Hyperthyroidism - ClinicalKey

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FIRST CONSULT

Hyperthyroidism

Revised: January 26, 2012

Copyright Elsevier BV. All rights reserved.

Key points

Hyperthyroidism, the presence of excessive thyroid hormone produced by the thyroid gland, is
usually caused by Graves disease, toxic multinodular goiter, toxic uninodular goiter, and
thyroiditis

Diagnosis involves testing to assess levels of thyroid-stimulating hormone (TSH) and thyroid
function
Treatment is aimed at relieving symptoms and restoring metabolic function
Take immediate action in patients with thyroid storm, a life-threatening condition

characterized by exaggerated signs and symptoms of hyperthyroidism, including fever,

arrhythmia, and altered mental status. It is usually precipitated by concurrent illness or injury
but also occurs following withdrawal of antithyroid medications

Background
Description

Hyperthyroidism refers to conditions caused by excessive thyroid hormone produced by

thyroid gland
Most common causes of hyperthyroidism are Graves disease, toxic multinodular goiter,
toxic uninodular goiter, and thyroiditis
Less common causes of hyperthyroidism are thyroid-stimulating hormone (TSH)-producing
tumors, pituitary resistance to thyroid hormone, trophoblastic disease, and iodine ingestion
Signs and symptoms generally result from stimulation of adrenergic nervous system
Overt hyperthyroidism is defined as low serum TSH with elevated peripheral thyroid
hormone values (free T3and/or free T4), while subclinical hyperthyroidism is defined as low
serum TSH with normal peripheral thyroid hormone values

Epidemiology

Incidence and prevalence

Women: 100/100,000
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Men: 33/100,000

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Demographics
Age:
Graves disease peaks in third to fourth decade of life, rare before 10 years of age
Toxic multinodular goiter is more common in patients older than 50 years and with history
of nontoxic goiter

Toxic solitary nodules are most common in patients in third and fourth decades of life
Gender:
Graves disease affects more women than men in a ratio of 7:1
Toxic multinodular goiter is more common in women
Genetics:
Graves disease has a familial predisposition and can overlap clinically and immunologically
with Hashimoto disease

Graves disease has a genetic predisposition that is polygenic in nature

Increased frequency in human leukocyte antigen (HLA) haplotype B8/DR3 in white
population, HLA Bw36 in Japanese population, and HLA Bw46 in Chinese population
Geography:
Iodine-induced hyperthyroidism: Outbreaks of thyrotoxicosis have occurred when thyroid
supplements added into diets of previously iodine-deficient populations

Causes and risk factors

Causes

Common causes:
Toxic diffuse goiter or Graves disease (most common cause): an autoimmune disease in
which thyroid gland is being stimulated by thyrotropin receptor antibodies, also known as
thyroid-stimulating immunoglobulin

Toxic multinodular goiter: multiple areas in thyroid gland overproduce thyroid hormone
independently of TSH

Toxic uninodular goiter (adenoma): solitary nodule in thyroid gland overproducing thyroid
hormone independently of TSH

Subacute thyroiditis : usually idiopathic but sometimes can be result of virally mediated
inflammation and destruction of thyroid gland. Consequently, stored thyroid hormones are
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released into circulation, causing transient thyrotoxic state and thyroid pain

Postpartum or sporadic thyroiditis: painless autoimmune inflammation of thyroid gland, in

which stored thyroid hormones are released into circulation, causing a transient thyrotoxic
state

Amiodarone-induced (types I and II): Type I is iodine-induced, while Type II is type of

thyroiditis

Iatrogenic or factitious thyrotoxicosis: due to intentional or inadvertent ingestion of

exogenous thyroid hormone
Rare causes:
TSH-secreting tumors: TSH-secreting pituitary adenoma or pituitary resistance to thyroid
hormones

Functioning trophoblastic tumors: includes hydatidiform mole, choriocarcinoma, or

metastatic embryonal carcinoma of the testis

Iodine-induced hyperthyroidism (Jod-Basedow disease): occurs when excess iodine is given

to patients with autonomous nodular goiter
Widely metastatic follicular thyroid cancer
Struma ovarii
Interferon-induced
Risk factors
Positive family history of hyperthyroid condition
Gender: females predisposed to hyperthyroid condition
Other autoimmune disorders
Iodide repletion after deprivation

Associated disorders
Myasthenia gravis

Pernicious anemia
Type I diabetes mellitus
Vitiligo
Rheumatoid arthritis
Systemic lupus erythematosus
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Addison disease

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Screening

Not applicable.

