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Transcript of THYROIDITIS Inflammatory diseases of the thyroid gland with different etiologic, biologic,...
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THYROIDITIS
Inflammatory diseases of the thyroid gland with different etiologic, biologic, histologic and clinical aspects
CLASSIFICATION
• ACUTE: bacterial, viral
• SUBACUTE: de Quervain’s thryoiditis
• CHRONIC:
• chronic autoimmune thyroidits
• Tuberculous
• Mycotic
• Riedel’s thyroidits
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ACUTE BACTERIAL THYROIDITIS
Signs and symptoms• Fever
• Pain profound and severe
• Dysfagia - 90 % din cazuri
• Dyspnea – 50 %
• Spasmodic cough
Laboratory data
• increased ESR
• leukocytosis with neutrophilia
• Ultrasound: small or large hypoechoic areas
• FNB: isolation of germs
Treatment : antibiotics
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ACUTE BACTERIAL THYROIDITIS
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Acute thyroiditis - histology
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SUBACUTE ”DE QUERVAIN’S” THYROIDITIS
PREVALENTA
Sex ratio F/M: 3,6/1 – 10,6 /1
1 caz TS for 5 cases of Graves disease and for 20 cases of AIT
• 0,01 % of all hospitalized patients
• 1,89 % of all patiens hospitalized for thyroid diseases
• 9,9 % of subjects presenting with thyrotoxicosis
• 1,52 % of patients investigated by FNB
Szabolosz I. Subacute thyroidits Budapesta 2000
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SUBACUTE THYROIDITIS
ETIOLOGY• probably the disease is a response to a viral infection
GENETICS• those with HLA-Bw35 have a risk to develop the disease of 8-56.6 %
• HLA-Bw35 allows the development of clincal symtoms
• it has no relatioship with the evolution of the disease
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SUBACUTE THYROIDITIS
PATOGENICITY• interleukine 6 produced by monocytes si macrophages determine inflammation
• interleukine 2 +TNF + interferon determine destructive thyroiditis in 10 % of cases
• VEGF, basic FGF, PDGF determine granulomatous reaction
• EGF determines by mitogenic effect the regeneration of the follicles
PATHOLOGY • Follicular disruption with thyroglobulin liberation is responsible for the initial phase of thyrotoxicosis
• granuloma:
• a center of giant cells surrounded by macrophages
• epithelial cells surrounded by a crown of macrophages involved with antigen presentation
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SUBACUTE THYROIDITIS
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SUBACUTE THYROIDITIS
Clinical signs and symptomsClassical
formNon
classical form
History of viral infectionPainful thyroid Fever DysfagyPainful thyroid enlargement
Pain irradiates to the earsSimptoms of thyrotoxicosisMalaise
1 / 390 %90 %
90 %50 %
76 %
18 %
42 %
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SUBACUTE THYROIDITIS
Laboratory data Imagery
Important increase of ESR Leukocytosis FT4 si FT3 increasedSuppressed TSH Increased thyroglobulin Transitory increased antithyroid antibodiesHLA-Bw 35+
Hipoechogenicity generalized or disseminated points Localized hipoechogenicityAbsent Tc 99 m uptakeReduced iodine uptake 67 Gallium citrat: scintiscan
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SUBACUTE THYROIDITIS
Differential diagnosis Evolution and complications
Cyst with intracystic hemorrhage Tirotoxicosis induced by iodine loading (amiodarone)Interpheron induced thyroiditisThyroid cancer: FNB
Painless forms
Transient hypothyroidism second phase of evolution Recurrent disease is unpredictable Heeling Definitive hypothyroidism <1/10
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Subacute thyroiditis: generalized hypoechogenicity
Subacute thyroiditis: patchy hypoechogenicity
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SUBACUTE THYROIDITIS
Color Doppler ultrasound examination scintiscan
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SUBACUTE THYROIDITIS – TREATMENT
FORME SEVERE:
GLUCOCORTICODS:
• Prednisone: 30-40 mg / day at the beginning of the disease with further reduction of the dosage
• Dexametazone: 3-4 mg /zi
FORME USOARE:
Nonsteroidal anti inflammatory drugs: indometacin
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AUTOIMMUNE THYROIDITIS
INCIDENCE
• 3,5 – 4,5 % of population present autoimmune thyroid diseases
• 4,6 % of women and 1,23 %of men have antithyroid antibodies
• 15 % of women over 60 years
• lymphocytic infiltrations: 6,8 5 of women and 2,7 % of men
• 50 % of those with antithyroid antibodies have TSH > 6 U.I./ml
