniversity, Affiliated ofMedical Hospital and Metabolism, The First 1 Department ofEndocrinology In recent years, high titers of thyrotropin-receptor years, hightitersofthyrotropin-receptor In recent 99m technetium ( t isgenerallyknownthattheuptakeofradioactive Tc slightlyintheright-side uptakeincreased 99m Tc uptakeintheacuteSAT phase;thelevel 99m Tc) orradioactive iodinebythe Levels then kept normal in the following four years. Inconclusion,high normalinthefollowingfouryears. Levels thenkept resolvedspontaneouslyafterTRAb-positivity 22months,and TSH levelswereslightlylowfor22months. antibody (TRAb)positive. After ashort ofprednisolone,SAT-like course symptomsandsignsimproved. fibrosisintheleft interstitial lobe.in therightlobe,withmarked Thepatient was thyrotrophin-receptor Histologicalexaminationshowedcellulardestructionandgranulomatousinflammatory uptake. changes normais nosquatroanosseguintes.Concluiu-sequeaaltaabsorçãode de 22 meses.Osníveis TSH permaneceramlevementebaixos por22mesese,depois,semantiveram os sintomasesinaisdaSAT melhoraram. para A positividade TRAb foiresolvidaespontaneamenteem para anticorposantirreceptores datireotropina(TRAb). Após umcurto tratamentocomprednisolona, marcada noloboesquerdo.Opacientefoipositivo lomatosas nolobodireito,comfibroseintersticial ção geralnormal.Oexamehistológicomostroudestruiçãocelularealteraçõesinflamatóriasgranu levementeelevadosde níveis da. Entretanto,umpacientecomSAT apresentousinaisnatiroidedireita,comtirotoxicose transitóriae A absorçãotiroidianade SUMÁRIO Thyroidal SUMMARY Zhe Zhang com absorção incomum de Acompanhamento decasotiroidite subaguda thyroid thyroiditis withuncommon Follow-up ofacasesubacute devida àcombinaçãoentre TRAb efibrosedatiroideesquerda. due tothecombined effects of TRAb andleft thyroid glandfibrosis. slightly high However, apatientwithSAT hadsignsintheright-sidethyroid glandwithtransientthyrotoxicosis and 99m Tc uptakeinthecourse 99m Tc uptake intheacutethyrotoxicTc uptake phaseofsubacutethyroiditis (SAT) isalways inhibited. 99m 1 , ChengjiangLi Tc uptake levelsinthe right lobe,low Tc uptake 99m 99m Tc uptake Tc noestadotirotóxico agudodatireoiditesubaguda(SAT) ésempreinibi 99m Tc nolobodireito,baixaabsorçãode 1 of gland,andnotthewholeshowedhigh and thyroid was not palpable and was painless. There were were wasnotpalpable andwaspainless.There thyroid andtender.slightly enlarged, firm Theleftlobeofthe and regular. id glandwas Theright lobeofthethyro was110/72mmHgandpulserate80bpm pressure infection. Physicalexamination showedthathisblood tract tory an upperrespira from hehad suffered before, week.Onemonth fortheprevious and fingertremors -side neckpain,rightshoulderweightlossof2kg, right nic complainingofhighfever(39.0°C)withsevere On May12 CASE REPORT of the thyroid glandinthispatientanddetectedTRAb. of thethyroid the courseofthisdisease,weinvestigatedhistology the possiblepathogenicmechanismsthatoccurduring uptake at diagnosis of SAT. to discuss in order Therefore, TSAb (4-7). However, in the present case, some parts TSAb (4-7).However, case,someparts inthepresent 99m Tc pelatiroide th , 2006,a44-year-old mancametoourcli 99m Tc uptake intheleftTc uptake lobe,andnormaloverall Arq BrasEndocrinolMetab. 2013;57(8):659-62 Arq BrasEndocrinolMetab. 2013;57(8):659-62 99m 99m Tc uptake bytherightlobewas Tc uptake Tc noloboesquerdoeabsor 99m Tc pelo lobo direito foi Tc pelolobodireitofoi case report 99m 659 Tc Tc - - - - -