Primary prevention
Preventive measures
Tobacco:

Encourage reduction and cessation of tobacco use

Diet:
Maintain diet adequate in iodine
Other:
Patients with family history of hyperthyroidism should be made aware of signs and
symptoms of hyperthyroidism to assist with early diagnosis
Family history of autoimmune disease is an identifiable risk factor for Graves disease

Diagnosis

Summary approach

If hyperthyroidism is suspected clinically, obtain high-sensitivity TSH and thyroid function

tests consisting of T4, T3resin uptake, and free thyroid index or free T4. In overt
hyperthyroidism, TSH should be undetectable (very low) and T4levels elevated.
Occasionally T4is not significantly elevated, and T3radioimmunoassay or free T3should be
checked to confirm T3toxicosis

When hyperthyroidism and exophthalmos are present, diagnosis is Graves disease

In absence of exophthalmos, thyroid scan and uptake is warranted to define nature of
thyroid disease
Low or absent uptake with poor imaging of gland suggests thyroiditis, iodine-induced
hyperthyroidism, use of exogenous thyroid hormone, amiodarone-induced thyroiditis, or
autoimmune hypothyroidism

Normal or high uptake is seen in Graves disease and toxic uninodular or toxic multinodular
goiter. Falsely elevated uptake may also be seen in patients recently treated with diuretics,
which may deplete endogenous iodine. Thyroid scan helps discriminate between these
entities

Erythrocyte sedimentation rate (ESR) may be elevated in subacute thyroiditis, and

antiperoxidase antibodies are useful in diagnosing autoimmune thyroid disease (including
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Hashimoto thyroiditis and Graves disease) and as risk factor for postpartum and
drug-related thyroiditis

In patients who are thyroglobulin antibody-negative, serum thyroglobulin is elevated in all

conditions characterized by excess endogenous thyroid hormone but is low in factitious
hyperthyroidism

Clinical presentation
Symptoms

Nervousness
Sweating
Sensitivity to heat
Fatigue
Eye irritation
Palpitations
Dyspnea
Increase in appetite
Increased frequency of bowel movement, or diarrhea
Oligomenorrhea or amenorrhea
Swelling in legs
Signs
Tachycardia
Fever
Weight loss (although weight gain can occur in up to one third of patients due to increased
appetite)

Warm, moist skin

Tremor and hyperreflexia
Eye signs (erythema, lid retraction, stare)
Exophthalmos (Graves disease)
Goiter
Bruit over thyroid (Graves disease)
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Tenderness of thyroid gland (subacute thyroiditis)

Gynecomastia
Splenomegaly
Gynecomastia
Thyroid acropachy (Graves disease)

In elderly patients:
Unexplained weight loss
Congestive heart failure
Atrial fibrillation
Proximal muscle weakness
In children:
Accelerated linear growth
Eye signs are more common
Examination
Note appearance of toxicity or confusion. Consider thyroid storm
Assess vital signs, including weight. Patients will usually be tachycardic at rest, and there
may be orthostasis secondary to decreased intravascular volume
Examine hands for warmth and fine tremor
Check eyes for erythema, stare, lid lag, and proptosis. Comparison of a photograph from the
past with patient's current appearance can bring out subtle changes in proptosis

Inspect neck for goiter, thyroid nodules, lymphadenopathy, asymmetry, and thyroid bruit
Perform cardiac exam to check for arrhythmia and for cardiac bruit, which may have
resulted from long-standing hyperthyroidism and high-output failure
Inspect muscle strength and reflexes, especially proximal muscle weakness. Have patient
squat; usually he/she has difficulty standing back up

Patients will have brisk reflexes with rapid relaxation phase and may even exhibit clonus
Questions to ask
Presenting condition:
What symptoms are you experiencing? For how long? Have you ever experienced them
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before? Graves disease can have periods of remission

Has anyone commented that your appearance is changed? Patients frequently report that
others have commented that they look flushed or bright-eyed
Do you have any difficulty swallowing or pain in your throat? Suggests significant goiter
size, recent change in goiter size, or possibly subacute thyroiditis
Do you have any history of head or neck irradiation? Patients with nodular thyroid disease
and history of irradiation are at increased risk of thyroid cancer
Do you have difficulty climbing steps, arising from a chair, or lifting objects over your
head? Suggests weakness of proximal muscles
Have you taken any over-the-counter or illicit drugs? Ephedrine, pseudoephedrine, and
phenylpropanolamine all mimic and exacerbate the symptoms of hyperthyroidism, as do
several illicit drugs

Do you have any medication allergies? Allergy to thioamides will affect choice of therapy
Are you pregnant or breastfeeding? Affects choice of therapy
Contributory or predisposing factors:
What other medical conditions do you have? Other autoimmune diseases may suggest
predisposition to Graves disease

Do you use tobacco? Tobacco usage may aggravate Graves ophthalmopathy and may
influence therapy
Have you recently taken intravenous radiographic contrast, expectorants, amiodarone, or
health foods containing kelp or seaweed? These agents have high iodine contents and may
exacerbate hyperthyroidism and confound thyroid uptake testing
Family history:
Any family history of thyroid problems? Autoimmune thyroid disease can present as
hyperthyroidism or hypothyroidism in a family