• 60 % of those with TSH > 6 U.I./ml have antithyroid antibodies
• 80 % of those with TSH > 10 6 U.I./ml have antithyroid antibodies
• 5 % of those with TSH > 6 U.I./ml develop overt hypothyroidism each year
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AUTOIMMUNE THYROIDITIS
PATOGENY
• genetic predisposition
•Viral aggression
• excessive iodine supply
GENETIC PREDISPOSITION
• relatives with autoimmune thyroid diseases
• patients with genetic abnormalities :Turner, Klinefelter, Down syndrome
• association with other autoimmune diseases:
• multiple autoimune endocrine diseases type I and II (ICSR, ovarian failure with precocious menopause ) autoimmune hypophysitis Biermer disease , sd, Sjogren, lupus, rheumatoid arthritis , miastenia gravis, interstitial lung disease
• HLA-DR3 si HLA-DR4
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AUTOIMMUNE THYROIDITIS
ANTIBODIES THIROIDITIS
ANTI-TPO (PEROXIDASE) HH, PTP
ANTI – Tg Ab HH
TSH -receptor stimulating antibodies hashitoxicosis
TGI – thyroid growth immunoglobulins HT with goiter
Thyroid stimulating blocking Ab Atrophic thyroiditis
Spontaneous mixoedema
TGBI – thyroid growth blocking immunoglobulins
Atrophic thyroiditis
Spontaneous mixoedema
Anti T3 –Ab , anti T4 - Ab May interfere with hormone assessment
Anti pancreatic islet
Anti salivary ducts
Anti other nedocrine glands Multiple autoimmune endocrine diseases
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AUTOIMMUNE THYROIDITIS
HASHIMOTO’S thyroiditis
• goiter
• metabolic state
• eutiroidism – 80 %
• hipothyroidism – 15 %
• hiperthyroidism – 5 %
LABORATORY DATA
• T4, T3 frequently normal
• TSH normal or slightly elevated
• increased response of TSH to TRH
• anti TPO – ab – 100 %
• anti TG-ab – 90 %
• TBII – 15-20 %
ULTRASOUND EXAMINATION
THYROID VOLUME: Increased, normal or decreased
Intense hypoechogenicity
Scintiscan : patchy hypoechogenicity FNB: lymphocytes and Hurthle cells
TREATMENT
THYROID HORMONES
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AUTOIMMUNE THYROIDITIS
CLINICAL FORMS• HASHOTOXICOSIS
• IN CHILDREN AND ADOLESCENTS: diffuse euthyroid goiter 10-15 % of goiters at these ages
• ATROPHIC
• SILENT or PAINLESS
• POSTPARTUM THYROIDITIS : TPO-Ab are detectable in predisposed cases in the 6th month of pregnancy: hiperthyroid state + depression it occurs postpartum weeks 11-12 and is followed by transient or definitive hypothyroidism
• AUTOIMMUNE THYROIDITIS SI MALIGN LYMPHOMA
• AUTOIMMUNE THYROIDITIS and THYROID CANCER
• IATROGENIC: interpheron, increased iodine intake, external radiotherapy
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AUTOIMMUNE THYROIDITIS-HISTOLOGY
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AUTOIMMUNE THYROIDITIS CLINICAL ASPECT
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AUTOIMMUNE THYROIDITIS CLINICAL ASPECT
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AUTOIMMUNE THYROIDITIS CLINICAL ASPECT
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POSTPARTUM - AUTOIMMUNE THYROIDITIS
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AUTOIMMUNE THYROIDITIS - ULTRASOUND
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AUTOIMMUNE THYROIDITIS
ATROPHIC VARIANT
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THYROID NODULES
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THYROID NODULES• CLINICAL : 4-7 % (5-20%)
• NECROPSIES:40-50 % (30-60%)
• ULTRASOUND EXAMINATION 16-67 %
CLINICA OF ENDOCRINOLOGY IASI:
- MEN : 27,37 %
- WOMEN: 30,3 %
CHILDREN: 1-2%
•THE PREVALENCE INCREASES WITH AGE BY : 0,08 % / year
THYROID CANCER: < 10 % OF PALPABLE NODULES, <5 % OF NODULES DETECTED BY US
NODULS 4 % OF POPULATION X 4% RISK= POSSIBLE INCIDENCE: 1,6/103
TRUE PREVALENCE : 0.025-0,050/103
1/30 MICROCANCERS BECOME CLINICALY DETECTABLE (MEYER 2000)
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THYROID NODULES
•CYST
• HETEROGENOUS ENDEMIC GOITER
• ADENOMA
• THYROIDIS
• CANCER
• LYMPHOMA
• EXTRATHYROIDAL LESION
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THYROID NODULESAUTHOR (YEAR) INVESTIGATED AREA INCIDENCE OF NODULS
Reshetnikov 1990 CIS 18,8 %
Filatov 1991 CIS 3,45 %Brander 1991
Finlanda27,3 %Solitar – 57 %
Multinodular 43 %
Hintze 1992 Germany > 60 YEARS
ENDEMIC AREA24,78 %
Grun 1992 GermanyGoiter prevalence: 37,7 %,
27,6 %women 36 %, men: 18,8 %
Mettler1992 Ukrain, Cernobil area children: 0,5 %
Adults 14,9 %
Mogos 1994 Iasi, Romania women: 30,3 %
meni: 27,7 %61,84 < 1 cm, 21 % 1-2 cm.9,2
%> 3 cm
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THYROID CANCERS
