2. • 15 year old girl known case of graves
disese diagnosed at age of 9 yaers.
• At that time started on carbimazole ,
dose weaned gradually recently she
is off of medication.
3. • in 1835, Graves Give
the classic description
of the disease.
• Also called Basedow-
Graves disease.
4. • Pediatric Graves' disease accounts
for 10-15% of thyroid disorders in
patients less than 18 yr of age.
• Graves disease is the most common
cause of hyperthyroidism in pediatric
patients.
• It May result in significant morbidity,
and even rarely death.
6. • Graves' disease is most common cause of
hyperthyroidism in children. (96 % of cases).
• Overall, the prevalence in children is
approximately 0.02 % of children (1 in 5000) .
• The incidence increases with age and peaks
during adolescence.
• mostly in the 11- to 15-year age group.
Pik-shun Cheng , Treatment Choices of ChildhoodGraves'
Disease. Medical Bulletin
VOL.13 NO.4 APRIL 2008
7. • 38 % of cases are prepubertal at diagnosis.
• Girls are affected more
• F:M is 5:1 .
• The ratio is considerably lower among
younger children.
8. • The cause of GD remains unclear.
• it is believed to result from a complex
interaction between genetic background
(heredity), environmental factors and the
immune system.
9. • there is a high prevalence of GD or other
autoimmune disese in first-degree relatives .
• Incidence of Graves disease in identical
twins is 30-50%.
• Graves disease has been reported to be
associated with the HLA gene on
chromosome 6p, the CTL4 gene on
chromosome 2q33 and the PTPN22
(lymphoid tyrosine phosphatase) gene on
chromosome 1p13.
10. • Graves disease results from the production
of thyroid-stimulating immunoglobulins (TSI)
by stimulated B lymphocytes.
• These immunoglobulins bind to the thyroid-
stimulating hormone (TSH) receptor to
mimic the action of TSH ,resulting in
follicular cell growth, an increase in
vascularity and the excessive synthesis and
secretion of thyroid hormone.
Pathophysiology
11. • An imbalance between pathogenic and
regulatory T cells is thought to be involved
in both the development of Graves disesas
and its severity .leading to production of
autoantibodies.
Pathophysiology
12.
13. • Patient with GD may have an increased
frequency of other autoimmune endocrine
diseases (eg, diabetes mellitus, celiac
disease and primary adrenal insufficiency)
and nonendocrine autoimmune disorders (eg,
vitiligo, SLE, rheumatoid arthritis, myasthenia
gravis .ITP,
Pathophysiology
Brea Prindaville, Incidence of vitiligo in children with Graves’
disease and Hashimoto’s thyroiditis. International Journal of
Pediatric Endocrinology 2011, 2011:18
14. • Children with trisomy 21 have an increased
risk for Graves' disease .
• And tended to be diagnosed at an earlier
age .
• Graves' disease has been reported in
association with moyamoya disease.
• Patients with Turner syndrome may also
be at increased risk for hyperthyroidism.
Pathophysiology
15. • Graves' ophthalmopathy may result from
antibodies against a TSH receptor-like
protein in retroorbital connective tissue .
• in children with Graves' disease, positive
association between elevated levels of
thyroid stimulating immunoglobulin (TSI)
and the development of ophthalmopathy
was reported.
Pathophysiology ophthalmopathy
16.
17.
18. • The onset of the disease is often insidious,
and the changes may be present for months
or years before the diagnosis is made.
• Interestingly, manifestation of GO begins to
resemble the adult findings more closely
when adolescence approaches.
GogakosAl, Pediatric aspects in Graves'
orbitopathy. Pediatr EndocrinolRev. 2010
Mar;7 Suppl 2:234-44
19. SYMPTOM SIGN
hyperactivity Goiter
palpitation Tachycardia
Sleep disturbance Weight loss
Fatigue Heat intolerance
Poor school performance Tremor
Emotional lability Systolic hypertensuion
Neck fullness or lump Increased pulse pressure
Irritabilityand nervousness Hair loss
Increased stool frequency Enuresis
Increased appitite Advanced bone age
opthalmopathy
20. G E Krassas. Treatment of juvenile Graves’ disease and its
ophthalmic complication: the ‘European way’. European
Journal of Endocrinology (2004) 150 407–414
21. • Most children with Graves' have a diffuse
goiter .
• The surface tends to be smooth, fleshy in
consistency, without palpable nodules.
