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Review Article On Graves’ Disease
Dan L. Longo, M.D., Editor
Terry J. Smith, M.D., and Laszlo Hegedüs, M.D., D.M.Sc.
Published in The New England Journal of
Medicine 375;16 October 20, 2016
Presenter:
Dr. Farhana Faruque
IMO, Medicine unit-2; SSMC & MH
Introduction
• Graves’ disease was first recognized in the
19th century as a syndrom comprising
an enlarged and overactive thyroid gland,
an accelerated heart rate, and ocular
abnormalities.
Introduction
• Graves’ disease has adverse effects on
quality of life, as a consequence of
somatic and psychiatric symptoms and an
inability to work and is associated with an
increased risk of death.
Introduction
• Debate persists concerning the diagnosis of
hyperthyroidism and adequate clinical care of
affected patients. Thyroid-associated
ophthalmopathy , the most common and
serious extrathyroidal manifestation, results
from underlying autoimmunity, but insights
into its pathogenesis and care remain elusive.
Epidemiology
• Graves’ disease is the most common
cause of hyperthyroidism, with an annual
incidence of 20 to 50 cases per 100,000
persons. The incidence peaks between
30 and 50 years of age, but people can
be affected at any age. The lifetime risk is
3% for women and 0.5% for men.
Epidemiology
• The annual incidence of Graves’ disease–
associated ophthalmopathy is 16 cases
per 100,000 women and 3 cases per
100,000 men. It is more common in
whites than in Asians.
Epidemiology
• Hyperthyroidism and ophthalmopathy
typically occur within 1 year of each
other but can be separated by decades.
Clinical Manifestations of Graves’
Disease.
Major Symptoms and Physical Signs
in Graves’Disease.
Symptoms:
• Weight loss (weight gain in 10% of patients).
• Palpitations.
• Dyspnea.
• Tremor.
• Tiredness, fatigue, muscle weakness.
• Heat intolerance, increased sweating.
• Increased stool frequency.
• Anxiety, altered mood, insomnia.
Major Symptoms and Physical Signs
in Graves’Disease.
Symptoms:
• Nervousness, hyperactivity.
• Pruritus.
• Thirst and polyuria.
• Menstrual disturbances in women
(oligomenorrhea or amenorrhea).
• Loss of libido.
• Neck fullness.
• Eye symptoms (swelling, pain, redness, double
vision.
Major Symptoms and Physical Signs
in Graves’Disease.
Physical signs of hyperthyroidism
• Tachycardia, atrial fibrillation.
• Systolic hypertension, increased pulse
pressure.
• Cardiac failure.
• Weight loss.
• Fine tremor, hyperkinesis, hyperreflexia.
Major Symptoms and Physical Signs
in Graves’Disease.
Physical signs of hyperthyroidism
• Warm, moist skin.
• Palmar erythema and onycholysis.
• Muscle weakness.
• Hair loss.
• Diffuse, palpable goiter and thyroid bruit.
• Mental-status and mood changes.
Clinical presentation
In elderly person(most common):
• Weight loss.
• Decrease appetite.
• Cardiac manifestation.
In adult (<60years):
• Palpable goitre (most common)
• Atrial fibrilation due to hyperthyroidism is
rare in patient less than 60 years of age but
more than 10% common in > 60 years.
Clinical presentation
• Diffuse thyroid enlargement is most
frequent, but many patients with Graves’
disease who live in iodine-deficient
regions have coexisting nodular goiter.
Clinical presentation
• Ophthalmopathy can be disfiguring and
can threaten sight. Its clinical course
typically follows a pattern originally
described by Rundle and Wilson.
Clinical presentation
• Proptosis, eyelid swelling, and diplopia
may prompt initial medical attention.
Some patients have dry eye, increased
tearing, and ocular discomfort early in
the active phase. This is followed by an
inactive phase in which the ocular
manifestations become stable.
Clinical presentation
The prevalence of distinct abnormalities
was as follows:
- Eyelid retraction, 92%;
-Exophthalmos, 62%;
-Extraocular muscle dysfunction, 43%;
-Ocular pain, 30%;
-Increased lacrimation,23%;
-Optic neuropathy, 6%.
Clinical presentation
• Mild eyelid retraction or lag may occur in
thyrotoxicosis from any cause, as a result of
increased sympathetic tone.