Diagnostic testing

High-sensitivity thyroid-stimulating hormone (TSH) (178807)is the best single screen for

hyperthyroidism. Normal test rules out all sources of thyrotoxicosis except those from
excess TSH

Peripheral thyroid function tests (281595): Free T4is preferred as lead thyroid function test after

TSH. Regular T4and T3resin uptake are alternatives to assess level of circulating T4levels.
Useful to assess severity and follow therapy

T (1214352) 3 (1214352) radioimmunoassay or free T (1214352) 3 (1214352): Occasionally a thyroid

gland will produce excess of T3rather than T4. Useful if T4is normal but patient is clinically

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hyperthyroid. May also be useful in assessing severity and monitoring therapy

Radioiodine uptake (178815)measures avidity with which thyroid gland is absorbing iodine.

High or normal in cases of hyperthyroidism from Graves disease or toxic nodular goiter but
low or absent in thyroiditis

Thyroid scan (178831)can be done with either 123-iodine or 99-technetium and identifies

areas in thyroid gland that are taking up iodine. Useful in evaluating palpable nodules in
thyroid gland to tell if they are functioning and in differentiating Graves disease from toxic
nodular goiter

Thyroperoxidase antibodies (1190096)are usually elevated in Graves disease and often in

autoimmune thyroiditis and may help to differentiate between autoimmune and

non-autoimmune causes of hyperthyroidism

Testing for thyrotropin receptor autoantibodies (1214353)is useful in the pregnant Graves patient
to assess likelihood that newborn will have hyperthyroidism

Erythrocyte sedimentation rate (ESR) (1190097)is elevated in subacute thyroiditis

High-sensitivity thyroid-stimulating hormone (TSH)

Description

Cuffed venous blood sample

Normal range
High-sensitivity TSH: 0.5 to 4.6 U/mL
Comments
Can detect TSH as low as 0.01 U/mL
May combine with other thyroid function test (T4, T3resin uptake, and free thyroid index,
or free T4, T3radioimmunoassay)

Peripheral thyroid function tests

Description

Thyroxine (T4), triiodothyronine (T3) resin uptake, and free thyroid index or free T4,
T3radioimmunoassay, or free T3
Cuffed venous blood sample
Normal ranges
Serum T4: 5.5 to 12.5 g/dL
Serum T3resin uptake: 25% to 35%
Serum T3: 60 to 180 ng/dL

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Free T4: 0.9 to 2.3 ng/dL

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Free T3: 130 to 450 pg/dL

Comments
Confirms hyperthyroid state

T3 radioimmunoassay or free T3

Description

Venous blood test to measure circulating unbound T3

Normal result
0.2 to 0.5 ng/dL
Comments
Most accurate and direct measurement of T3
May be clinically helpful in states in which total hormone levels may be abnormal due to
alterations in serum protein levels ( eg , severe illness, pregnancy)

Radioiodine uptake

Description

123-iodine or 99-technetium is used to assess thyroid function as measured by gland's

ability to trap iodine. Tracer dose of radioactive isotope is administered and then
followed by measuring external radiation present in gland at given times
Normal ranges
Measured at 6 hours after administration: 5% to 15%
Measured at 24 hours after administration: 8% to 30%
Comments
Useful in calculating the dose of 131-iodine for therapy of hyperthyroidism
Contraindicated in pregnancy because of risk of low levels of radiation to developing
thyroid in fetus
Lactating women may undergo radioiodine uptake testing with I-123 if they pump and
discard breast milk for 2 to 3 days after test in order to avoid delivering radioactive
iodine to nursing infant

Costly and inconvenient

Thyroid scan

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Description

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Nuclear medicine test using a radioactive iodine tracer to measure thyroid functionality
Normal result
Lobes of thyroid appear as pear-shaped homogenous structures connected by thin
isthmus on scintiscan
Dimensions of normal thyroid are up to 5 cm x 3 cm
Comments
Useful in delineating structural abnormalities of thyroid; helps distinguish Graves
disease from multinodular goiter and toxic adenoma from cold nodule
Patient must return for scanning at 24 hours
Contraindicated in pregnancy and breastfeeding because of risk of radiation to
developing thyroid in fetus or infant
Similar to uptake function test. Imaging can be performed in combination with thyroid
uptake but requires larger dose of isotope
Overall, of limited use in evaluation of hyperthyroidism

Thyroperoxidase antibodies tests

Description

Immunoassay for antibodies to thyroid peroxidase and thyroglobulin. Also called

antiperoxidase (antimicrosomal) and antithyroglobulin antibodies
Normal result
Absence of antibodies
Comments
Useful in diagnosis of autoimmune thyroid diseases such as Hashimoto thyroiditis and
Graves disease