• A large goiter may cause dysphagia and
tracheal compression with complaints of
dyspnea.
• A bruit can often be auscultated over the
gland in hyperthyroid patients.
22.
23. • Ophthalmic abnormalities are less severe
in children than in adults.
• less severe eye findings in prepubertal as
compared with postpubertal children .
24.
25. • The stare and wide palpebral fissures are
the commonest.
• It is presumed that these eye findings are
the direct consequence of excessive
thyroid hormone action, and that they are
not immunologically mediated.
• These findings remit when the
thyrotoxicosis is controlled
G E Krassas. Treatment of juvenile Graves’ disease and its
ophthalmic complication: the ‘European way’. European
Journal of Endocrinology (2004) 150 407–414
26.
27.
28. • restricted eye muscle motility, severe
strabismus and optic neuropathy are
practically absent
• Ophthalmopathy is caused by inflammation
of the extraocular muscles and orbital fat
and connective tissue, which results in
proptosis (exophthalmos), impairment of
eye muscle function, and periorbital edema.
GogakosAl, Pediatric aspects in Graves'
orbitopathy. Pediatr EndocrinolRev. 2010
Mar;7 Suppl 2:234-44
29.
30. • Patients with gravs have an increase in
cardiac output, caused by both increased
peripheral oxygen needs and increased
cardiac contractility.
• pulse pressure is widened, and peripheral
vascular resistance is decreased .
• Mitral valve prolapse is two to three times
more prevalent in hyperthyroid patients
• Atrial fibrillation, is rare in children.
31. • Acceleration of growth is accompanied by
advancement of epiphyseal maturation.
• The acceleration is usually subtle.
• And related to the duration of
hyperthyroidism
32. • The age of onset of puberty does not
appear to be altered by hyperthyroidism.
• Girls may develop oligomenorrhea or
secondary amenorrhea
• anovulatory cycles are common .
33. • Failure to gain weight or weight loss, despite
an increase in appetite.
• Weight loss is caused by increased
calorigenesis, increased gut motility and
malabsorption.
• Mild elevation of liver enzymes.
Magdalena .Graves’ disease, celiac disease and liver function
abnormalitiesin a patient —clinical manifestation and diagnostic
difficulties. The Journal of the Polish Biochemical Society Vol.
61, No 2/2014. 281-284
36. • Thyroid hormone stimulates bone
resorption,
• Serum alkaline phosphatase and
osteocalcin concentrations are high,
• The increase in bone resorption may
lead to an increase in serum calcium
concentrations, thereby inhibiting
parathyroid hormone secretion
• The net effect is osteoporosis and an
increased fracture risk.
37. • tremor are common.
• Deep tendon reflexes are hyperactive.
• Ataxia and chorea have been reported .
• Benign intracranial hypertension, has
been reported.
• Speech and language delay .
38. • Children with hyperthyroidism tend to have
greater mood swings and disturbances of
behavior
• Their attention span decreases, they are
usually hyperactive, they sleep poorly, and
their school performance deteriorates.
• Among very young children (<4 years), it
may cause neurodevelopmental delay
39. • The skin is warm in hyperthyroidism
because of increased blood flow; it is
also smooth because of a decrease in
the keratin layer .
• Sweating is increased .
• Onycholysis (loosening of the nails from
the nail bed, Plummer's nails) .
40. • Patients with hyperthyroidism tend to
have low serum total and high-density
lipoprotein (HDL) cholesterol
concentrations.
41. clinical
• history and physical
examination.
lab
• Thyroid function test.
• antibodies.
imaging
• Iodine uptake.
• Thyroid US.
42. • Serum TSH is suppressed. ( < 0.3 mU/l)
• Most children with hyperthyroidism have
very high serum FT4 and FT3 concen.
• Rarely, some children will have typical
physical features of Graves’ disease, but
thyroid function tests will be normal, so-
called “euthyroid Graves’ disease”.
43. • some patients may have normal FT4
concentrations and high FT3
concentrations –
a condition termed T3
toxicosis, which may be observed at
diagnosis or at times of relapse during the
course of the disease.
44. • (TSHR-Ab) to confirm Graves' disease as
the etiology.
• TRAbs are specific to GD.
• They are detected in most patients.(60-
94%)
• The most accurate TSHR-Ab test is a
measurement of thyroid stimulating
immunoglobulin (TSI).