Clinical presentation
• Ophthalmopathy can be graded by assigning 1
point for each of the following manifestations:
eyelid erythema and edema, conjunctiva
injection, caruncular swelling, chemosis,
retrobulbar pain, and pain with eye
movement.
• A score of 3 or higher indicates active disease.
Clinical presentation
• Thyroid dermopathy occurs in 1 to 4% of
patients with Graves’ disease.
• It most frequently localizes to the
pretibial region but can occur elsewhere,
especially after trauma to the skin.
Clinical presentation
• Acropachy resembles clubbing of the
fingers or toes and occurs only in patients
with dermopathy.
Pathogenesis
• Theoretical modelof intrathyroidal Graves’Disease:
Pathogenesis
• Theoretical model of the pathogenesis of thyroid-
associated ophthalmopathy:
Diagnosis
• If pathognomonic features such as
ophthalmopathy or dermopathy are
absent and a diffuse goiter is not detected,
radionuclide scanning can confirm the
diagnosis.
Diagnosis
• Routine measurement of thyrotropin-
receptor antibodies is not mandatory, but
when such assays are performed, they
have 99% sensitivity and specificity for
Graves’ disease.47 They are also helpful in
diagnosing Graves’ disease in patients
with concomitant nodular goiter.
Diagnosis
Thyroid-Associated Ophthalmopathy:
• Computed tomography or magnetic
resonance imaging of the orbit is
warranted when the cause of ocular
manifestations remains uncertain.
Diagnosis
Thyroid-Associated Ophthalmopathy:
• These imaging studies are useful in
distinguishing extraocular muscle
enlargement from fat expansion.
Especially in cases of asymmetric
proptosis, ruling out orbital tumor and
arteriovenous malformation is important.
Diagnosis
Thyroid-Associated Ophthalmopathy:
• Several other imaging techniques,
including orbital ultrasonography,
scintigraphy with radiolabeled octreotide,
gallium scanning, and thermal imaging,
may be useful in more precisely defining
the orbital disease.
Diagnosis
• The diagnosis of hyperthyroidism is
based on characteristic clinical features
and biochemical abnormalities. Figure
shows a commonly used diagnostic
algorithm.
Diagnosis
Suspected
Graves’ disease
Measure serum Thyrotropin
and free thyroxine levels
Normal
thyrotropin
and free thyroxine
Normal or high serum
thyrotropin and
high free thyroxine
Hyperthyroidism
ruled out Thyrotropin-secreting
pituitary tumor
Thyroid hormone
resistance
Assay interference
Low
thyrotropin
and
high free
thyroxine
Low
thyrotropin
and normal
free
thyroxine
Hyperthyroidism
Measure free
triiodothyronine
Diagnosis
Hyperthyroidism
Measure free
triiodothyronine
Normal free
triiodothyronine
Subclinical
hyperthyroidism
Evolving Graves’
disease
Evolving toxic nodular
goiter
Excess thyroid
hormone
intake
Nonthyroidal illness
High free
triiodothyronine
Triiodothyronine
toxicosis
Measure
thyrotropinreceptor
antibodies
Present
Graves’
disease
Absent
Assess
radioiodine
uptake, obtain
radionuclide
scan, or both
Diagnosis
• Assess radioiodine
• uptake, obtain
• radionuclide scan, or both
Homogeneous,
increased uptake
Patchy uptake
or single nodule
Low or no uptake
Graves’
disease
Toxic nodular
goiter
Subacute thyroiditis
Excess thyroid hormone
Intake HCG-secretingtumor
Therapy
• Spontaneous remission occurs in a small
proportion of patients with Graves’ disease.
• Patients who currently smoke or formerly
smoked tobacco, the efficacy of medical
therapy is reduced and the importance
of smoking cessation cannot be overstated.
Therapy
• Autoimmune hypothyroidism develops in
10 to 20% of patients during long-term
follow-up.
Therapy
Antithyroid Drugs:
• Methimazole, carbimazole (which is
converted tomethimazole and is not
available in the United States), and
propylthiouracil inhibit thyroid peroxidase
and thus block thyroid hormone synthesis.
Therapy
Antithyroid Drugs:
• Methimazole is preferred for initial therapy
in both Europe and North America because
of its favorable side-effect profile.
• Durable remission occurs in 40 to 50% of
patients.
Therapy
Antithyroid Drugs:
• The recurrence rate is not further
decreased by providing treatment for more
than 18 months or by combining
antithyroid drugs with levothyroxine.