Thyrotropin receptor autoantibodies

Description

Venous blood sample

Normal result
Thyroid stimulating hormone: < 130% basal activity
Comments
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Several types of autoantibodies to thyrotropin receptors occur, and several are capable of
activating thyroid hormone production

The most clinically relevant marker in Graves disease is thyroid-stimulating hormone

Thyroid-stimulating hormone can cross the placenta, causing Graves disease in an infant
born to a woman with Graves disease

Erythrocyte sedimentation rate

Description

Venous blood sample

Normal ranges
Adults (Westergren method):
Men under 50 years old: less than 15 mm/h
Men over 50 years old: less than 20 mm/h
Women under 50 years old: less than 20 mm/h
Women over 50 years old: less than 30 mm/h
Children (Westergren method):
Newborn: 0 to 2 mm/h
Neonatal to puberty: 3 to 13 mm/h
Comments
Elevated ESR is seen in subacute and suppurative thyroiditis but is nonspecific for those
conditions

Differential diagnosis
Anxiety

Anxiety is an abnormal and overwhelming sense of apprehension that is often

accompanied by physiologic signs

Characterized by palpitations, irritability, tremulousness, fatigue, and insomnia. Fatigue

differs from hyperthyroidism in that anxiety patient has no desire to be active and may
be fatigued upon awakening
Tachycardia is present on exam, but heart rate is normal during sleep
Palms of hands are cool and clammy
Thyroid function tests are normal in anxiety states
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Thyroid malignancy

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Malignancy may metastasize and terminate fatally

Hypermetabolism may be present as increased sweating and weight loss
If anemia is present, patient may be tachycardic
Goiter is absent, and thyroid function tests are normal

Acquired immune deficiency syndrome

Acquired immune deficiency syndrome (AIDS) leaves individual vulnerable to illnesses that a

healthy immune system would readily overcome

Weight loss
Sweats, fever
Fatigue
Tachycardia

Goiter is absent, and thyroid function tests are normal

Thyroiditis

Thyroiditis may be difficult to distinguish from hyperthyroidism if goiter is present, but

radioiodine uptake can be diagnostic

In Hashimoto thyroiditis, thyroid gland is firmer and more lobulated than in Graves
disease
Antithyroid antibodies may be elevated in both conditions
In subacute thyroiditis, antibodies are negative, gland is usually tender to touch, there is
often a viral prodrome, and ESR is elevated
In post-partum or sporadic thyroiditis, antibody levels may also be elevated, but course
more closely resembles that of subacute thyroiditis. Patient may subsequently develop
permanent hypothyroidism

Pheochromocytoma

Pheochromocytoma most commonly arises from chromaffin cells of adrenal medulla but

may be found wherever chromaffin tissue is located

Tachycardia, hypermetabolism, tremulousness, sweating, and irritability are frequently

present

Eyelid retraction my be present in pheochromocytoma

In pheochromocytoma, patients have diastolic hypertension as opposed to reduced
diastolic pressures in thyrotoxicosis

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In pheochromocytoma, urinary excretions of vanillylmandelic acid, metanephrines, and

catecholamines are increased, and thyroid function tests are generally normal

Consultation

Patients with significant ophthalmopathy ( eg , weakness in extraocular muscles, diplopia,

corneal ulcerations, papilledema, venous congestion, and visual field defects) require urgent
referral to endocrinologist and/or ophthalmologist experienced with orbitopathy from
Graves disease

Patients suspected of thyroid storm should be referred for specialist care in an

intensive-care setting

Infiltrative orbitopathy of Graves disease may follow a course independent from thyroid

disease and may be uninfluenced by treatment of thyroid disease. Nonsurgical therapies

may be undertaken by endocrinologist or surgical intervention made available by a
specialist with experience in this disorder

Significant hyperthyroidism in elderly patients is poorly tolerated and may lead to

psychosis, cardiac ischemia, or arrhythmia, which can be difficult to manage with
conventional therapies unless hyperthyroidism is controlled

Treatment

Summary approach
Immediate action

Thyroid storm is a life-threatening condition which can be precipitated by general

anesthesia or serious infection and needs swift attention and aggressive therapy. Treat any
concurrent illness, but also start several measures to control thyroid dysfunction
Thyroid storm is treated with a regimen that includes -blocker, thioureylene,
glucocorticoids, and iodine solution
Hyperthyroidism
Goals for treatment are to alleviate signs and symptoms, return metabolism to normal state,
and prevent long-term complications

Radioactive 131-iodine (178920)is very effective at ablating hyperthyroidism. Frequently used

except in children and pregnant women. Achieves permanent cure of hyperthyroidism and
has lower costs and complications when compared to surgery. However, there is risk of
permanent hypothyroidism and thyroiditis, as well as usual risks associated with radiation

Thioureylenes (253548)are antithyroid medications that inhibit thyroid hormone biosynthesis.