45. • There is a positive correlation between
serum TRAb and FT4 levels.
• Serum TRAb levels are significantly higher
in young patients and in patients with a
severe initial clinical presentation.
46. • An alternative TSHR-Ab test is thyrotropin
binding inhibitor immunoglobulin (TBII).
• (up to 100%).
• TBII may be helpful if TSI is negative.
48. • If the TSI level is not elevated, the next step
is to perform radioactive iodine (RAI) uptake.
• 123-I is the radionucleotide of choice for
thyroid uptake and scans, as it has a shorter
half-life (13.2 hours) .
• And delivers a much smaller radiation dose
to the thyroid gland as compared with 131-I.
49. • The RAI uptake is elevated in Graves'
disease.
• scan typically will show diffuse uptake
throughout the gland.
• a thyroid scan should be added to work
up in the presence of thyroid nodularity.
50.
51.
52. • The thyroid gland is diffusely enlarged, and
often homogeneous.
• parenchymal hypervascularity is observed.
• Goiter size is variable,
Florentia K, Graves’ Disease in Childhood:Advances in
Management withAntithyroid Drug Therapy. Horm Res
2009;71:310–317
53.
54. • The optimal treatment of GD in childhood
remains a matter of debate
• Treatment is directed at alleviating
symptoms and reducing thyroid hormone
production.
• The choice of therapy is determined by
individual consideration of the risks and
benefits of the three treatment modalities
55.
56. • Most pediatric endocrinologists recommend
antithyroid drug therapy as initial treatment .
• There is, however, a growing acceptance
of radioactive iodine therapy for children
older than 10 years and adolescents as a
second, and in some cases initial treatment.
• Surgical near-total thyroidectomy is an
equally effective and safe treatment too.
57. • Antithyroid drugs are the best-established
treatment in this age group, and provide a
chance of permanent remission with
euthyroidism.
• Improvement is gradual.
• the course of treatment is long.
• and patients must be monitored for
potential side effects.
Antithyroid drugs
58. • Most children and adolescents with Graves'
respond well to an antithyroid drug, with 87
to 100% becoming euthyroid within a few
weeks to a few months .
• More prolonged use of ATD (at least 2–4
years) in children may be required to
achieve remission.
• carbimazole and its active metabolite,
methimazole are the drug of choice.
Antithyroid drugs
59. • Propylthiouracil is also effective.
• PTU may not be suitable for initial use
in children and adolescents with GD,
even with the risk of major adverse
reactions such as liver failure
excluded.
Antithyroid drugs
Sato H, Comparison of methimazole and propylthiouracil in
the management of children and adolescents withGraves'
disease: efficacy and adverse reactions duringinitial
treatment and long-term outcome. J Pediatr Endocrinol
Metab. 2011;24(5-6):257-63.
60. • may be reserved for:
• children who experience a minor side
effect with MMI that is not a
contraindication to continued
antithyroid drug use, and for whom
radioactive iodine or surgery are not
treatment option.
Antithyroid drugs
61. • Mechnisim of action:
• They inhibit thyroid hormone synthesis
by inhibiting the oxidation of iodide and
block the coupling of iodotyrosyl
residues in thyroglobulin.
• PTU can also block the peripheral
conversion of T4 to T3.
Antithyroid drugs
62. • The initial starting dose is based on clinical
severity, size of goiter, and biochemical
severity.
• PTU:
• 5–10mg/kg/day, with a maximum of 300
mg/ day in three equal doses.
• carbimazole or MMI
• 0.5–1 mg/kg/day, with a maximal dose of
30 mg per day.
Antithyroid drugs
64. • beta-blockers :
• during the first 2 weeks of management
may help to reduce the patient’s
symptoms.
• stopped when the patient becomes
euthyroid.
• Atenolol is preferred over propranolol.
65. • L –thyroxine:
• Giving levothyroxine in combination with
ATDs to enhance remission rates is no
more recommended.
Scott A. Rivkees .Pediatric Graves’ Disease:
Controversies in Management .Horm Res Paediatr
2010;74:305–311
66. • Dose adjustment:
• Moniter serum free T4 and total T3 every
four to six weeks initially.
• If these values are elevated, then increase
the dose of methimazole by approximately
0.25 mg/kg increments until thyroid
function is normal.
Antithyroid drugs
67. • Stopping therapy :
• When only a low dose is needed to
maintain a euthyroid state drug can be
stopped with close follow up.