Therapy
Radioactive Iodine:
• It offers relief from symptoms of
hyperthyroidism within weeks.
• Treatment with antithyroid drugs may be
suspended 3 to 7 days before and after
radiotherapy in order to enhance its
efficacy, although this interval remains
controversial.
Therapy
Radioactive Iodine:
• Radioiodine is not associated with an
increased risk of cancer but is known to
provoke or worsen ophthalmopathy.
• Postablation thyroid function should be
monitored throughout life, and if
hypothyroidism develops, it should be
treated immediately.
Therapy
Surgery:
• Before patients undergo surgical
thyroidectomy, their thyroid hormone
levels should be normal to minimize the
risk of complications or a poor outcome,
which is higher for total thyroidectomy
than for subtotal thyroidectomy.
Therapy
Surgery:
• Treatment with inorganic iodide
commencing 1 week before surgery may
decrease thyroid blood flow, vascularity,
and blood loss but does not otherwise
influence surgical risk.
Therapy
Surgery:
• It is recommended that women who have
undergone surgery wait until the serum
thyrotropin level stabilizes with
levothyroxine therapy before attempting
conception.
Therapy
• Main Treatment Options for Graves’ Hyperthyroidism.
Treatment Mode of
Action
Route of
Administr
ation
Advantages Disadvantages Special
Considera-
tions
Beta-blockers Beta-blockers
competitively
block β-
adrenergic
receptors;
propranolol
may block
conversion
of thyroxine
to
triiodothyro-
nine.
Oral; may
be
administer
ed
intravenou
sly in
acute
cases
Ameliorates
sweating,
anxiety,
tremulousn
ess,
palpitations
, and
tachycardia
Does not
influence
course of
disease; use
cautiously in
patients with
asthma,
congestive
heart failure,
bradyarrhythm
ias,
or Raynaud’s
phenomenon
Use
cardioselectiv
e beta-
blockers,
especially in
patients with
COPD; use
calcium-
channel
blockers as
alternative
Therapy
• Main Treatment Options for Graves’ Hyperthyroidism.
Treatment Mode of Action Route of
Administration
Advantages Disadvantages Special
Considera-
tions
Antithyroid
drugs
(methimazol
e,
carbimazole,
and
propylthiour
acil)
Methimazole,
carbimazole,
and
propylthiouracil
block thyroid
peroxidase
and thyroid
hormone
synthesis;
propylthiouracilal
so blocks
conversion
of thyroxine to
triiodothyronine
Given as either
a single,
high fixed dose
(e.g.,
10–30 mg of
methimazole
or 200–600 mg
of
propylthiouracil
daily)
and adjusted as
euthyroidism
is achieved or
combined with
thyroxine
to prevent
hypothyroidism
(“block–
replace”
Regimen)
Outpatient
therapy; low
risk
of
hypothyroidi
sm; no
radiation
hazard or
surgical
risk;
remission
rate, 40–
50%
High recurrence
rate; frequent
testing required
unless
block-
replacement
therapy
is used; minor
side effects
in ≤5% of patients
(rash,
urticaria,
arthralgia, fever,
nausea,
abnormalities of
taste and smell)
Major side effects in
0.2–0.3% of
patients, usually
within first
3 months of therapy;
agranulocytosis
in <0.2% of patients;
hepatotoxicity
in ≤0.1%; cholestatic
for
the thionamides and
hepatocellular
necrosis for
propylthiouracil;
antineutrophil
cytoplasmic
antibody–associated
vasculitis
in ≤ 0.1% of patients
Therapy
• Main Treatment Options for Graves’ Hyperthyroidism.
Treatment Mode of
Action
Route of
Administr
ation
Advantages Disadvantages Special
Considera-
tions
Radioactive
iodine
(iodine-131)
Irradiation
causes
thyroid
cell damage
and cell
Death.
Oral;
activity
either fixed
(e.g., 15 mCi
[555 MBq])
or
calculated
on the
basis
of goiter
size
and uptake
and
turnover
Investigatio
ns.
Normally
outpatient
procedure,
definitive
therapy,
low cost,
few side
effects,
effectively
reduces
goiter size
Potential
radiation
hazards,
adherence to a
country’s
particular
radiation
regulations,
radiation
thyroiditis,
decreasing
efficacy with
increasing
goiter size,
eventual
hypothyroidism
in most patients.