They offer patients a chance of permanent remission; advantages include low cost and no
risk of permanent hypothyroidism. May be used as monotherapy in patients with mild

disease or to treat symptoms before patients are treated with radioactive iodine or surgery.
Remember that both thioureylenes and 131-iodine are effective only in patients producing
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excess thyroid hormone ( eg , Graves disease) but not in those with thyroiditis

Subtotal or total thyroidectomy (178904)is rarely treatment of first choice. May be recommended

in young children, pregnant women who have had adverse reaction to pharmacotherapy,

patients with compressive symptoms, those in whom there is concern about possibility of
thyroid cancer, and when rapid control of hyperthyroidism is needed or avoidance of

exacerbation of symptoms is required ( ie , cardiac patients). Like radioactive iodine, there

is risk of permanent hypothyroidism and severe adverse effects; cost may also be an issue

with surgery. Surgery may be more effective in treating Graves ophthalmopathy than other
treatment modalities
Treatment with alternative agents, such as lithium, potassium perchlorate, iodine ipodate

and cholestyramine may be considered in certain circumstances as adjunctive treatment or

in patients intolerant to thioureylenes but are not commonly used
-blockers are used to reduce adrenergic manifestations of hyperthyroidism and may be
used concomitantly with antithyroid therapies. Propranolol is often considered -blocker of
choice since it is thought to have additional benefit of blocking peripheral conversion of
T4to T3. Atenolol is also sometimes used

Calcium-channel blockers are rarely used (unless -blockers are contraindicated) as they do
not have any antiadrenergic properties. Diltiazem may be useful for rate control in patients
intolerant to propranolol

Hyperthyroid patients should be educated about relevant lifestyle (2395139)matters, such as

avoidance of tobacco, especially in the setting of Graves disease, as there is some correlation
between smoking and worsening eye disease

There is no evidence that moderating amount of iodine in diet will have any clinical effect in
hyperthyroid patients
Graves disease
Graves disease may remit in up to 40% of cases and can be treated with thioureylenes for 6
to 18 months
If no remission is achieved, patient can receive radioactive 131-iodine or thyroidectomy
There is some evidence to suggest that Graves ophthalmopathy improves after thyroid
surgery but not after radioactive iodine ablation. Rituximab has been used to treat Graves
ophthalmopathy

Active Graves ophthalmopathy may benefit from various means of eye protection, such as
sunglasses, artificial tears, elevation of head of bed, and eye protection at night

Steroids, surgical decompression, or external radiation may be required in patients with

sever ophthalmopathy
Goiter
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Patients with toxic uninodular and multinodular goiter do not go into remission and require
surgery or radioactive 131-iodine. Thioureylenes and/or -blockers may be given prior to
definitive therapies

Medications

Thioureylenes

Indication

Treatment of hyperthyroidism
Dose information
Methimazole :

Adult: 15 to 60 mg/d by mouth given in divided doses every 8 hours

Pediatric: 0.4 mg/kg/d by mouth given in divided doses every 8 hours
Propylthiouracil :

Adult: 300 to 450 mg/d initially by mouth given in divided doses every 8 hours; usual
maintenance dose is 100 to 150 mg/d, given in divided doses every 8 hours to a
maximum of 1200 mg/d
Pediatric: 5 to 7 mg/kg/d by mouth given in divided doses every 8 hours
Major contraindications
Breastfeeding (methimazole)
Comments
Safety and efficacy of propylthiouracil in patients younger than 6 years of age have not
been established

Propylthiouracil is considered second-line agent in pediatric patients due to case reports

of fulminant hepatic failure associated with its use in children
Use caution in patients with bone marrow suppression

Evidence

A small randomized trial that compared a single daily dose of methimazole versus a
single daily dose of propylthiouracil for 12 weeks in 71 patients with newly diagnosed
Graves disease found that methimazole (15 mg/d) was more effective than
propylthiouracil in promoting euthyroidism. [1] Level of evidence: 2

A randomized trial compared radioactive iodine (with or without subsequent

corticosteroids for 3 months) versus 18 months of methimazole in 443 patients with
hyperthyroidism. It found that radioactive iodine treatment was more frequently
associated with appearance or worsening of ophthalmopathy compared with

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treatment with methimazole. However, this effect was often transient and could be
prevented by administration of prednisone. [2] Level of evidence: 2

A meta-analysis of 12 trials involving different regimens concluded that optimal

duration of treatment with antithyroid drugs in Graves disease is 12 to 18 months. [3]

Level of evidence: 2

References

Propranolol

Indication

Propranolol is indicated to reduce adrenergic manifestations of hyperthyroidism

This is an off-label indication

Dose information
Adult: 10 to 40 mg orally every 6 hours
Pediatric: 2 mg/kg/d orally, given in equally divided doses every 6 to 8 hours
Major contraindications
Asthma
AV block
Bradycardia
Cardiogenic shock
Sick sinus syndrome
Comments
Safety and efficacy in pediatric patients have not been established
Doses should be gradually reduced before ceasing therapy. Do not stop treatment
abruptly, risk of withdrawal syndrome