Antithyroid drugs
68. • Remission :
• The rate of remission of Graves'
hyperthyroidism in children and
adolescents varied from 25 to 65 % .
• 25 % of children went into a remission
every 2 years.
Antithyroid drugs
69. • prepubertal children may take longer to
enter remission than pubertal children .
• and are also less likely to enter remission
even after prolonged treatment.
Gemli J [Graves's disease in children and adolescent:
study of seven cases.Tunis Med. 2008 Aug;86(8):728-34.
Antithyroid drugs
70. • Predictors of remission:
• lower thyroid hormone concentrations at
presentation.
• older age.
• euthyroid status after three months of
antithyroid drug therapy .
• smaller goiter size.
• high body mass index (BMI).
Antithyroid drugs
71. • Relapse :
• is defined as the presence of suppressed
levels of TSH (< 0.05 mIU/l) combined with
FT4 > 21 pmol/l or FT3 >11 pmol/l.
• the relapse rate in children varied from 3 to
47 % .
Florentia K, Graves’ Disease in Childhood:Advances in
Management withAntithyroid Drug Therapy. Horm Res
2009;71:310–317
Antithyroid drugs
72. • About 75% of patients relapse within
6 months of the end of drug
treatment.
• only 10% relapse after 18 months.
Antithyroid drugs
73. • Relapse risk factors:
• non-Caucasians.
• patients with higher initial free T4.
• the risk decreases with increasing age and
with longer duration of antithyroid drug
therapy.
• history of previous relapse
• Relapse pridictor:
• measurement of (TSHR-Ab) is the most
useful predictor of subsequent outcome
Antithyroid drugs
74. • Side effects :
Antithyroid drugs
MAJOR
MINOR
agranulocytosis
papular or urticarial skin rashes
vasculitis (lupus-like syndrome)
arthralgias
polyarthritis
nausea
Hepatitis
pruritis
cholestatic jaundice
Hair loss
liver failure
abnormal taste sensation.
thrombocytopenia
Stevens-Johnson syndrome *
Andrew J. Bauer.Approach to the Pediatric Patient with
Graves’ Disease: When Is Definitive Therapy Warranted?.J
Clin Endocrinol Metab 96: 580 –588, 2011
75. • In case of minor side effects:
• discontinue the drug for a few days until
the symptom subsides, and then resume.
• In case of major side effects:
• Patient should be treated with radioactive
iodine or surgery instead of antithyroid
medication
76. • agranulocytosis :.
• Agranulocytosis occurs in 0.1 to 0.5 %
• If a patient develops a febrile illness or
pharyngitis, antithyroid drug treatment
should be stopped immediately and
WBC measured.
Antithyroid drugs
77. • If the granulocyte count is normal,
antithyroid drug treatment may be restarted.
• If the granulocyte count is low but not
meeting criteria for agranulocytosis
( <500/mm3) neutrophil counts usually
recover spontaneously within one to two
weeks.
• Agranulocytosis (<500/mm3) is a
contraindication to future antithyroid drug
treatment .
Antithyroid drugs
78. • Severe hepatitis develops in up to 1:1000 of
children treated with PTU.
• liver failure occurring in 1:2000 to 1:4000 .
• Prior to initiating antithyroid drug therapy,
patients should have, as a baseline,
complete blood cell count and a liver profile .
Antithyroid drugs
79. • Pregnancy risks: .
• MMI is associated with an embryopathy
characterized by cutis aplasia and
omphalocele,osephegal and choanal
atresia.
• PTU with malformations of the face and
neck.
• both assosiated urinary tract malformations.
Antithyroid drugs
80. • RAI of graves was introduced for more
than 60 years more than one million
individual have been treated.
• (RAI) is an effective alternative treatment
for children and adolescents with Graves.
• some pediatric endocrinologists consider it
the initial treatment of choice in children
>10 years of age and adolescents.
Radioactive iodine
81. • Its recommend it for :
• patients who have recurrent hyperthyroidism
who request definitive treatment.
• those who have a major side effect while
receiving an antithyroid drug.
Radioactive iodine
82. • its recommend that if radioactive iodine is
used in children between 5 and 10 years
of age the total dose should be limited to
<10 milliCi.
• it should not be used at all in children <5
years of age.
