10° Congresso Associazione Italiana della Tiroide · APS II FT3,FT4, TSH and ultrasonography...
Transcript of 10° Congresso Associazione Italiana della Tiroide · APS II FT3,FT4, TSH and ultrasonography...
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“Sapienza” Università di Roma UOC Endocrinologia - Latina
Prof. Marco Centanni
10° Congresso Associazione Italiana
della Tiroide Cagliari 15-17 Dicembre 2016
LA TIROIDITE CRONICA ASSOCIATA ALLE MALATTIE AUTOIMMUNI NON ENDOCRINE
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TOLLERANZA PERIFERICA : delezione linfociti che riconoscono antigeni self
Y
Y
Y
Y
Y
Y
Y
Y
APOPTOSI
TOLLERANZA
Linfocitaself-rea9vo
An;geneestraneo
TIMO:CENTRALE
ORGANILINFOIDI:PERIFERICA
AIRE:espressionedian;geniselfeconseguenteapoptosidellecelluleautorea9ve
EisenbarthGSetal,NEnglJMed-2004
Treg MOLECULAR MIMICRY
Linfocitaself-rea9vo
An;geneself
TOLLERANZA CENTRALE E PERIFERICA: delezione dei cloni che riconoscono antigeni self
EspressionediFoxp3eproduzionediTreg
Clonilinfocitariimmaturi
Clonilinfocitarimaturi
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APS tipo I
AITD + autoimmunopatie non endocrine:
APS III?
APS tipo II
APS tipo IV
Sindromi associative autoimmuni endocrine e non endocrine
IPEX MONOGENICHE
FOXP3
AIRE
POLIGENICHE HLA
CTLA-4 PTPN-22
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MALATTIA AUTOIMMUNE TIROIDEA
Candidiasi cronica
Ipoparatiroidismo
AITD
POF
DM 1
DM 1
Ipofisite
Gastrite atrofica
Anemia perniciosa
Morbo celiaco
Epatite cronica
autoimmune
Cirrosi biliare primitiva
Vitiligine
Alopecia
Miastenia gravis
Sclerosi multipla
Sindrome da Ab anti Fosfolipidi
LES
Artrite reumatoide
Sclerodermia
Sjogren
AITP
+ + + + +
a b d c
SINDROME POLIENDOCRINA AUTOIMMUNE
+ M. DI ADDISON
I II III GIOVANILE dell’
ADULTO Betterle C. et al Endocrine Reviews 2002
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PATOGENESI MULTIFATTORIALE
- Fattori genetici ed associazione con aplotipi HLA
- Alterazione della risposta immune cellulare
- Eventi scatenanti e meccanismi “trigger”
ASPETTI FISIOPATOLOGICI COMUNI NELLE SPA DELL’ADULTO
Anticorpi circolanti diagnostici in fase preclinica e clinica
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MARCATORIDELRISCHIODIMALATTIA
MARCATORIDIMALATTIA
EFFETTORIDELDANNOPATOGENETICO
ESPRESSIONEDELDANNOPATOGENETICO
Test di screening in: • Familiari di pazienti con autoimmunopatie endocrine e non
endocrine • Pazienti con autoimmunopatie endocrine per la ricerca di altre
immunopatie
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PATOLOGIA ORGANO BERSAGLIO
AUTOANTIGENi
Morbo di Graves, Tiroidite di Hashimoto, Tiroidite atrofica
Tiroide Recettore del TSH, Perossidasi tiroidea, Tireoglubulina, cotrasportatore Na/I
Morbo celiaco, Malassorbimento idiopatico
Intestino Transglutaminasi, Triptofano idrossilasi
Epatite cronica autoimmune, Cirrosi biliare primitiva
Fegato P450 (IID6, IA2), Mitocondrio
Gastrite atrofica del corpo-fondo, anemia perniciosa
Stomaco H/K pompa ATPasi, Fattore intrinseco
Diabete mellito tipo 1 Pacreas endocrino Acido glutammico decarbossilasi (GAD65), Tirosin fosfatasi, Insulina
Ipoparatiroidismo Paratiroidi Recettore calcio-sensibile
Vitiligine, Alopecia Cute SOX9,SOX10,Tirosinasi, Tirosina idrossilasi
Morbo di Addison Surrene 21 – idrossilasi
Ipogonadismo Gonadi Enzima di clevage della catena laterale p450, 17αidrossilasi
Ipofisite linfocitaria Ipofisi 68, 49, 43 kD
Miastenia gravis Muscolo Recettore dell’acetilcolina
Principalimala9eautoimmuniorgano-specificheerela;viautoan;geni
BeNerleetal,ClinExpImmunol-2004
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PATOLOGIA Frequenza di associazione
alla TAI
Ipofisite linfocitaria 69 %
Gastrite autoimmune 50 %
Vitiligine 8-55 %
Malattia celiaca 17-48 %
Diabete mellito tipo 1 5.5-46 %
Cirrosi biliare primitiva 26-43 %
Artrite reumatoide 10.2-38 %
Sindrome di Sjögren 29-34 %
Lupus eritematoso sistemico 4.4-31.7 %
Sclerosi multipla 5.7-21.7 %
Modificata da Betterle C. L’Endocrinologo 2009
Frequenza di associazione delle principali patologie autoimmuni alla TAI
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TPO Ab 10-40%
Ab anti-insula 3-8%
ASIMMETRIA DELLE POSITIVITÀ ANTICORPALI
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Frequenza di alcuni autoanticorpi
Frequenza di differenti malattie autoimmuni
Bagnasco M. Et al Autoimmunity Reviews 2007
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• Virus e retrovirus
• Antigeni batterici
• Heat shock proteins
• Stress
• Farmaci
EVENTI SCATENANTI
MOLECULAR MIMICRY !!
