2. INTRODUCTION
These days the terms thyrotoxicosis and hyperthyroidism are used
interchangeably
refer to the classic or subtle physiologic manifestations of excessive quantities of
the thyroid hormones
5. INTRODUCTION
DEFINITION :
single autonomously functioning thyroid nodule (AFTN) in the thyroid gland
causing clinical and biochemical hyperthyroidism
surrounding normal thyroid tissue is often, but not always, suppressed
7. EPIDEMIOLOGY
frequency of toxic adenomas in patients referred for thyrotoxicosis – varies btw
1.5 – 44.5 %
Autonomous adenomas were more frequent in iodine-deficient areas (10.1%)
than in iodine-sufficient areas (3.2%)
The female-to-male ratio was 14.9:1 for nontoxic AFTNs and 5.9:1 for toxic AFTN
patients
8. PATHOGENESIS
somatic gain-of-function mutations in the TSH receptor or the stimulatory Gsα
subunit (encoded by the GNAS1 gene)
Both result in constitutive activation of the cAMP pathway
This results in enhanced proliferation and function of thyroid follicular cells
9. PATHOGENESIS
somatic, constitutively activating TSH receptor mutations are more common,
compared to Gsα mutations
iodine deficiency may be a predisposing factor for the development of AFTNs
10. PATHOLOGY
a solitary toxic nodule is surrounded by normal thyroid tissue that is functionally
suppressed.
Histology –
encapsulated follicular neoplasms or adenomatous nodules without a capsule.
Hemorrhage, calcifications, and cystic degeneration are commonly present
11. PATHOLOGY
high level of NIS gene expression, a high TPO mRNA and protein content, and
low H2O2 generation.
cell proliferation was found to be modestly increased
12. CLINICAL FEATURES
signs and symptoms of thyrotoxicosis and/or a thyroid nodule.
Clinical findings suggestive for GD are missing.
onset of thyrotoxicosis is often insidious
more common in older patients, who typically have larger adenomas
13. CLINICAL FEATURES
Thyrotoxicosis may develop independent of age
much more common in nodules over 3 cm in diameter.
USG - the critical volume at which hyperthyroidism occurs is about 16 mL.
14. INVESTIGATIONS
serum TSH has the highest sensitivity and specificity - initial screening test
can be a/w overt or subclinical hyperthyroidism.
In overt hyperthyroidism, usually both serum fT4 and T3 are elevated
T3-thyrotoxicosis, the isolated elevation of T3, can also be found
15. IMAGING
thyroid scan – 123 iodine, 131 iodine, or 99 technetium labeled pertechnetate.
Iodine isotopes are preferred –
3% to 8% of nodules that appear functioning on pertechnetate scanning are
nonfunctioning on radioiodine scanning.
16. IMAGING
warm (uptake similar to surrounding tissue)
hot (uptake increased without suppression of surrounding tissue)
toxic (uptake increased with concomitant suppression of surrounding tissue).
18. IMAGING
USG - solitary nodule and may show a small contralateral thyroid lobe.
no indication to perform FNAC because the risk for thyroid carcinoma is
extremely low
19. MANAGEMENT
In patients with overt thyrotoxicosis - beta blocker
b-adrenergic blockade should be considered prior to RAI even in asymptomatic
patients who are at increased risk for complications due to worsening of
hyperthyroidism
i.e., elderly patients and patients with comorbidities
20. MANAGEMENT
ATD - used infrequently as it requires long-term therapy, and a relapse will almost
invariably occur after discontinuation of the medication
Prolonged (lifelong) ATD in some pts with limited life expectancy and increased
surgical risk
Widely used forms for definitive treatment include surgical excision of the nodule
or treatment with radioactive iodine.