Should not be
used in
patients with
active thyroid
ophthalmopat
hy;
contraindicate
d in women
who
are pregnant
or breast-
feeding
and for 6 wk
after breast-
feeding
has stopped.
Therapy
• Main Treatment Options for Graves’ Hyperthyroidism.
Treatment Mode of
Action
Route
of
Admi
nistra
tion
Advantages Disadvantages Special
Considera-
tions
Thyroidect
omy
Most or all
thyroid
tissue
is removed
surgically.
Rapid
euthyroidism,
recurrence
extremely rare,
no radiation
hazard,
definitive
histologic
results,
rapid relief of
pressure
symptoms.
Most expensive therapy,
hypothyroidism
is the aim, risks
associated with surgery
and anesthesiology, minor
complications in 1–2% of
patients (bleeding,
infection,
scarring), major
complications
in 1–4%
(hypoparathyroidism,
recurrent
laryngeal-nerve damage).
Does not
influence
course of
Graves’
ophthalmopat
hy; during
pregnancy,
is best
performed
during
the second
trimester.
Therapy
Treatment during Pregnancy:
• Graves’ disease affects approximately
0.1% of pregnancies.
• The lowest effective dose of an
antithyroid drug should be used to
maintain thyroid function at the upper
limit of the normal range in order to
avoid fetal hypothyroidism.
Therapy
Treatment during Pregnancy:
• Both propylthiouracil and methimazole
are associated with birth defects.
• The use of propylthiouracil in the first
trimester and methimazole during the
remainder of pregnancy is currently
recommended.
Therapy
Treatment during Pregnancy:
• Breast-feeding is safe with either
methimazole or propylthiouracil,but
methimazole is recommended for
postpartum therapy.
Treatments for Thyroid-Associated
Ophthalmopathy.
Therapy Mode of Action Pros and Cons Common
Doses
Mild active disease
-Topical solutions
Artificial tears
Glucocorticoids
Maintain tear film
Reduce inflammation
Rapid action, minimal side
effects
- Avoidance of wind,
light, dust, smoke
Reduces ocular
surface desiccation,
reduces irritation
-Elevation of head
during sleep
Reduces orbital
congestion
-Avoidance of eye
cosmetics
Reduces irritation Benefits not yet confirmed
-Selenium59 Uncertain Benefits not yet confirmed
Treatments for Thyroid-Associated
Ophthalmopathy.
Therapy Mode of Action Pros and Cons Common Doses
Moderate or severe active disease
-Systemic glucocorticoids
Oral
Glucocorticoids
Reduce inflammation
and orbital
congestion
Reduce inflammation
and orbital
congestion
Hyperglycemia,
hypertension,
Osteoporosis
Rapid onset of
anti-inflammatory
effect, fewer side
effects
than oral delivery,
liver
damage on rare
occasions
Up to 100 mg of
oral prednisone
daily, followed
by tapering of
The dose
Methylprednisol
one, 500 mg/wk
for 6 wk
followed by 250
mg/wk for 6 wk
Treatments for Thyroid-Associated
Ophthalmopathy.
Therapy Mode of Action Pros and Cons Common Doses
Moderate or severe active disease
-Orbital irradiation Reduces
inflammation
Can induce
retinopathy
2 Gy daily for 2
wk (20 Gy total)
-B-cell depletion Reduces autoreactive
B cells
Very expensive;
risks of infection,
cancer, allergic
reaction
Two 1000-mg
doses of
intravenous
rituximab 2 wk
apart
-Emergency orbital
decompression
Reduces orbital
volume
Treatments for Thyroid-Associated
Ophthalmopathy.
Therapy Mode of Action Pros and Cons Common
Doses
Stable disease (inactive)
-Orbital decompression
(fat removal)
Reduces orbital
volume
Postoperative diplopia,
pain
-Bony decompression
of the lateral and
medial walls
Reduces proptosis
by enlarging
orbital space
Postoperative diplopia,
pain,sinus bleeding,
cerebrospinal fluid leak
-Strabismus repair Improves eye
alignment,
reduces diplopia
-Eyelid repair Improves
appearance,
reduces
lagophthalmos,
and improves
function
Future Therapies
• Agents blocking the thyrotropin and insulin-
like growth factor receptors are under
consideration.