INCIDENCE B/106 F/106
• USA: 2,4-2,8 5,6-6,2
• Australia: 0,7 2,1
• Japan: 1.1 2
• Hawai: 3,1 4
• Germany: 2,7
•USA: ’85-’95: 13.856 cases
= 1 % Cancer Data Base
Necropsies:
Honolulu: 15,16%
Hiroshima 25,3
USA: 1,09-1,84
MORBIDITY:NEW CASES /106/ year
• SOKAL 1954: 12 / 106/ year
• CUTTLER 1975: femei: 52 /106/year
barbati: 21/ 106/year
• INGBAR 1981: 36 / 106/year
• IMPIERI 1984: 10-30 / 106/year
• MAZAFFERRY 1988 : 37 / 106/year
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THYROID CANCERS
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THYROID CANCERS
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THYROID CANCERS
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THYROID CANCERS
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THYROID CANCERS
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THYROID CANCERS
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THYROID CANCERS
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THYROID CANCER papillary form
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FOLLICULAR THYROID CANCER
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MEDULLARYTHYROID CANCER
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THYROID LYMPHOMA
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Steady increase of thyroid cancer all over the world
Between 1973-2002Between 1973-2002
2.4 times increase in 2.4 times increase in thyroid cancer incidencethyroid cancer incidence
All thyroid cancerAll thyroid cancer 3.6/103.6/1055
8.7/108.7/1055/year/year
Papillary cancerPapillary cancer 2.7/102.7/1055
7.7/107.7/1055/year /year
Small papillary Small papillary cancer cancer
87 % of the cancer 87 % of the cancer increaseincrease
Mortality decreased from Mortality decreased from 0.57 to 0.47/100.57 to 0.47/1055/year/year
external irradiation stopped external irradiation stopped after 1961after 1961
precocious diagnosis by precocious diagnosis by ultrasound and FNB ultrasound and FNB
increased incidence but increased incidence but stable mortalitystable mortality
Papillary cancer has a long Papillary cancer has a long evolution and excellent evolution and excellent survivalsurvival
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Trends in thyroid cancer
There was noticed steady increase of thyroid cancer all over the world
External irradiation is the only well documented cause in papillary thyroid cancer leading to RET/PTC re-arrangements
Iodine deficiency may play a role in the development of follicular cancer and may favor the development of anaplastic carcinoma
Iodine repletion is associated with increased incidence of papillary carcinoma with excellent prognosis
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The ratio of papillary to follicular thyroid cancer
(M.Goldust, S.Samankan etc al,2012)
(J. D. Cramer, 2010)
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Interval Number of cases
Age Females Males
1975 - 1979
19 45.7 ± 10.9
18 1
1980 - 1984
18 52.9 ± 14.9
15 3
1985 - 1989
17 49.5 ± 15.6
13 4
1990 - 1994
37 48.6 ± 16.8
32 5
1995 - 1999
52 51.5 ± 15.8
43 9
2000 -2004 71 53.1 ± 15
53 18
2005-2009 131 51.8 ± 14.2
109 22
1975 - 2009
345 51.3 ± 14.8
283 62
Table 1. Demographic data of 345 patients with thyroid cancer operated between 1975-2009 in the Ist. Surgery Clinic
of 5 years from the entire examined cohort
Figure 4. Percentage of thyroid cancer operated for each period
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Etiology and patogeny of thyroid cancers
external irradiation:“ ..until now the only carcinogenetic factor for the thyroid in man is external irradiation
Duffy si Fitzgerald 1936: firs obsercation of radiatioon induced thyroid cancer in children irradiated for benign lesions of head and neck
New cases of thyroid cancer in in Belarus 1990-1995 –Cernobil effect
( Pacini: J.Clin.Endorinol.Metab.1997)
1990 – 31, 1991 – 66, 1992 – 72, 1993 – 94, 1994 – 96, 1995 – 90 78.8 % sub 14 ani
Prezumed thyroid cancer: 10- 40 Excess of thryodi cancer due to external irradiation after Cernobil: 200 - 800
Increased susceptibility:
Irradiation of head and neck in all children
- external irradiation for othe rcancers
-Vage less than 20 years
-Female sex
-Genetic predisposition
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CONTAMINAREA RADIOACTIVA DUPA CERNOBIL 1986
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THYROID CANCER – CERNOBIL ACCIDENT
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Irradiation induced thyroid cancer
(E.Cardis,2005).