Copyright© ABE&M todos os direitos reservados. Copyright© ABE&M todos os direitos reservados. of the thyroid glandonJuly25 of thethyroid Ultrasonography and goiter size gradually decreased. taper, levels, withinnormal CRPandESRremained mm/h) onMay30 thyroid follicleswithlittlecolloid,eosinophilic dege thyroid bothrightandleftlobes showedsmall obtained from Histological examination of needle biopsy specimens range(0.12-1.67%at30min). higher than thenormal the leftlobe(2.01%vs.0.44%at30min),whichwas (9.86 mg/dL)onMay25 CRPconcentrationwasnormal loberesolved. thyroid intheright two days,thepatient’sfeverandtenderness 660 was commencedonMay22 1A,B,C). changesintherightlobe(Figures flammatory andgranulomatousin small lymphocytes,macrophages follicles, of thyroid sis intheleftlobe,withdestruction epithelialcells,andmarkedinterstitialfibro neration of ver, in bothlobes.Normal 1.9; right:4.4x2.52.9cm)andhypoechoiclesions ghtly enlarged goiter in the right lobe (left: 4.1 x 1.5 x negative. andinfluenzawere xsackievirus, x 10 bloodwhitecells, 7.9 dings showed thefollowingresult: fin Laboratory recorded. physicalfindingswere relevant no signsofGraves’ophthalmopathy. Nootherclinically July 30 drug onJuly16 drug in both lobes. The results ofthetotal in bothlobes.Theresults echoicchanges diffused were butthere disappeared, right: 4.0x2.01.6cm)andhypoechoiclesions (left:4.1x1.51.8cm; measurements treatment withbefore compared that goitersizewasdecreased of prednisolone from May 31 from of prednisolone 2 levelsonAugust tonormal of fT4andfT3returned in therightlobeand1.01% intheleftlobe).Thelevel m; normal range 0.24-3.34%) were observed. Howe observed. range0.24-3.34%)were m; normal co antibodiestocytomegalovirus, positive; otherserum were virus IgG antibodies toEpstein-Barr Ltd.). Serum by measured levelsoffT4,fT3,TSH,andTPOAbwere mL). Serum antibodies(TPOAb),10.4U/mL(<34U/ peroxidase TSH, 0.017µlU/mL(0.4-4.0µlU/mL);anti-thyroid (fT3),19.4pg/mL(3.1-6.8pg/mL); tri-iodothyronine (fT4), 77.2ng/dL(10.3-24.45ng/dL);free thyroxine functionwasasfollows:free 20.2 mg/dL.Histhyroid Thyroidal nd , 2006andSeptember 5 Treatment witha30-mgdailydoseofprednisolone glandshowedsli Ultrasonography ofthethyroid 9 99m /mm Tc thanin uptakein therightlobewasgreater th 99 , 2006 were slightlyelevated(4.15%:3.14% , 2006were mTc uptake insubacute thyroiditis 3 ; ESR, 66 mm/h; C-reactive protein (CRP), (CRP), protein ; ESR,66mm/h;C-reactive chemiluminescence (DPC TIANJIN Co. chemiluminescence (DPCTIANJINCo. th . During the course of prednisolone . Duringthecourseofprednisolone th . We thedose graduallyreduced 99m Tc uptakelevels (2.43%at30 th th nd . ESR was also normal (18 . ESRwasalsonormal , 2006. The levels of serum , 2006.Thelevels ofserum , 2006.Overthefollowing st , 2006 and stopped this th , 2006alsoshowed 99m Tc uptakeon ------These were negative by March 28 negativebyMarch These were October 14 forthesubsequent6months (detectedon normal levelsoffT4,fT3,andTSHremained patient’s serum body levels are shownintable1. body levelsare detectedonAugust2 TRAb antibodieswere negative, but antibodies (TPOAb) remained roxidase 28 levelsbyMarch tonormal returned foralongerperiodandonly suppressed TSH were degeneration of the epithelial cells, and interstitial fibrosis (HE stain, x400). thyroid glandshowssmallfollicle withlittlecolloid, eosinophilic the thyroidgland(HEstain, x400). (C)Histologicalexaminationoftheleft follicles (HEstain, x400). (B ) Giantcellswerepresentintheright sideof examination of the right-side thyroid glandrevealed destruction of thyroid Figure 1. Histologicalexaminationofthethyroid gland. (A)Histological thyrotoxicosis were minimal. were thyrotoxicosis and his symptoms of about their side effects concerned any the patientrefused thyroid function and thyroid-related autoimmune anti function and thyroid-related thyroid During the course of the disease, anti-thyroid pe During thecourseofdisease,anti-thyroid C B A th , 2008).Duringthecourseofthisdisease, anti-thyroid drugs, ashewas drugs, anti-thyroid Arq Bras Metab. Endocrinol 2013;57/8 