Use caution in patients with diabetes (may mask signs of hypoglycemia), severe
peripheral vascular disease, hyperthyroidism, pheochromocytoma, vasospastic angina,
coronary artery disease, bronchospastic disease, myocardial infarction, cardiac failure,
and those patients preparing for surgery

Evidence

A small, double-blind, crossover, placebo-controlled trial compared propranolol (40

mg/d) with placebo as adjunctive treatment (with carbimazole) for hyperthyroid
tremor and tachycardia in seven patients. All patients showed improvement, but
propranolol group showed greater improvement than placebo group. [4] Level of

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evidence: 2

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References

Non-drug treatments

Radioactive 131-iodine

Description

Destruction of an overactive thyroid gland using radioactive iodine

Indication
Hyperthyroidism
Complications
Hypothyroidism
Comments
Patient's dose is based on radioactive thyroid uptake, so this needs to be obtained first
Contraindicated in pregnancy or breast-feeding
Safety not yet established in children younger than 10 years of age
Elderly patients should receive antithyroid drugs prior to radioactive iodine and for
several weeks after to decrease any risk of worsening hyperthyroidism from postradiation
thyroiditis. However, antithyroid drugs should be interrupted for 3 to 7 days immediately
prior to radioiodine treatment
Moderate orbitopathy may worsen with radioactive 131-iodine therapy
Patients with active orbitopathy (and especially cigarette smokers) should avoid

radioactive 131-iodine if possible. Radioiodine therapy has been associated with

aggravating the eye disease. A trial for 6 to 24 months of antithyroid medications to see if
remission can be achieved is advisable. If radioactive iodine must be administered,
glucocorticoids should be added to decrease immune reaction

Very effective in ablating hyperthyroidism from Graves disease

Most common therapy in U.S.
Nodular goiter is more resistant to therapy, so it may require retreatment if
hyperthyroidism persists for more than 6 months after treatment

Thyroidectomy

Description

Surgical removal of thyroid gland

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Indication

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Often recommended in young children (in whom safety of radioactive iodide therapy is
not established)
Pregnant women who have had a major adverse reaction to antithyroid agents. If
thyroidectomy is necessary in pregnancy it is safest in second trimester
Patients in whom a large goiter is causing tracheal compression
Patients in whom there is concern about possibility of thyroid cancer
Potentially patients with Graves ophthalmopathy
When rapid control of hyperthyroidism is necessary or when avoidance of worsening of
symptoms is required ( ie , cardiac patients)
Complications
Bleeding:
Postoperative bleeding in neck is a particular problem because it occurs in confined
space with airway. Even small amounts of hematoma can cause airway compromise
Typical signs and symptoms of postoperative bleeding include expanding mass,
impending sense of doom, squeaky voice, patient sitting up and leaning forward, and
airway compromise

If bleeding is suspected, it is critical that incision and underlying tissue layers are opened
to trachea immediately. This should not be delayed by intubation or by returning patient
back to operating room

Recurrent laryngeal nerve injury:

Up to 5% of patients have temporary hoarseness that may be result of traction injury to
nerve
By definition, a temporary injury resolves within 6 months
Less than 1% of patients have permanent nerve injury, which can be ameliorated through
a variety of procedures that aim to tense vocal cord

Bilateral nerve injury can necessitate tracheostomy if airway is compromised

Hypocalcemia:
Temporary hypocalcemia occurs in up to 5% of patients and is usually due to reversible
ischemia of parathyroid glands
By definition, temporary hypocalcemia resolves within 6 months
Permanent hypocalcemia occurs in less than 1% of patients, and patients may require

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large doses of oral calcium and vitamin D supplements several times per day

Infection:
Infection is exceedingly rare in neck
Comments
Patient should receive thioureylenes to render them euthyroid preoperatively to decrease
risk of thyroid storm

Iodine (eg, 3-5 drops of Lugol solution three times a day by mouth for 10-14 days before
surgery) should be given preoperatively in patients with Graves disease to decrease
vascularity of gland and possibility of thyroid storm

-blockers may be added to reduce symptoms and sequelae of hyperthyroidism

High probability (more than 60%) of hypothyroidism and need for life-long thyroid
hormone replacement

Evidence

A meta-analysis of studies involving a total of 7241 patients with Graves disease found
that thyroidectomy (either partial or total) is successful treatment for
hyperthyroidism. All patients who underwent total thyroidectomy were rendered
hypothyroid. Of patients who underwent subtotal thyroidectomy, nearly 60% were

rendered euthyroid, about 26% became hypothyroid, and about 8% had persistent or
recurrent hyperthyroidism. [5] Level of evidence: 2
A comprehensive study of the English clinical literature from 1980 looked at the
experience in seven randomized, controlled trials (RCTs) of nearly 10,000 patients

undergoing total thyroidectomy for Graves disease and concluded that procedure was
effective therapy for both Graves disease and Graves ophthalmopathy. [6] Level of
evidence: 2