(E.Cardis,2005).
(E.Cardis,2005).
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THYROID CANCER
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THYROID CANCERFCMT MEN-2A MEN-2B CMT
sporadic
RET MUTATION germinal germinal germinal somatic
Exon 10,11,13,14,15 10,11 16,(15), 918 10,11,13,16
CMT 100% 100% 100% 100%
AGE <20,>50 <20 <20 <40
Multicentricity 100% 100% 100% rara
Bilateral lesions 100% 100% 100% rara
Hiperplasia of C cells 100% 100% 100% rar
Feocromocytoma 0 % 10-60% 50% 0 %
Hiperparathiroidism 0 % 10-25 % 0 % 0 %
Notalgia –cutaneous lichen amyloidosis
Hirschprung disease
0 % < 10 %
Codon: 618,620
0 % 0 %
Ganglioneuromatosis 0 % 0 % 100 % 0 %
Dismorphism 0 % 0 % 100 % 0 %
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MEN TYPE IIB - GORLIN’S SYNDROME
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MEN TYPE IIB - GORLIN’S SYNDROME
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THYROID CANCER- ultrasound exam
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THYROID CANCER- ultrasound exam
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THYROID CANCER
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THYROID CANCER - FNB
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Risk factors for malignancy in thryoid nodules
element benign malignant
history Endemic area, female sex, aged patients
History of cranial irradiation, other medullary thyroid carcinomas in the family, solitary thyroid nodule rapidly growing, compressive symptoms, male sex, child, young adult
Clinical data Multinodular goiter,soft nodule, lack of palpable lymph nodes,
Solitary ferm nodule, lymph node enlargement, distant metastases
Biologgical data AAT+, deceased TSH ,increased T3,T4 Increased calcitonine
ultrasoud Pure cyst, peripheral hallo, hyper, iso or hypoechoic, without calcification. Doppler exam:peripheral ring of vassels
Irregular margins, absence of hallo, increased intranodular vascularity
scintigraphy “worm nodule” a cold nodule is not surely a malignant one
“cold nodule”
ABC (FNB) “benign” Suspicious or malignant
Response to thyroid hormone treatment
Reduction of volume Increased volume under treatment
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FINE NEEDLE BIOPSY
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Algorithm for investigation and treatment of thyroid nodules
TYOROID NODULE
ULTRASOUNDCYST SOLID or partially cyst
FNB
MALIGNSUSPECT SAU NEOPL.FOLIC
SCINTIGRAPHY
COLDWARM
LOW RISK HIGH RISK
THYROIDECTOMY
Follow up
FNB
BENIGN
T4
ASPIRATION
SCLEROSING
REFACEREHeeled
E.Zbranca si col.Simp.Nat.Endocrinol.1995, Endocrinologie Clinica 1997
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Clinical staging of differentiated thyroid cancer
Patients under 45 years old Patients over 45 years old
STAGE I - any T, any N, M0 STAGE I - T1, N0, M0
STAGE II - any T, any N, M1 STAGE II - T2 / T3, N0, M0
STAGE III - T4, N0,M0, any T,N1,M0
STAGE IV – any T, any N, M1
Papillary and follicular
Clinical staging of medullary thyroid carcinoma
STAGE I - T1, N0, M0
STAGE II - T2 / T3 / T4 , N0, M0
STAGE III – any T, N1, M0
STAGE IV – any T, any N, M1
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Treatment of diffentiated thyroid cancers
Surgery
• total thyroidectomy +control of lymph nodes
• loboistmectomy: only in microcarcinomas with low risk (young age, female sex, well differentiated papillary
Complication:
• recurrent nerve palsy: 2-8 %
• hipoparathyroidism: 1-4 %
• intra or postoperative hemorrhage