th , 2008.Changesin th , 2008.The nd , 2006. - - we could not explain the normal uptakeof we couldnotexplainthenormal symptoms and, therefore, low levelsofTSHandsevere hormones, patient inthiscasehadhighlevelsofthyroid Arq Bras Metab. Endocrinol 2013;57/8 xicosis inSAT leakageof theuncontrolled from results and TSHlevels withoutdecreased normal function remains thyroid tissue.Therefore, of functiontheaffected tissuecancompensatefortheloss thyroid mild, normal Whentheillnessis issuppressed. and TSHproduction destroyed toxic phase,aslarge amountsofthegland are The uptakeof xic phasewasnotsuppressed. diagnosis. Firstly, thyroidal medications. any anti-thyroid without and 6)thefunctionTRAblevelsrecovered was effective; 5) prednisolone sient hyperthyroxinemia; changes; 4) the patient had symptoms and signs of tran biopsy specimensshowedgranulomatousinflammatory leukocytosis; 3)histological examination of needle butwithout sociated fever;2)ESRlevelwas increased, was enlarged andfindings: tender 1) with thyroid as was diagnosedwithSAT onthebasisoffollowing toIitaka’scriteriaforSATAccording (8),ourpatient DISCUSSION 2 After Aug antibodies. ESR: sedimentationrate;CRP: erythrocyte C-reactiveprotein;fT4: freethyroxin;fT3: freetri-iodothyronine; TSH: thyrotropin; TRAb: thyrotropin-receptorantibody; TPOAb: anti-thyroidperoxidase Table 1. findings Clinicalcourseoflaboratory without transient hypothyroidism. Transientwithout transienthypothyroidism. thyroto months, whichwaslongerthan thatoftypicalpatients, phase withamildillnessprofile. thyrotoxic June 2 May 2 May 30 Aug 2 Mar28 Feb16 Sep 5 July12 June 28 June 17 May 25 Aug 8 May 19 Aug14 May15 Normal range However, this existregarding severaldiscrepancies Second, the duration of the thyrotoxic phasewas22 Second, thedurationof thyrotoxic DATE th th nd 99m nd th th th th nd th , 2007 th th th , 2008 , 2006 th th nd , 2006, normalrangeschangedasfollows: fT4: 10.3-24.45pg/dL;fT3: 3.23-7.22ng/mL;sTSH: 0.4-4.0uIU/L; TpoAb: 0-35%, because thispatientwasfollowedupatthelocalhospital. Tc However, uptakelevelcanbenormal. the 12-22 ng/dL 99m 38.59 19.25 19.16 12.27 15.51 21.13 18.11 39.2 46.7 53.1 77.2 FT4 40 Tc inthethyro commonlydecreased 3.1- 6.8pg/mL 99m 30.21 10.3 4.17 3.82 4.12 7.52 7.59 7.98 12.3 6.13 19.4 4.52 FT3 This phenomenon is rare. This phenomenonisrare. Tc uptakein thethyroto 0.27-4.2 uIU/mL 0.004 0.004 0.005 0.013 0.005 0.022 0.017 STSH 2.06 0.02 0.03 0.02 1.34 99m Tc during TPOAB 0-34% 14.33 28.23 18.9 9.30 9.42 22.8 10.0 9.79 10.4 7.14 - - - - - TRAB continue to be impaired. However,continue tobeimpaired. thisisalsotran ensues asthe biosynthetic capabilities of thethyroid spontaneously. resolves thyrotoxicosis Hypothyroidism isexhausted, hormone when the supply of stored theinflamedgland.After2to8weeks, from thyroxine also can induce positive TRAb. Virus infectionincites also caninduce positiveTRAb.Virus influence thedegradation of TRAb. In addition, virus changesseemto anddestructive hand, inflammatory Ontheother in autoantibody production. resulting system, theimmune surveillance flammation affects TRAb.Ontheonehand, in toproduce ne reactivity intotheblood,whichinducesautoimmu is released (TSHR) theTSHreceptor glandisimpaired, thyroid listed asfollows.Fujiiandcols.(5)statedthatwhenthe SAT TRAb. mayproduce ves’ disease.Thisfindingmayexplainwhyonly10% after SAT toGra predisposing hadgeneticbackground positiveforTRAb found thatpatientswhoappeared highinseveralpatients(10).Iitakaandcols.(8) very ve in10%patientswithSAT (9,10).TRAbtiterswere TRAbpositi wever, studies,wefoundserum inrecent positive TRAbisusedtodiagnoseGraves’disease.Ho pathophysiologyofSAT.be explainedbythenormal inour patientcannot toxicosis withouthypothyroidism thelongdurationofthyro most patients.Therefore, functionin thyroid ofnormal subsequent restoration 1month,withthe sient, andcanlastforapproximately + + + + _ _ The possible mechanisms of TRAb production were were The possiblemechanismsofTRAbproduction thepatienthadpositiveTRAb.Ingeneral, Third, 0.24-3.34% 2.43 4.15 ECT ECT of left % 0.44 1.01 Thyroidal right % ECT of 2.01 3.17 99 mTc uptake insubacute thyroiditis 0-10 mg/dL 9.86 2.32 27.8 CRP 0-20 mm/h ESR 18 55 66 7 5 661 ------