Radioactive iodine
Scott A. Rivkees .Pediatric Graves’ Disease:
Controversies in Management .Horm Res Paediatr
2010;74:305–311
83. • Mechanisim of action:
• It is the beta radiation which destroys the
follicular cells.
• There would be epithelial swelling,
necrosis, oedema and leukocyte infiltration
of the thyroid gland.
• At the end, the thyroid gland becomes
fibrotic.
Radioactive iodine
84. • Dose:
• The dose of iodine-131 is usually from 50 to
200 microCi per gram of thyroid tissue
calculated according to the formula :
• Dose (mCi)=50-200microCi of I-131/gm of
thyroid X estimated thyroid weight.
• Usually, a dose of 150 microCi/g of thyroid
tissue yields radiation doses of 12,000 cGy
to the thyroid.
Radioactive iodine
85. • children with GD having free T4 estimates
>5 ng/dL (60 pmol/L) should be be
pretreated with methimazole and beta-
adrenergic blockade until total T4 and/or free
T4 estimates normalize
• Symptoms of hyperthyroidism may appear
4-10 days after iodine-131 administration.
• It can be controlled by beta-blockers or
Lugol's solution.
Radioactive iodine
86. • if radioactive iodine is to be used, it is
better to use a higher dose such that most
children become hypothyroid.
• To achieve hypothyroidism, doses of
radioactive iodine approximating 200 to
300 microCi/gram of thyroid tissue are
recommended.
Radioactive iodine
Scott A. Rivkees. An Optimal Treatment for Pediatric
Graves’ Disease Is Radioiodine. J Clin Endocrinol Metab
92: 797–800, 2007
87. • Cure rate:
• Hyperthyroidism persists in 25-40% if a dose
of 50-100 microCi/g thyroid tissue is given.
• It would be only 5-20% if 150-200 microCi/g
thyroid tissue is administered.
• The success rate is inversely related to the
size of the thyroid gland and the circulating
levels of TSAb
Radioactive iodine
Florentia K, Graves’ Disease in Childhood:Advances in
Management withAntithyroid Drug Therapy. Horm Res
2009;71:310–317
88. • factors that may predict a poorresponse to
RAI treatment in children.
• Graves’ eye disease .
• An interval of greater than 12 months from
diagnosis to RAI treatment .
• large thyroid glands ( > 80 g).
Radioactive iodine
Scott A. Rivkees .Pediatric Graves’ Disease:
Controversies in Management .Horm Res Paediatr
2010;74:305–311
89. • Pretreatment with ATD did not appear to
alter the efficacy or outcome after RAI
therapy.
• there was no relationship between ATD
use and an increased need for a second
dose of radioiodine.
Adriano N Cury. clinical experience with radioactive
iodine in the treatment of childhood and adolescent Graves’
Disease. Endocrine Connections.32-37 (2013)
Radioactive iodine
90. • When hyperthyroidism due to GD
persists after 6 months following 131-
I therapy.
• if there is minimal response 3 months
after therapy, retreatment with 131-I
is suggested.
Radioactive iodine
91. • Monitoring:
• We measure serum free T4 and TSH six
weeks after radioactive iodine treatment,
and then at three-month intervals then six
months.
Radioactive iodine
92. • Side effects:
• transient thyroid pain in about 5%.
• Nausea.
• transient hypocalcaemia
• thyroid storm.
Radioactive iodine
93. • There is no evidence that radioactive iodine
causes or worsens Graves' ophthalmopathy
in children or adolescents.
Radioactive iodine
Scott A. Rivkees. An Optimal Treatment for Pediatric
Graves’ Disease Is Radioiodine. J Clin Endocrinol Metab
92: 797–800, 2007
94. • four cases of thyroid malignancy in children
treated with iodine-131 were reported.
• They were all treated with low to moderate
doses of iodine-131.
• Recent studies have not revealed an
increased risk of thyroid cancer, leukemia,
or other cancers .
Radioactive iodine
Florentia K, Graves’ Disease in Childhood:Advances in
Management withAntithyroid Drug Therapy. Horm Res
2009;71:310–317
95. • The incidence of congenital anomalies
reported among the offspring of
patients treated with RAI does not differ
from the incidence in the general
population.
Radioactive iodine
Scott A. Rivkees .Pediatric Graves’ Disease:
Controversies in Management .Horm Res Paediatr
2010;74:305–311
96. • The association between the
development of parathyroid hyperplasia
and hyperparathyroidism after
radioactive iodine therapy is another
point of controversy.