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“molecularmimicry”fraanDgeniesogenieautoanDgeni
Mimetismo molecolare
Wucherpfennig,Strominger–Cell,1995
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M.M.D’Eliosetal./MicrobesandInfecDon6(2004)1395–1401
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GENE Patologia associata HLA DR3-DQ2, DR4-DQ8 T1D
DR3;DR5 AIT
DR3-DQ2 CD
DR3-DQ2, DR4-DQ8 (DRB1*0404) AD
MIC-A T1D
CD
AD
PTPN22 T1D
AIT
AD
CTLA-4 T1D
AIT
MHC I related gene A
Maturazione timica delle cellule T
Cascata di trasduzione del segnale dal TCR
gene della tirosin-fosfatasi linfocitaria
Lega molecole costimolatorie inibendo l’attivazione delle cellule T
Barker J.M. 2006
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Simultaneous recognition of a specific major histocompatibility complex (MHC)–peptide complex by the T-cell receptor (TCR) and of B7-1 (CD80) or B7-2 (CD86) by the co-stimulatory receptor CD28 results in T-cell activation, cytokine production, proliferation and differentiation. In the absence of CD28 ligation, T
cells undergo apoptosis or become anergic. After T-cell activation and upregulation of cytotoxic T-lymphocyte antigen 4 (CTLA-4; CD152), co-ligation of the TCR and CTLA-4 results in cell-cycle arrest and
termination of T-cell activation. APC, antigen-presenting cell.
Alegre M.L. et al 2001
CTLA-4
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U
MHC II TCR
APC Th0 autoreattivo
IL-2 IFN-γ
IL-4 IL-5
Th1
Th2
IL-17 IL-23
T reg TGF-β IL-10
TGF-β
TGF-β IL-6
Th17
Pathway
effeZrice
Pathway
regolatoria
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GJ Kahaly, European Journal of Endocrinol 2009
PAS Tipo II
Prevalenza RARA
Incidenza
M/F 1:3
Età d’insorgenza Giovane-adulta
Eredità Poligenica
Endocrinopatie associate AITD (70-75%)
Ipoparatiroidismo (3%)
Ipopituitarismo(0-2%)
Malattia concomitante NO candidiasi
Malattie non endocrine Vitiligo, Alopecia areata, GCA
1-2:10000/anno
Diabete tipo 1 (50-60%) M.Addison (40%)
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IlmorbodiAddisonèlaendocrinopa;aautoimmunepivotalediquestasindrome.Èquindipresentenel100%deicasi.
EndocrinopaDeautoimmuniassociate:TireopaDaautoimmune–S.Schmidt(70-75%)
DiabeteDpo1–S.Carpenter(50-60%)IpoparaDroidismocronico(3%)
Ipopituitarismo(0-2%)
Mala_eNONendocrine:ViDligine–AlopeciaAreata
GastriteCronicaAtrofica–Ipogonadismo
BeNerleetal,EndocrineReviews,2002
BeNerle,ZaccheNa,ActaBioMedica,2003
GJKahaly,EuropeanJournalofEndocrinol2009
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Prevalenza 3-4 % della popolazione adulta
Epidemiologia:
Tiroidite cronica autoimmune
Prevalenza 0.00008% della popolazione adulta
6-8 casi per 100000 abitanti
Morbo di Addison
Tiroidite/Addison ratio = 50.000:1
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Addison patient
+ =AUTOIMMUNE - = NON AUTOIMMUNE TPOAb, TGAb, GAD65Ab and ICA
Re-evaluated every few yrs
All normal
Re-evaluated every 6-12 mo.