21. MANAGEMENT
SURGERY
risk of treatment failure is <1% after surgical resection (ipsilateral thyroid
lobectomy or isthmusectomy)
prevalence of hypothyroidism varies from 2% to 3% following lobectomy
22. MANAGEMENT
RAI therapy
6%–18% risk of persistent hyperthyroidism and a 3%– 5.5% risk of recurrent
hyperthyroidism
In patients treated with ATD prior to RAI, the increase in TSH may reactivate
suppressed thyroid tissue and iodide uptake, resulting in more damage by
131iodine.
23. MANAGEMENT
RAI therapy
Therefore, some clinicians administer LT4 for 2 weeks prior to therapy in order to
assure that the tissue surrounding the TA is suppressed.
therapy with 131iodine may trigger the development of TRAB
fixed activity of approximately 10–20 mCi or an activity calculated on the basis of
nodule size
24. MANAGEMENT
PEA
injection of ethanol (average dose 10 mL) into the TA or autonomous area of a
TMNG.
In one study, the average patient required four sessions at 2-week intervals
The injection results in necrosis and thrombosis of small vessels.
25. MANAGEMENT
PEA
S/E –
local pain - extravasation of the ethanol to extranodular locations
transient thyrotoxicosis, permanent ipsilateral facial dysesthesia, paranodular
fibrosis, and toxic necrosis of the larynx and adjacent skin
In studies evaluating the outcomes at 12 or 30 months, about 85% of patients
were euthyroid
26. MANAGEMENT
Percutaneous laser thermal ablation (LTA)
In hyperfunctioning nodules, LTA induced a nearly 50% volume reduction with a
variable frequency of normalization of TSH
RFA can also be used
27. MANAGEMENT
IF PERSISTENT HYPERTHYROIDISM
If hyperthyroidism persists beyond 6 months following RAI therapy for TMNG or
TA, retreatment with RAI is suggested.
In selected patients with minimal response 3 months after therapy additional RAI
may be considered.
28. MANAGEMENT
IF PERSISTENT HYPERTHYROIDISM
In severe or refractory cases of persistent hyperthyroidism, following treatment
with RAI, surgery may be considered.
Preoperative iodine therapy is not indicated because of the risk of exacerbating
the hyperthyroidism
ALTERNATIVELY - use of MMI with close monitoring may be considered to allow
control of the hyperthyroidism until the RAI is effective
31. PATHOGENESIS
hyperfunctioning adenomas within MNG or autonomous areas within euthyroid
goiters may also harbor somatic gain-of function mutations in the TSH receptor
studies demonstrate distinct clonal origins of different thyroid adenomas within
the same MNG
32. CLINICAL FEATURES
signs and symptoms associated with hyperthyroidism
locoregional compression causing dysphagia, shortness of breath, stridor,
dysphonia, or obstruction of the thoracic inlet (Pemberton sign).
33.
34. MANAGEMENT
ATD –
Therapeutically, hyperthyroidism can be controlled with thionamides.
This does not offer a definitive treatment and does not result in volume
reduction.
35. MANAGEMENT
Therefore, surgery and radioiodine therapy are frequently the preferred
therapeutic modalities
The activity of RAI used to treat TMNG is usually higher than that needed to treat
GD.
In addition, the RAIU values for TMNG may be lower, necessitating an increase in
the applied activity of RAI.
38. DEFINITION
Very rarely, well-differentiated thyroid carcinomas, secrete excessive amounts of
thyroid hormone resulting in thyrotoxicosis
usually follicular carcinomas and exceptionally PTCs
39. PATHOGENESIS
In well-differentiated thyroid cancers, mutations in the Gsα subunit and the TSH
receptor genes occur only very rarely
Although constitutive activation of the cAMP pathway results in enhanced growth,
it does not result in malignant transformation of otherwise normal thyrocytes.