Copyright© ABE&M todos os direitos reservados. Copyright© ABE&M todos os direitos reservados. 662 of theetiology,nation (13,14). Regardless small folli painless SAT byhistologicalexami hasbeenconfirmed gland.However,symptoms orsignsintheleft thyroid isunlikely,ory asthe patientdidnothaveanyprevious nosis ofSAT lobe.However, inleftthyroid thisthe thediag Thisfindingsupports left lobedisappeared. hypoechoiclesionsin lobes, atfirst.Aftertreatment, glandshowedhypoechoiclesionsinboth the thyroid phase. Ultrasonography of have been in the recovery the patientwasdiagnosed,whileleftglandcould side oftheglandwasinacutephaseSAT when gland.Theright locationsofthethyroid in different SAT, ofSAT degrees canoccur progression asdifferent These histologicalchangesmayhavebeencausedby bothnegative. titersofTgAbandTPOAbwere serum state after therapy.or a hypothyroid Atthe same time, Hashimoto’sdisease tological indicationofdestructive wasnohis Hashimoto’s diseasewasexcluded,asthere gland. intheleftthyroid cles andinterstitialfibrosis gland. intheleftthyroid marked interstitialfibrosis follicleswithlittlecolloid, and smallthyroid thyroid, intheright follicles,granulomaformation of thyroid destruction disease. Histologicalexaminationrevealed wasnohistologicalevidence ofGrave’s patient, there (11,12).However, inour waseffective drugs -thyroid epithelium andlittlecolloid,therapywithanti follicles,whichhaveacolumnar andfolded of thyroid and hyperplasia hypertrophy Graves’ disease:diffuse thetypicalchangesof logical examinationsconfirmed TRAbfollowingGrave’sdisease,ashisto circulating long durationthyrotoxicosis. TRAb could havecaused the and, therefore, recovery timeofTRAbwasconsistentwithtoTSH very tivity couldalsoexplainthenormal ofTRAbistransient.posi that theproduction theviewpoint Thissupports drugs. use ofanti-thyroid spontaneously without the can resolve Thyrotoxicosis tonormal. ly whileTSHlevelssimultaneouslyreturned spontaneous ned for22months,andthendisappeared with time.Inourpatient,positiveTRAbstatusremai systemmayrecover because theimmunesurveillance intheSAT,spontaneously negativewithimprovement (5,7),TRAb alsobecame tive TRAb.Insomereports inposi resulting which leadstoautoimmunereaction ofMHCII, induceexpression to thatofTSHreceptors SAT. similar that havemolecularstructure Someviruses during the thyrotoxic phase.Inthispatient,thereco during thethyrotoxic Thyroidal We astothecauseofsmallfolli uncertain remain Some patientswithSATtohave havebeenreported 99 mTc uptake insubacute thyroiditis 99m Tc uptakefound ------ral Science Foundation of Zhejiang Province ofChina,N ral ScienceFoundationofZhejiangProvince bytheNatu Acknowledgements: thestudywassupported autoimmune antibody, inpatientswithSAT. isproduced isa need tostudywhyTRAb,ratherthananother there gland. ofleftthyroid and interstitialfibrosis We feel that ofboththeTRAbandsmallfollicles the presence lobeinthispatientwasdueto take intherightthyroid madefortheweightofgland. tions were why theuptakeof oftheleftlobecouldexplain cles andinterstitialfibrosis REFERENCES 14. 13. 12. 11. 10. 9. 8. 7. 6. 5. 4. 3. 2. 1. . was reported. relevant tothisarticle nopotentialconflictofinterest Disclosure: Y2090448. was greater thanthepainlessleft-sidelobe,aftercorrec was greater

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