References

Other measures

Adequate diet high in protein, vitamins, and calories

Avoidance of physical exertion
Smoking cessation may slow deterioration in Graves orbitopathy
Monitor patient's weight and tobacco consumption at each visit

Special circumstances
Comorbidities

Hyperthyroidism in pregnancy results in increased rates of fetal loss and required

treatment

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Due to reports of fulminant hepatic failure in pregnant women taking propylthiouracil, it

is recommended that methimazole be first-line drug except in first trimester of
pregnancy, when propylthiouracil is preferred because of concerns about methimazoleinduced embryopathy

Frequently, pregnancy has an ameliorative effect on Graves disease, and patients can be
maintained on low dose of antithyroid medication. Patients should be seen at 4- to
6-week intervals. Thyroid-stimulating antibodies can be checked at 22 to 26 weeks
gestation and will help predict risk for neonatal hyperthyroidism

Patients should be seen 6 weeks postpartum because Graves is likely to worsen then.
Radioactive 131-iodine is contraindicated in pregnancy and when nursing. Patients with

postpartum thyroiditis can be reassured that it is self-limiting; however, regular

monitoring of thyroid function is warranted. During hyperthyroid phase, -blockers can
be used to alleviate symptoms

Radioactive 131-iodine has been used safely in patients under 20 years of age but has
limited experience in patients younger than 10 years

Elderly patients benefit from pretreatment with antithyroid drugs to achieve

euthyroidism before treatment with radioactive iodine because postradiation thyroiditis

with exacerbation of hyperthyroidism is a possible complication and may have
particularly severe consequences in the elderly

Patient satisfaction/lifestyle priorities

Pregnancy must be avoided for 6 months after radioactive therapy

Radioactive iodine cannot be administered to a breast-feeding patient

Consultation

Patients with worsening clinical status despite initiating therapy

Preoperative surgical evaluation for thyroid surgery
Patients with thyrotoxicosis of unclear etiology

Follow-up

Plan for review

Therapy with antithyroid medications can continue for 6 months to 2 years for Graves disease
During this time, patients are monitored with thyroid function tests every 3 months
Dosages of antithyroid medications are adjusted to maintain peripheral thyroid hormone tests
in high-normal range and patients free from symptoms

-blockers can be discontinued when symptoms of tachycardia abate

Patients receiving radioactive 131-iodine should be seen 6 weeks after therapy is received, at

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which time thyroid function tests are ordered to check for hypothyroidism. Thyroid function
tests should be monitored every 6 to 8 weeks until euthyroidism is achieved

Secondary prevention
Patients must be followed with TSH annually after therapy. Hyperthyroidism may recur in
patients treated with thioureylenes, and hypothyroidism can develop in patients treated with
radioiodine or surgery
Prognosis
Prognosis is good with therapy. There will be some failures with initial therapy, but therapy
can be repeated or different therapy tried
Therapeutic failure:
Patients who develop serious allergic reactions to thioureylenes will need alternative therapy,
usually radioiodine
To achieve temporary control of thyrotoxicosis while awaiting effects of radioiodine,
propranolol can be prescribed for symptomatic relief
Patients who fail to respond to radioactive iodine within 6 to 9 months should be retreated
with larger dose
Pretreatment with propylthiouracil may decrease effectiveness of 131-iodine ablation
Recurrence:
About 50% of patients may not achieve sustained remission with thioamides, in which case
therapy can be repeated. However, it is more common to give definitive therapy with
radioiodine or thyroidectomy if Graves disease recurs or fails to remit
Clinical complications
Hyperthyroidism is risk factor for development of osteoporosis later in life
Untreated hyperthyroidism, even subclinical hyperthyroidism, puts patient at risk for atrial
fibrillation

Patient education

Information for patient or caregiver:

Patients given radioactive 131-iodine frequently develop hypothyroidism and require lifelong
thyroid hormone supplementation
Weight gain is common during therapy for hyperthyroidism and is due to reduced caloric

needs of euthyroid patient compared with hyperthyroid patient. Patients should concentrate
on healthy eating habits
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Patients receiving treatment for hyperthyroidism frequently experience hair loss, a result of
fluctuating hormone levels and not an adverse effect of medication

Questions patients ask:

Patients may be so frightened by prospect of radioactive iodine scanning and therapy that they
refuse radioactive therapy, thus limiting therapeutic options
Patients may refuse radioactive therapy because they have seen large weight gains in friends
and family members who have had it. In some cases, they refuse any therapy for
hyperthyroidism

Patients with a history of hyperthyroidism are at risk for osteoporosis and will need to be
advised and counseled

Online information for patients

Mayo Clinic: Hyperthyroidism (overactive thyroid) (http://www.mayoclinic.com/health/hyperthyroidism