However, a few patients with hyperthyroidism due to autonomously functioning
thyroid cancers with mutations in the TSH receptor have been identified
40. CLINICAL PRESENTATION
signs of thyrotoxicosis and the finding of a thyroid nodule prompting FNAC
Most commonly, thyrotoxicosis and the thyroid malignancy are diagnosed at the
same time
41. TREATMENT
Treatment does not differ from the therapy of thyroid cancer patients without
thyrotoxicosis
appropriate control of the hyperthyroid state with beta blockers and ATD before
thyroid surgery or 131iodine therapy.
43. DEFINITION
An excess of iodine through dietary intake, drugs, or other iodine-containing
compounds can lead to thyrotoxicosis through increased thyroid hormone
synthesis
particularly in MNGs that contain zones of autonomy
often called Jod-Basedow phenomenon
44.
45. For adults, the Dietary Reference Intake for iodine is 150 mcg
The Tolerable Upper Intake Level for adults has been set to 1100 mcg/day
The thyroid gland needs only 70 mcg/day to synthesize the required daily
amounts of T4 and T3
46. PATHOGENESIS
The normal thyroid gland protects itself from acute excessive amounts of iodide
by the Wolff-Chaikoff effect
most individuals with a normal thyroid gland can tolerate a chronic excess of 30
mg up to 2 g of iodide per day without clinical symptoms.
However, in some individuals, even exposure to modest amounts of excessive
iodine can induce IIT or hypothyroidism.
47. PATHOGENESIS
the incidence of IIT appears to be inversely related to the nutritional iodine intake
In regions with iodine deficiency, the prevalence of nodular goiter decreases after
the introduction of iodine supplementation
the incidence of hyperthyroidism then gradually falls over the years.
48. PATHOGENESIS
chronic excessive iodine intake may modulate thyroid autoimmunity and thereby
lead to thyrotoxicosis in genetically susceptible individuals
Epidemiologic studies in China, Turkey, Denmark, and Brazil
supplementation with iodized salt increases the prevalence of autoimmune thyroid
disease, clinical or subclinical hypothyroidism, autoimmune hyperthyroidism
49. CLINICAL PRESENTATION
similar to the diagnosis of hyperthyroidism due to other causes.
O/E, many patients have a thyroid nodule or a MNG
others may have underlying autoimmune thyroid disease.
50. CLINICAL PRESENTATION
IIT often develops several weeks after the administration of contrast agents
Patients deemed to be at high risk of developing iodine-induced hyperthyroidism
or whose cardiac status is tenuous at baseline may be considered for prophylactic
therapy with ATDs.
51. TREATMENT
IIT is usually self-limited lasting from a few weeks to several months provided that
the source of iodine is discontinued.
Beta blocker for symptomatic relief
In patients with prolonged IIT, the administration of methimazole should be
considered
52. TREATMENT
Dosing of MMI - 20–40 mg/d, given either as a daily or twice daily dosing.
There may be relative resistance to ATD in patients with iodine-induced
hyperthyroidism
53. TREATMENT
urinary iodine excretion returns to baseline within 1–2 months in most patients
Radioiodine treatment for an underlying adenoma or MNG may not be possible
after iodine exposure for several weeks to months because the exogenous iodine
will limit the uptake of iodide by the thyroid.
55. INTRODUCTION
37% iodine by weight
daily dissociation rate of iodine from the drug of about 10%
about 3 mg of iodine (i.e., ∼200 times the RDA of 150 mcg) are released into the
circulation per 100 mg of amiodarone.
Approximately 15– 20% of amiodarone-treated patients develop either AIT or AIH
56. INTRODUCTION
The huge iodine content of amiodarone increases plasma inorganic iodide 40-
fold and urinary iodide excretion up to 15,000 μg per 24 h
AIH is relatively more frequent in iodine-replete
AIT in iodine-deficient geographical areas
May occur early or late in the course of treatment
57.