• A randomized, placebo-controlled clinical
trial of the efficacy and safety of
teprotumumab, an insulin-like growth
factor 1 receptor–blocking monoclonal
antibody, in patients with active, severe
ophthalmopathy has recently been
completed.
Future Therapies
• Graves’ disease appears to be an ideal
candidatefor antigen-specific therapy, since
the identity of a dominant self-antigen is
known.
• Restoring immune tolerance to the
thyrotropin receptor and other relevant
autoantigens remains the ultimate goal,
sparing patients nonspecific
immunosuppression and toxic drugs.
THANK YOU

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Presentation graves journal

  • 1. Review Article On Graves’ Disease Dan L. Longo, M.D., Editor Terry J. Smith, M.D., and Laszlo Hegedüs, M.D., D.M.Sc. Published in The New England Journal of Medicine 375;16 October 20, 2016 Presenter: Dr. Farhana Faruque IMO, Medicine unit-2; SSMC & MH
  • 2. Introduction • Graves’ disease was first recognized in the 19th century as a syndrom comprising an enlarged and overactive thyroid gland, an accelerated heart rate, and ocular abnormalities.
  • 3. Introduction • Graves’ disease has adverse effects on quality of life, as a consequence of somatic and psychiatric symptoms and an inability to work and is associated with an increased risk of death.
  • 4. Introduction • Debate persists concerning the diagnosis of hyperthyroidism and adequate clinical care of affected patients. Thyroid-associated ophthalmopathy , the most common and serious extrathyroidal manifestation, results from underlying autoimmunity, but insights into its pathogenesis and care remain elusive.
  • 5. Epidemiology • Graves’ disease is the most common cause of hyperthyroidism, with an annual incidence of 20 to 50 cases per 100,000 persons. The incidence peaks between 30 and 50 years of age, but people can be affected at any age. The lifetime risk is 3% for women and 0.5% for men.
  • 6. Epidemiology • The annual incidence of Graves’ disease– associated ophthalmopathy is 16 cases per 100,000 women and 3 cases per 100,000 men. It is more common in whites than in Asians.
  • 7. Epidemiology • Hyperthyroidism and ophthalmopathy typically occur within 1 year of each other but can be separated by decades.
  • 8. Clinical Manifestations of Graves’ Disease.
  • 9. Major Symptoms and Physical Signs in Graves’Disease. Symptoms: • Weight loss (weight gain in 10% of patients). • Palpitations. • Dyspnea. • Tremor. • Tiredness, fatigue, muscle weakness. • Heat intolerance, increased sweating. • Increased stool frequency. • Anxiety, altered mood, insomnia.
  • 10. Major Symptoms and Physical Signs in Graves’Disease. Symptoms: • Nervousness, hyperactivity. • Pruritus. • Thirst and polyuria. • Menstrual disturbances in women (oligomenorrhea or amenorrhea). • Loss of libido. • Neck fullness. • Eye symptoms (swelling, pain, redness, double vision.
  • 11. Major Symptoms and Physical Signs in Graves’Disease. Physical signs of hyperthyroidism • Tachycardia, atrial fibrillation. • Systolic hypertension, increased pulse pressure. • Cardiac failure. • Weight loss. • Fine tremor, hyperkinesis, hyperreflexia.
  • 12. Major Symptoms and Physical Signs in Graves’Disease. Physical signs of hyperthyroidism • Warm, moist skin. • Palmar erythema and onycholysis. • Muscle weakness. • Hair loss. • Diffuse, palpable goiter and thyroid bruit. • Mental-status and mood changes.
  • 13. Clinical presentation In elderly person(most common): • Weight loss. • Decrease appetite. • Cardiac manifestation. In adult (<60years): • Palpable goitre (most common) • Atrial fibrilation due to hyperthyroidism is rare in patient less than 60 years of age but more than 10% common in > 60 years.
  • 14. Clinical presentation • Diffuse thyroid enlargement is most frequent, but many patients with Graves’ disease who live in iodine-deficient regions have coexisting nodular goiter.
  • 15. Clinical presentation • Ophthalmopathy can be disfiguring and can threaten sight. Its clinical course typically follows a pattern originally described by Rundle and Wilson.
  • 16. Clinical presentation • Proptosis, eyelid swelling, and diplopia may prompt initial medical attention. Some patients have dry eye, increased tearing, and ocular discomfort early in the active phase. This is followed by an inactive phase in which the ocular manifestations become stable.