Radioactive iodine
Christopher Breuer1 ,Pediatric Thyroid Disease: When is
Surgery Necessary, and Who Should be Operating on Our
Children? J Clin Res Pediatr En docrinol 2013;5(Suppl 1):79-
85 DO I: 10.4274/Jcrpe.817
97.
98. • the risks and outcomes for surgery have
been known since Kocher’s first successful
series of thyroidectomies in 1883.
• Surgery provides the most rapid resolution
of hyperthyroidism.
• avoids the theoretical risk of radiation.
• most of the patient is rendered hypothyroid,
and requires lifelong thyroid hormone
replacement therapy.
99. • indications for thyroidectomy include :
• Suspicious nodules or known cancer.
• pregnancy.
• large glands> (80 g).
• requirement for immediate control .
• obstructive or compressive symptoms.
• age younger than 5 yr.
James A. Lee,CONTROVERSY IN CLINICAL
ENDOCRINOLOGY The Optimal Treatment for Pediatric
Graves’ Disease Is Surgery. The Journal of Clinical
Endocrinology & Metabolism 92(3):801–803
100. • The operation of choice is total or near-total
thyroidectomies to reduce the risk of high
recurrence rate associated with subtotal
thyroidectomy.
• The complications of surgery in children are
similar to those in adults, and mortality is
very rare.
Christopher K Breuer,Effect of patient Age on surgical
outcomes for Graves’ disease: a case–control study of 100
consecutive patients at a high volume thyroid surgical center.
International Journal of Pediatric Endocrinology 2013, 2013:1
101. • Methimazole is typically given for one to
two months in preparation for
thyroidectomy.
• The vascularity of the gland is decreased
by adding iodine to ATD (5–10 drops of
Lugol’s solution) for 1 week before surgery.
Florentia K, Graves’ Disease in Childhood:Advances in
Management withAntithyroid Drug Therapy. Horm Res
2009;71:310–317
103. • when the thyroid remnant is less than 4 g,
the likelihood of recurrent thyrotoxicosis is
small.
• Surgical management of GD is technically
more challenging in children as evidenced
by longer operative times.
Christopher K Breuer,Effect of patient Age on surgical
outcomes for Graves’ disease: a case–control study of 100
consecutive patients at a high volume thyroid surgical center.
International Journal of Pediatric Endocrinology 2013, 2013:1
104. • Surgery should be performed by a
high-volume thyroid surgeon .
• temporary hypocalcemia occurs more
commonly in children than adults.
105. Ophthalmopathy treatment
• In children most physicians prefer a 'wait-
and-see' policy.
• Lubricants ,Head elevation at night
• Stop smoking (Adolescence)
• steroid therapy.
• orbital decompression.
• Recent studies have shown successful
therapy with the long-acting somatostatin
analogs (SM-a), octreotide and lanreotide.
GogakosAl, Pediatric aspects in Graves' orbitopathy.
Pediatr Endocrinol Rev. 2010 Mar;7 Suppl 2:234-44
106.
107. • No matter how children and adolescents
are treated, lifelong monitoring of thyroid
function is indicated.
• serum free T4 and TSH shoulde be
monitored every six months.
MONITORING
108. • problems with schooling.
• chronic loss of bone mineralization.
• thyroid storm.
109.
110. • Graves’ disease (GD) is the most
common cause of thyrotoxicosis in
children and adolescents.
• Caused by immunologic stimulation of the
thyroid-stimulating hormone receptor.
• lasting remission occurs in only a minority
of pediatric patients treated with
antithyroid drugs (ATDs) for many years.
111. • Thus the majority of pediatric patients
with GD will need thyroidectomy or
treatment with radioactive iodine.
• When ATDs are used in children, only
methimazole should be used.
• Propylthiouracil is associated with an
unacceptable risk of severe liver injury in
children and should never be used as
first-line therapy.
112. • If remission is not achieved after 2 years
of ATD therapy, 131- I or surgery may be
considered.
• When 131 I is used, administered doses
should be>150 Ci/g of thyroid tissue.
• When surgery is performed, near total or
total thyroidectomy is recommended.
113. • Choosing a treatment approach for
childhood GD is often a difficult and
highly personal decision.
• Discussion of the advantages and risks
of each therapeutic option by the
physician is essential to help the patient
and family select a treatment option.