58. TYPES OF AIT
TYPE – I
caused by excessive, uncontrolled biosynthesis of thyroid hormone by
autonomously functioning thyroid tissue in response to iodine load
typically develops in underlying nodular goitre or latent GD
59. TYPES OF AIT
TYPE – 2
destructive thyroiditis occurring in an otherwise substantially normal thyroid
gland
more prevalent in iodine-sufficient areas
most frequent form of AIT
60. TYPES OF AIT
A mixed/indefinite type is also recognized where patients acquire an
overlapping condition of both types
61. PATHOGENESIS
AIT type 1 results from the iodine-induced increase in thyroid hormone synthesis.
Patients typically present with a preexisting nodular goiter.
AIT type 2 is caused by the cytotoxic effects of amiodarone and thus results in the
release of preformed thyroid hormones
62. CLINICAL PRESENTATION
Often not readily apparent because of the underlying cardiac condition and a
paucity of adrenergic manifestations in patients treated with amiodarone.
Weight loss, exacerbation of arrhythmias and a decrease in cardiac function may
be observed in a subset of patients.
Some patients have a nodular goiter, a finding that can point to AIT type1
63. DIAGNOSIS
increased serum FT4 and FT3 and suppressed serum TSH levels.
In rare cases of AIT associated with severe non-thyroidal illness, FT3 may be
normal
Anti-thyroid antibodies, such as anti-TPO, are often positive in AIT 1 and negative
in AIT 2
64.
65. DIAGNOSIS
The diagnosis of AIT 2 is based on
the usual absence of goitre
reduced RAIU in areas of iodine deficiency
absence of hypervascularity on CFDS
anti-thyroid antibody negativity
Serum interleukin 6 levels are normal to high in AIT type 1 and markedly elevated
in AIT type 2 - significant overlap, so insufficient sensitivity
66. DIAGNOSIS
Thyrotoxicosis may be heralded by an unexplained increased sensitivity to
warfarin due to an increased degradation of vitamin-dependent coagulation
factors
67. TREATMENT
If possible, amiodarone should be discontinued.
in patients treated with amiodarone for life threatening ventricular arrhythmias,
this may not be possible
68. MANAGEMENT OF AIT 1
AIT 1 is best treated by ATD when a medical therapy is advisable
In some circumstances, an emergency or salvage thyroidectomy may be the initial
therapeutic choice
The iodine-replete thyroid gland of AIT patients is less responsive to thionamides
very high daily doses of the drug (40–60 mg/day of MMZ) for longer than usual
periods of time
69. MANAGEMENT OF AIT 1
potassium perchlorate - decreases thyroid iodine uptake
increases the sensitivity and response of the thyroid gland to thionamides
doses not exceeding 1 g/day for no more than 4–6 weeks
sodium perchlorate is an alternative option – solution - 21 drops corresponding
to about 300 mg perchlorate
70. MANAGEMENT OF AIT 1
After restoration of euthyroidism, a definitive therapy of the hyperfunctioning
thyroid gland is usually advised
If amiodarone can be discontinued, RAI therapy can be performed when iodine
contamination is over (up to 6–12 months after cessation of amiodarone).
Otherwise, total thyroidectomy should be considered.
71. MANAGEMENT OF AIT 2
prednisone was considered as the most effective treatment modality
0.5 to 0.7 mg/kg body weight per day for 1 to 2 months before gradual tapering.
If AIT presents an emergency, salvage thyroidectomy can be considered
72. MANAGEMENT OF MIXED/INDEFINITE AIT
2 alternatives
The first one is to start with ATD (± sodium perchlorate) as for AIT 1
to add GC in the absence of a biochemical improvement within a relatively short
period of time (4–6 weeks)
An alternative approach is represented by a combined treatment (ATD and GC)
from the very beginning
73. MANAGEMENT OF MIXED/INDEFINITE AIT
Thyroidectomy represents a valid option in the event of a poor response also to
the combined treatment
74. TREATMENT
Salvage thyroidectomy should be considered in the following conditions:
patients with deterioration of cardiac function: patients with a reduced LVEF have
an increased mortality risk.
patients with a severe underlying cardiac disease (e.g ARVD) or patients with
malignant arrhythmias
75. TREATMENT
Surgery, by rapidly restoring euthyroidism, can improve cardiac function within 2
months
plasmapheresis may be helpful in preparing thyrotoxic patients prior to surgery
76. TREATMENT
In addition to the emergency setting, total thyroidectomy can be considered in
the following conditions
(a) as a definitive therapy of hyperthyroidism in alternative to RAI therapy
(b) in patients who need to continue amiodarone therapy.