  • 17. Clinical presentation The prevalence of distinct abnormalities was as follows: - Eyelid retraction, 92%; -Exophthalmos, 62%; -Extraocular muscle dysfunction, 43%; -Ocular pain, 30%; -Increased lacrimation,23%; -Optic neuropathy, 6%.
  • 18. Clinical presentation • Mild eyelid retraction or lag may occur in thyrotoxicosis from any cause, as a result of increased sympathetic tone.
  • 19. Clinical presentation • Ophthalmopathy can be graded by assigning 1 point for each of the following manifestations: eyelid erythema and edema, conjunctiva injection, caruncular swelling, chemosis, retrobulbar pain, and pain with eye movement. • A score of 3 or higher indicates active disease.
  • 20. Clinical presentation • Thyroid dermopathy occurs in 1 to 4% of patients with Graves’ disease. • It most frequently localizes to the pretibial region but can occur elsewhere, especially after trauma to the skin.
  • 21. Clinical presentation • Acropachy resembles clubbing of the fingers or toes and occurs only in patients with dermopathy.
  • 22. Pathogenesis • Theoretical modelof intrathyroidal Graves’Disease:
  • 23. Pathogenesis • Theoretical model of the pathogenesis of thyroid- associated ophthalmopathy:
  • 24. Diagnosis • If pathognomonic features such as ophthalmopathy or dermopathy are absent and a diffuse goiter is not detected, radionuclide scanning can confirm the diagnosis.
  • 25. Diagnosis • Routine measurement of thyrotropin- receptor antibodies is not mandatory, but when such assays are performed, they have 99% sensitivity and specificity for Graves’ disease.47 They are also helpful in diagnosing Graves’ disease in patients with concomitant nodular goiter.
  • 26. Diagnosis Thyroid-Associated Ophthalmopathy: • Computed tomography or magnetic resonance imaging of the orbit is warranted when the cause of ocular manifestations remains uncertain.
  • 27. Diagnosis Thyroid-Associated Ophthalmopathy: • These imaging studies are useful in distinguishing extraocular muscle enlargement from fat expansion. Especially in cases of asymmetric proptosis, ruling out orbital tumor and arteriovenous malformation is important.
  • 28. Diagnosis Thyroid-Associated Ophthalmopathy: • Several other imaging techniques, including orbital ultrasonography, scintigraphy with radiolabeled octreotide, gallium scanning, and thermal imaging, may be useful in more precisely defining the orbital disease.
  • 29. Diagnosis • The diagnosis of hyperthyroidism is based on characteristic clinical features and biochemical abnormalities. Figure shows a commonly used diagnostic algorithm.
  • 30. Diagnosis Suspected Graves’ disease Measure serum Thyrotropin and free thyroxine levels Normal thyrotropin and free thyroxine Normal or high serum thyrotropin and high free thyroxine Hyperthyroidism ruled out Thyrotropin-secreting pituitary tumor Thyroid hormone resistance Assay interference Low thyrotropin and high free thyroxine Low thyrotropin and normal free thyroxine Hyperthyroidism Measure free triiodothyronine
  • 31. Diagnosis Hyperthyroidism Measure free triiodothyronine Normal free triiodothyronine Subclinical hyperthyroidism Evolving Graves’ disease Evolving toxic nodular goiter Excess thyroid hormone intake Nonthyroidal illness High free triiodothyronine Triiodothyronine toxicosis Measure thyrotropinreceptor antibodies Present Graves’ disease Absent Assess radioiodine uptake, obtain radionuclide scan, or both
  • 32. Diagnosis • Assess radioiodine • uptake, obtain • radionuclide scan, or both Homogeneous, increased uptake Patchy uptake or single nodule Low or no uptake Graves’ disease Toxic nodular goiter Subacute thyroiditis Excess thyroid hormone Intake HCG-secretingtumor
  • 33. Therapy • Spontaneous remission occurs in a small proportion of patients with Graves’ disease. • Patients who currently smoke or formerly smoked tobacco, the efficacy of medical therapy is reduced and the importance of smoking cessation cannot be overstated.
  • 34. Therapy • Autoimmune hypothyroidism develops in 10 to 20% of patients during long-term follow-up.