APS II FT3,FT4, TSH and
ultrasonography Fasting blood glucose
and OGTT
Clinical or subclinical hypothyroidism
Clinical or subclinical hyperthyroidism
Pathological Both normal
TRAb,RAIU, Scintiscan TIDM/LADA Re-evaluated every
6-12 mo
TTGAb in children
GAD65Ab+and/or ICA+ TPOAb+and/or TGAb+ All negative
21OHAb and/or ACA
Falorni A et al. Endocrinol Metab Clin N Am, 2002
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MALATTIA AUTOIMMUNE TIROIDEA
Gastrite atrofica
Anemia perniciosa
Morbo celiaco
Epatite cronica autoimmune
Cirrosi biliare primitiva
Malattie infiammatorie dell’intestino
Vitiligine
Miastenia
gravis
Sclerosi multipla
LES
Artrite reumatoide
Sclerodermia
Sjogren
Piastrinopenia autoimmune
Sindrome da anti-fosfolipidi
+ + +
Non Endocrine Autoimmune Diseases NEAD
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CARATTERISTICHE CLINICHE COMUNI ALLE PATOLOGIE AUTOIMMUNI DELL’APS II/III
1. Marcata familiarità per autoimmunopatie 2. Lunga fase prodromica
3. Predominanza nel sesso femminile e nelle età adulte
4. Aspetti clinici caratteristici
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Hashimoto K et al Horm Res 2005
HLA-DQA1*0301-associated susceptibility for autoimmune polyglandular syndrome type II and III
Wallaschofski et al Horm Metab Res. 2003
Kriegel MA et al J Exp Med 2004
Santaguida MG et al Clin Exp Immunol 2011
COMMON GENETIC AND IMMUNOLOGICAL FEATURES
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Clusterizzazione Familiare
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
20% 24%30%
40%
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
SPAIII TiroipaDaAutoimmune
50% 52%
…inalcunepatologieaforteimprontafamiliare
…nellaTireopaDaAutoimmuneenellaSPAIII
M Centanni - Unpublished data
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11%
89%
DIFFERENZA DI GENERE
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3 11
99
137
70
3
0
40
80
120
160
Età
Pazienti 3 11 99 137 70 3
0-10 11-20 20-39 40-59 60-79 80-99
DISTRIBUZIONE PER ETA’
M Centanni - Unpublished data
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MALASSORBIMENTO DI FERRO E VIT.B12
ANEMIA MALASSORBIMENTO DI
L-TIROXINA
ABORTIVITA’ RIPETUTA
ASPETTI CLINICI PECULIARI
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SibillaRetal–ClinEndo2008
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CentanniM-HotThyrolidology2007
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Pazienti con Malassorbimento N° %
215 12.7
Pazienti tireopatici esaminati 3488
Pazienti in terapia con l-T4 1688 48.3
n° %
M.Centanni unpublished observation
AITD N° % 160 74.4
NATD N° % 55 25.6
RR= 4.125
MALASSORBIMENTO DI L-T4
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2% 6%
AITDSPAIII
p<0.0266
MCentanni-Unpublisheddata
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0
0,5
1
1,5
2
2,5
Pre
vale
nza
plur
iabo
rtiv
ità
(%)
2.17%
0,48%
p=0.0044 OR=7.438
SPA III ATD
SUBFERTILITA’ associata a POLIABORTIVITA’
ATD isolata (3/836) ed SPA III (6/230)
NATD
0,11%
p<0.0001; OR=23.91
p=0.228
M.Centanni unpublished observation
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SPA III (n=21; 6%)
POLIABORTIVITA’ N° POLIABORTIVITA’INPAZIENTISUBFERTILI
N°
SindromedaAban;-fosfolipidi/LES
8 SindromedaAban;-fosfolipidi/LES
4
Gastritecronicaatrofica 7 Gastritecronicaatrofica 2
Morboceliaco 3
S.diSjogren 1
Conne9viteIndifferenziata
2
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1) In un paziente affetto da tiroidite cronica autoimmune esiste una probabilità del 14% circa di sviluppare una seconda patologia autoimmune;
2)LeSPAIIIriconoscono:unaneNaprevalenzadellaDroiditediHashimoto,unamaggiorfrequenzanelsessofemminileenellafasciadietàgiovane-adulta.Sievidenzia,inoltre,unruoloimportantedellaclusterizzazionefamiliare
3) Le patologie che più frequentemente si accompagnano alla tireopatia autoimmune e definiscono una SPA III sono: la gastrite cronica atrofica, la vitiligine, il morbo celiaco, la sclerosi multipla
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1) In pazienti con SPA III c’è una significativa prevalenza di malassorbimento di ferro e levotiroxina
2)L’anemiamicrocitemicaèmaggiormentepresenteneipazien;SPAIII,aragioneanchedellaassociazioneconautoimmunopaDedeltraZogastrointesDnale
3) La poliabortività è più frequente nelle pazienti con autoimmunopatie, tiroidee e non, a motivo dell’imbalance immunitario e della associazione anche con la sindrome da anticorpi antifosfolipidi
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Take Home Message
Le autoimmunopatie multiple costituiscono un complesso sindromico che:
1. Non rappresenta una semplice aggregazione statistica di patologie
2. Indebolisce il concetto di organospecificità delle autoimmunopatie endocrine
3. Necessita di un modulato algoritmo diagnostico
4. Consente la diagnosi precoce di patologie silenti a partire da una immunopatologia nota
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Dr.ssa Lucilla Gargano
Dr.ssa Maria Giulia Santaguida
Dr.ssa Camilla Virili
Dr.ssa Miriam Cellini
Dr.ssa Nunzia Brusca
Dr.ssa Silvia Capriello
Laboratorio di Fisiopatologia Endocrina e Molecolare
UOC ENDOCRINOLOGIA Latina