(c) in patients showing adverse effect to medical therapy.
77. TREATMENT
CAN AMIODARONE BE CONTINUED IN SOME CASES OF AIT?
This decision should be individualized with respect to risk stratification and taken
jointly by cardiologists and endocrinologists
amiodarone should be continued in critically ill patients with life-threatening
cardiac disorders responsive to the drug.
Continuation of amiodarone treatment is also feasible in AIT 2, as it is often self-
limiting
78. TREATMENT
CAN AMIODARONE BE CONTINUED IN SOME CASES OF AIT?
If cardiac conditions are stable and non-severe, amiodarone can be safely
discontinued
if needed, can be restarted after restoration of euthyroidism
82. DEFINITION
caused by constitutively activating mutations in the TSH receptor
affected individuals carry monoallelic gain-of-function mutations in the TSH
receptor in the germ line
The distinction from GD is important because of the need for a definitive
treatment
appropriate counseling of the families - offspring have a 50% risk for inheriting
the mutated allele
83. CLINICAL FEATURES
The thyroid gland is diffusely enlarged
signs associated with autoimmune hyperthyroidism are absent.
age of onset of hyperthyroidism is variable - between 18 months to 74 years in
various studies
84. DIAGNOSIS
suppressed TSH and elevated peripheral hormones in the absence of TSAB and
TPO antibodies.
The family history is key in order to demonstrate familial clustering indicative for
an AD disorder.
The diagnosis requires sequence analysis of the TSH receptor gene
85. TREATMENT
If these patients are treated with ATDs or insufficient amounts of radioiodine,
their hyperthyroidism frequently relapses.
Therefore, appropriate ablative therapy, either by thyroidectomy followed by
radioiodine therapy, or radiotherapy alone, is indicated for the majority of these
patients.
In younger patients, temporary therapy with ATDs can be considered.
87. Occurs in less than 2% of newborns that are the offspring of a mother with a
history of GD
caused by transplacental passage of stimulating TRAB
Antibody-induced neonatal hyperthyroidism resolves within the first few weeks or
months of life as the maternal antibodies are cleared from the circulation
89. can occur in sporadic patients with de novo germ line gain-of-function mutations
in the TSH receptor
patients tend to have severe hyperthyroidism that may necessitate surgery and
ablative radioiodine therapy early in life
Some of the children with severe neonatal hyperthyroidism were reported to have
mild mental retardation
90. high levels of thyroid hormone may have a negative impact on brain
development
alternatively, mental development may have been impaired because of premature
closure of the cranial sutures.
A few of these children presented with proptosis.
92. DEFINITION
account for less than 2% of all pituitary adenomas
syndrome of “inappropriate TSH secretion”
defined by normal or elevated TSH levels in combination with increased (free) T4
and T3 levels
93. CLINICAL PRESENTATION
present with signs and symptoms of hyperthyroidism that are usually mild
Symptoms are sometimes masked by the concomitant hypersecretion of other
pituitary hormones
The thyroid gland is enlarged.
94. CLINICAL PRESENTATION
The peripheral hormones are elevated and the TSH is inappropriately normal or
elevated TSH because the negative feedback is not operational
95. DIAGNOSIS
MRI of the pituitary gland will reveal a pituitary adenoma
Very rarely, TSH-secreting tumors are ectopic
The α subunit and the α subunit : TSH ratio are typically elevated in patients with
TSHomas
96. DIAGNOSIS
The secreted TSH is normal in terms of amino acid sequence
has variable biological activity and is secreted in fluctuating amounts.