  • 35. Therapy Antithyroid Drugs: • Methimazole, carbimazole (which is converted tomethimazole and is not available in the United States), and propylthiouracil inhibit thyroid peroxidase and thus block thyroid hormone synthesis.
  • 36. Therapy Antithyroid Drugs: • Methimazole is preferred for initial therapy in both Europe and North America because of its favorable side-effect profile. • Durable remission occurs in 40 to 50% of patients.
  • 37. Therapy Antithyroid Drugs: • The recurrence rate is not further decreased by providing treatment for more than 18 months or by combining antithyroid drugs with levothyroxine.
  • 38. Therapy Radioactive Iodine: • It offers relief from symptoms of hyperthyroidism within weeks. • Treatment with antithyroid drugs may be suspended 3 to 7 days before and after radiotherapy in order to enhance its efficacy, although this interval remains controversial.
  • 39. Therapy Radioactive Iodine: • Radioiodine is not associated with an increased risk of cancer but is known to provoke or worsen ophthalmopathy. • Postablation thyroid function should be monitored throughout life, and if hypothyroidism develops, it should be treated immediately.
  • 40. Therapy Surgery: • Before patients undergo surgical thyroidectomy, their thyroid hormone levels should be normal to minimize the risk of complications or a poor outcome, which is higher for total thyroidectomy than for subtotal thyroidectomy.
  • 41. Therapy Surgery: • Treatment with inorganic iodide commencing 1 week before surgery may decrease thyroid blood flow, vascularity, and blood loss but does not otherwise influence surgical risk.
  • 42. Therapy Surgery: • It is recommended that women who have undergone surgery wait until the serum thyrotropin level stabilizes with levothyroxine therapy before attempting conception.
  • 43. Therapy • Main Treatment Options for Graves’ Hyperthyroidism. Treatment Mode of Action Route of Administr ation Advantages Disadvantages Special Considera- tions Beta-blockers Beta-blockers competitively block β- adrenergic receptors; propranolol may block conversion of thyroxine to triiodothyro- nine. Oral; may be administer ed intravenou sly in acute cases Ameliorates sweating, anxiety, tremulousn ess, palpitations , and tachycardia Does not influence course of disease; use cautiously in patients with asthma, congestive heart failure, bradyarrhythm ias, or Raynaud’s phenomenon Use cardioselectiv e beta- blockers, especially in patients with COPD; use calcium- channel blockers as alternative
  • 44. Therapy • Main Treatment Options for Graves’ Hyperthyroidism. Treatment Mode of Action Route of Administration Advantages Disadvantages Special Considera- tions Antithyroid drugs (methimazol e, carbimazole, and propylthiour acil) Methimazole, carbimazole, and propylthiouracil block thyroid peroxidase and thyroid hormone synthesis; propylthiouracilal so blocks conversion of thyroxine to triiodothyronine Given as either a single, high fixed dose (e.g., 10–30 mg of methimazole or 200–600 mg of propylthiouracil daily) and adjusted as euthyroidism is achieved or combined with thyroxine to prevent hypothyroidism (“block– replace” Regimen) Outpatient therapy; low risk of hypothyroidi sm; no radiation hazard or surgical risk; remission rate, 40– 50% High recurrence rate; frequent testing required unless block- replacement therapy is used; minor side effects in ≤5% of patients (rash, urticaria, arthralgia, fever, nausea, abnormalities of taste and smell) Major side effects in 0.2–0.3% of patients, usually within first 3 months of therapy; agranulocytosis in <0.2% of patients; hepatotoxicity in ≤0.1%; cholestatic for the thionamides and hepatocellular necrosis for propylthiouracil; antineutrophil cytoplasmic antibody–associated vasculitis in ≤ 0.1% of patients
  • 45. Therapy • Main Treatment Options for Graves’ Hyperthyroidism. Treatment Mode of Action Route of Administr ation Advantages Disadvantages Special Considera- tions Radioactive iodine (iodine-131) Irradiation causes thyroid cell damage and cell Death. Oral; activity either fixed (e.g., 15 mCi [555 MBq]) or calculated on the basis of goiter size and uptake and turnover Investigatio ns. Normally outpatient procedure, definitive therapy, low cost, few side effects, effectively reduces goiter size Potential radiation hazards, adherence to a country’s particular radiation regulations, radiation thyroiditis, decreasing efficacy with increasing goiter size, eventual hypothyroidism in most patients. Should not be used in patients with active thyroid ophthalmopat hy; contraindicate d in women who are pregnant or breast- feeding and for 6 wk after breast- feeding has stopped.