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Treatment of diffentiated thyroid cancers
Radioactive iodine - 131I
Indication (Schlumberger 2000)- incomplete surgery
- compete surgery with risk of reccurence: less than 16 years or > 45 ani
- papillary variant less differentiated: columnar, diffuse sclerozing
- faollicular variant: invasive, less differentiated, Hurthle cell
- large tumors with capsular invasion
- Tiroglobulin over 3 ng/ml after 3 month of treatment
Ablative iodine therapy: 30 mCi or more if a certain volume of cancer tissue was left in place
Iodine therapy after previous ablation: 100-150 mCi for local recurrences or distant metastases
for children: 1 mCi/Kg bw
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Treatment and follow up of differentiated thyroid cancers
Suppressive thyroxine treatment :
• L-Thyroxine >/= 200 g/day
• 2,1-2,8 g/Kg.bw/day
• for TSH < 0.1 UI/ml
Suppression is switched to replacement dosage if there are not risk factors, serum Tg levels are less than 1 ng/mL
Follow Up:
Tiroglobuline (IRMA) after total thyrodectomy
• not detectable in 98 % of those with remission
• detectable in 5 % of those with reccurences
• in those with reccurences or metastases increaeses after T4 withdrawal (56 %) of after rhTSH (52%)
• errors: AAT tg.
• RT-PCR mARN for Tg
WBS: every 6-12 luni:Tg < 10 ng/ml : 100 mCi2-5 mCi
Tg . 10 ng/ml: 100 mCi
For Tg + si WBS negativ: 18 F-FDG-PET
Protocol for hr TSH adminstration prior diagnostic or therapeutic 131 Iodine administration0.9 mg hrTSH day 1 and 2131 Iodine id given day 3TG measurements in days 1-3-5WBS in day 5
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Treatment of diffentiated thyroid cancer
Total thyroidectomy131 I ablation + WBS
3 month fT4:FT3-TSH-Tg Tg> 5 ng/ml
131I100 mCi+WBS
6-12 luni- stop T4TSH/Tg
131 I WBS (2-5 mCi
Not detectable
Yearly Tg control on T4
Tg < 10 ng/ml
Tg +131I WBS ( 2-5 mCi)
Negative: repeat every 2-5 years
Tg > 10ng/ml or WBS +
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DIFFERENTIATED THYROID CANCER TREATMENT
1. THYROIDECTOMY AND LYMPH NODE DISSECTION
2. RADIOIODINE TREATMENT
3. HIGH DOSES OF THYROID HORMONE – LT4 TO SUPPRESS TSH
4. INTERRUPTION OF THYROID HORMONE FOR 4 WEEKS TO ALLOW TSH TO INCREASE AND TO STIMULATE IODINE UPTAKE IN NEOPLASTIC CELLS
5. THYROGLOBULIN ASSESSMENT: IF > 10 ng/dL
6. THYROID AND WHOLE BODY SCANNING + RADIOIODINE TREATMENT IF METASTASES OR LOCAL RECURENCE ARE DETECTED
7. THYROID HORMONE AT SUPPRESSIVE DOSES
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Treatment and follow up of medullary thyroid cancers
Total thyroidecotmy
Every 6 month
CEA,CT,Test PG
N Repeat yearly
N Repeat at 2
years
No meta
Incomplete surgery
Micrometa
PG – CT =N
Repat anually
Distant meta
Medical treat.
CT<50
Pg-CT<500
CT>50
PG-CT>500
Repat yearly
Stable.follow
increasedUS,CT,RMIN
negatives
Immunoscintigraphy
No tumor
Repeat annually
Lymph nodes meta
Modigliani 2000
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MEN 2A or 2B
Patient with MTC (index case)
Germ line mutation of RET analysis
RET pozitive/hereditary disease
RET mutation analysis in first degree relatives
Negative
No other investigation needed
•RET positive
RET negative
PG-CT test
No calcitonine increaseSurgery as
soon as possible if some aggressive mutation are detected
Surgery postponed
Test PG-CT
Positive- surgery Negative repeat PG- CT every year
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THYROID CANCER- SURVIVAL RATE
0
20
40
60
80
100
120
0 5ANI 10 ANI 15 ANI
PAPILAR
FOLICULAR
MEDULAR
NEDIF