TSH burst frequency and basal secretion are increased and the secretion patterns
is more irregular
diurnal rhythm is preserved at a higher mean in all patients
97. DIAGNOSIS
T3 suppression test (80 to 100 mcg/day of T3 for 8 to 10 days) - does not result in
complete inhibition of T3 secretion
TRH stimulation test - After injection of TRH (200 mcg IV), TSH and the α subunit
do not increase in patients with TSHomas
98. TREATMENT
The first-line treatment is transsphenoidal resection of the adenoma.
Complete resection is not always possible because of invasion into the sinus
cavernosus or other adjacent structures.
Prior to surgery, the hyperthyroidism should be controlled with thionamides and
beta blockers
99. TREATMENT
In patients with residual tumor tissue and persistent secretion of TSH,
somatostatin analogues such as octreotide and lanreotide or γ-knife radiotherapy
(10 to 25 Gy) are therapeutic options
effective in reducing TSH secretion in more than 90% and goiter size in about
30% of patients.
Tumor shrinkage does occur in about 40% of patients
101. DEFINITION
rare entity consisting of thyroid components that are part of a teratoma or
dermoid in the ovary.
accounts for less than 1% of all ovarian tumors and 2% to 4% of all ovarian
teratomas
5% to 10% are bilateral, and 5 to 10% are malignant
102. DEFINITION
More commonly, they consist of papillary cancers, but follicular carcinomas have
also been reported.
Thyrotoxicosis occurs in about 8% of patients with struma ovarii.
103. CLINICAL PRESENTATION
finding of an abdominal mass, ascites, pelvic pain, and, rarely, a pseudo-Meigs
syndrome with pleural effusions.
A subset of women present with subclinical or overt thyrotoxicosis.
Goiter is only present in patients who have concomitant thyroid disease
104. DIAGNOSIS
suppressed TSH and elevated peripheral thyroid hormones.
Radioiodine uptake will reveal uptake in the pelvis, while the uptake in the thyroid
gland is usually diminished
CT or MRI demonstrates unilateral or bilateral ovarian masses.
105. DIAGNOSIS
CA125 may be elevated.
Malignant thyroid tissue shows the characteristic patterns of papillary or follicular
thyroid cancer
can be positive for mutations in the BRAF gene
106. TREATMENT
Unilateral or bilateral laparoscopic or open oophorectomy is the primary therapy.
Thyrotoxic women should be treated with ATD and beta blockers in preparation
for surgery.
malignant struma ovarii - thyroidectomy followed by treatment with 131iodine.
108. DEFINITION
caused by the voluntary or involuntary intake of supraphysiologic amounts of
exogenous thyroid hormone.
MC iatrogenic - either intentionally in order to suppress TSH in thyroid cancer
patients or unintentionally in patients treated for primary hypothyroidism
109. DEFINITION
Non-iatrogenic - patients who are taking excessive amounts of thyroid hormones
or supplements containing thyroid hormones for weight loss, treatment of
depression, or infertility
hamburger thyrotoxicosis –
due to consumption of meat containing bovine thyroid tissue
110. CLINICAL FEATURES
clinically thyrotoxic but do not show signs of endocrine ophthalmopathy
Patients with an intact thyroid gland may have a small thyroid gland because of
the TSH suppression.
111. DIAGNOSIS
Serum TSH is suppressed, and (free) T4 and T3 levels are variably elevated.
T4 and T3 levels depend on the type of ingested thyroid hormone preparation.