  • 46. Therapy • Main Treatment Options for Graves’ Hyperthyroidism. Treatment Mode of Action Route of Admi nistra tion Advantages Disadvantages Special Considera- tions Thyroidect omy Most or all thyroid tissue is removed surgically. Rapid euthyroidism, recurrence extremely rare, no radiation hazard, definitive histologic results, rapid relief of pressure symptoms. Most expensive therapy, hypothyroidism is the aim, risks associated with surgery and anesthesiology, minor complications in 1–2% of patients (bleeding, infection, scarring), major complications in 1–4% (hypoparathyroidism, recurrent laryngeal-nerve damage). Does not influence course of Graves’ ophthalmopat hy; during pregnancy, is best performed during the second trimester.
  • 47. Therapy Treatment during Pregnancy: • Graves’ disease affects approximately 0.1% of pregnancies. • The lowest effective dose of an antithyroid drug should be used to maintain thyroid function at the upper limit of the normal range in order to avoid fetal hypothyroidism.
  • 48. Therapy Treatment during Pregnancy: • Both propylthiouracil and methimazole are associated with birth defects. • The use of propylthiouracil in the first trimester and methimazole during the remainder of pregnancy is currently recommended.
  • 49. Therapy Treatment during Pregnancy: • Breast-feeding is safe with either methimazole or propylthiouracil,but methimazole is recommended for postpartum therapy.
  • 50. Treatments for Thyroid-Associated Ophthalmopathy. Therapy Mode of Action Pros and Cons Common Doses Mild active disease -Topical solutions Artificial tears Glucocorticoids Maintain tear film Reduce inflammation Rapid action, minimal side effects - Avoidance of wind, light, dust, smoke Reduces ocular surface desiccation, reduces irritation -Elevation of head during sleep Reduces orbital congestion -Avoidance of eye cosmetics Reduces irritation Benefits not yet confirmed -Selenium59 Uncertain Benefits not yet confirmed
  • 51. Treatments for Thyroid-Associated Ophthalmopathy. Therapy Mode of Action Pros and Cons Common Doses Moderate or severe active disease -Systemic glucocorticoids Oral Glucocorticoids Reduce inflammation and orbital congestion Reduce inflammation and orbital congestion Hyperglycemia, hypertension, Osteoporosis Rapid onset of anti-inflammatory effect, fewer side effects than oral delivery, liver damage on rare occasions Up to 100 mg of oral prednisone daily, followed by tapering of The dose Methylprednisol one, 500 mg/wk for 6 wk followed by 250 mg/wk for 6 wk
  • 52. Treatments for Thyroid-Associated Ophthalmopathy. Therapy Mode of Action Pros and Cons Common Doses Moderate or severe active disease -Orbital irradiation Reduces inflammation Can induce retinopathy 2 Gy daily for 2 wk (20 Gy total) -B-cell depletion Reduces autoreactive B cells Very expensive; risks of infection, cancer, allergic reaction Two 1000-mg doses of intravenous rituximab 2 wk apart -Emergency orbital decompression Reduces orbital volume
  • 53. Treatments for Thyroid-Associated Ophthalmopathy. Therapy Mode of Action Pros and Cons Common Doses Stable disease (inactive) -Orbital decompression (fat removal) Reduces orbital volume Postoperative diplopia, pain -Bony decompression of the lateral and medial walls Reduces proptosis by enlarging orbital space Postoperative diplopia, pain,sinus bleeding, cerebrospinal fluid leak -Strabismus repair Improves eye alignment, reduces diplopia -Eyelid repair Improves appearance, reduces lagophthalmos, and improves function
  • 54. Future Therapies • Agents blocking the thyrotropin and insulin- like growth factor receptors are under consideration. • A randomized, placebo-controlled clinical trial of the efficacy and safety of teprotumumab, an insulin-like growth factor 1 receptor–blocking monoclonal antibody, in patients with active, severe ophthalmopathy has recently been completed.
  • 55. Future Therapies • Graves’ disease appears to be an ideal candidatefor antigen-specific therapy, since the identity of a dominant self-antigen is known. • Restoring immune tolerance to the thyrotropin receptor and other relevant autoantigens remains the ultimate goal, sparing patients nonspecific immunosuppression and toxic drugs.