Both T4 and T3 levels are high with excessive intake of levothyroxine
only T3 is elevated with the intake of T3
112. DIAGNOSIS
serum thyroglobulin levels - very low or undetectable
RAIU is decreased
Doppler - absent thyroidal vascularity and low-normal peak systolic velocity
113. TREATMENT
adjustment or discontinuation of the thyroid hormone preparation
Temporary use of beta blockers
In instances of severe acute intoxication with large amounts of thyroid hormone :
induced emesis, activated charcoal, gastric lavage, and, rarely, plasmapheresis and
exchange transfusion
In a relatively large prospective European multicenter study (17 centers in 6 countries)
Gain-of-function mutations in Gsα impair the hydrolysis of guanine triphosphate (GTP) to guanine diphosphate (GDP), resulting in persistent activation of adenylyl cyclase.
Mosaicism for Gsα mutations with onset during blastocyst development causes McCune-Albright syndrome, which can also be associated with toxic adenomas
PCNA and Ki 67 – markers of cell proliferation
Clinical findings suggestive for Graves’ disease such as endocrine ophthalmopathy, (pretibial) myxedema, and acropachy are missing. The onset of thyrotoxicosis is often insidious
all patients with TMNG or TA who are older than 60 years of age and those with cardiovascular disease or severe hyperthyroidism
The required dose of MMI to restore the euthyroid state in TMNG or TA patients is usually low (5–10 mg/d)
if volume reduction is a goal, at the expense of an increased risk of hypothyroidism, pretreatment with MMI, allowing the TSH to rise slightly prior to RAI administration, results in greater volume reduction after fixed doses of RAI
about 5% of patients treated with 131iodine fo toxic or euthyroid multinodular goiter develop stimulating TSH receptor antibodies and Graves’ disease.
using 150– 200 lCi RAI per gram corrected for 24-hour RAIU
MANAGEMENT SIMILAR TO TA
calculated on the basis of goiter size to deliver 150–200 lCi (5.55–7.4 MBq) per gram of tissue corrected for 24-hour RAIU,
(Jod = iodine in German; Karl von Basedow = German physician who described the signs of thyrotoxicosis associated with exophthalmos and goiter, i.e., Graves’ disease, in 1840
Iodochlorohydroxyquinolone – antifungal
Dihydroiodohydroxyquinolone – antiamoebic
Benziodarone – uricostatic and uricosuric
Isopropamide – anticholinergic used for petic ulcer and hypermotility disorders
Metrimazide – for cisternography
Wolff-Chaikoff effect, which consists of an immediate reduction in iodide uptake, iodide organification, thyroid hormone biosynthesis, and secretion
Individuals who are the most susceptible are elderly patients with autonomously functioning nodular goiters (557) and, less commonly, patients with occult GD (558) or patients with a prior history of GD who are in remission after a course of ATDs
The absolute levels of FT4 and FT3 at presentation have no discriminatory value between AIT 1 and AIT 2, although they tend to be higher in AIT 2
RAIU has low diagnostic value in differentiating AIT 1 from AIT 2 in iodine-replete areas
), as suggested by normalized iodine urinary excretion and adequate RAIU values
Mean t1/2 of amiodarone – 58 days
(or equivalent doses of other glucocorticoids)
arrhythmogenic right ventricular dysplasia
In contrast to toxic adenomas, which contain somatic mutations
signs associated with autoimmune hyperthyroidism, such as endocrine ophthalmopathy, myxedema, and lymphocytic infiltration of the thyroid gland, are absent.
in order to evaluate it for the presence of a monoallelic mutation.
BRAF – classical, tall cell
RAS, PAX8-PPARG – follicular
RET
Determination of the cause of hyperthyroidism based on the 123I uptake in the gland. In the setting of a suppressed thyroid-stimulating hormone (TSH) a normal or increased uptake is indicative of something else driving uptake rather than endogenous TSH. In the absence of uptake the gland has either been damaged or an external factor such as exogenous hormone or iodine is playing a role. Rarely, ectopic thyroid hormone production may occur. hCG, human chorionic gonadotropin.