/DS00344)

American Academy of Family Physicians: Hyperthyroidism (http://familydoctor.org/familydoctor

/en/diseases-conditions/hyperthyroidism.html)

Cleveland Clinic: Hyperthyroidism (http://my.clevelandclinic.org/disorders/hyperthyroidism

/hic_hyperthyroidism.aspx)

Resources

Summary of evidence
Evidence

A small randomized trial that compared a single daily dose of methimazole versus a
single daily dose of propylthiouracil for 12 weeks in 71 patients with newly diagnosed
Graves disease found that methimazole (15 mg/d) was more effective than
propylthiouracil in promoting euthyroidism. [1] Level of evidence: 2

A randomized trial compared radioactive iodine (with or without subsequent

corticosteroids for 3 months) versus 18 months of methimazole in 443 patients with

hyperthyroidism. It found that radioactive iodine treatment was more frequently

associated with appearance or worsening of ophthalmopathy compared with treatment
with methimazole. However, this effect was often transient and could be prevented by
administration of prednisone. [2] Level of evidence: 2

A meta-analysis of 12 trials involving different regimens concluded that optimal duration

of treatment with antithyroid drugs in Graves disease is 12 to 18 months. [3] Level of
evidence: 2

A small, double-blind, crossover, placebo-controlled trial compared propranolol (40

mg/d) with placebo as adjunctive treatment (with carbimazole) for hyperthyroid tremor
and tachycardia in seven patients. All patients showed improvement, but propranolol

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group showed greater improvement than placebo group. [4] Level of evidence: 2

A meta-analysis of studies involving a total of 7241 patients with Graves disease found
that thyroidectomy (either partial or total) is successful treatment for hyperthyroidism.

All patients who underwent total thyroidectomy were rendered hypothyroid. Of patients
who underwent subtotal thyroidectomy, nearly 60% were rendered euthyroid, about 26%
became hypothyroid, and about 8% had persistent or recurrent hyperthyroidism. [5]
Level of evidence: 2

A comprehensive study of the English clinical literature from 1980 looked at the
experience in seven RCTs of nearly 10,000 patients undergoing total thyroidectomy for
Graves disease and concluded that procedure was effective therapy for both Graves
disease and Graves ophthalmopathy. [6] Level of evidence: 2

References

References

Evidence references

1. Homsanit M, Sriussadaporn S, Vannasaeng S, Peerapatdit T, Nitiyanant W, Vichayanrat A.

Efficacy of single daily dosage of methimazole vs. propylthiouracil in the induction of
euthyroidism. Clin Endocrinol (Oxf). 2001;54:385-90
View In Article (refInSitucid_05363)

2. Bartalena L, Marcocci C, Bogazzi F, et al. Relation between therapy for hyperthyroidism

and the course of Graves' ophthalmopathy. N Engl J Med. 1998;338:73-8

View In Article (refInSitucid_05361) | CrossRef (http://dx.doi.org/10.1056%2FNEJM199801083380201)

3. Abraham P, Avenell A, Park CM, Watson WA, Bevan JS. A systematic review of drug
therapy for Graves' hyperthyroidism. Eur J Endocrinol. 2005;153:489-98
View In Article (refInSitu47149) | CrossRef (http://dx.doi.org/10.1530%2Feje.1.01993)

4. Henderson JM, Portmann L, Van Melle G, et al. Propranolol as an adjunct therapy for
hyperthyroid tremor. Eur Neurol. 1997;37:182-5
View In Article (refInSitucid_05362)

5. Palit TK, Miller CC 3rd, Miltenburg DM. The efficacy of thyroidectomy for Graves' disease:
a meta-analysis. J Surg Res. 2000;90:161-5
View In Article (refInSitucid_05365) | CrossRef (http://dx.doi.org/10.1006%2Fjsre.2000.5875)

6. Stlberg P, Svensson A, Hessman O, Akerstrm G, Hellman P. Surgical treatment of

Graves' disease: evidence-based approach. World J Surg. 2008;32:1269-77
View In Article (refInSitu36053) | CrossRef (http://dx.doi.org/10.1007%2Fs00268-008-9497-9)

Guidelines

The American Association of Clinical Endocrinologists (http://www.aace.com/)has produced the

following:
Baskin HJ, Cobin RH, Duick DS, et al; AACE Thyroid Task Force. Medical guidelines for
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clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism

(https://www.aace.com/sites/default/files/hypo_hyper.pdf). Endocr Pract. 2002,8:457-69

Gharib H, Papini E, Paschke R, et al; AACE/AME/ETA Task Force on Thyroid Nodules.

Medical guidelines for clinical practice for the diagnosis and management of thyroid nodules

(https://www.aace.com/sites/default/files/ThyroidGuidelines.pdf). Endocr Pract. 2010;16:1-43

Gharib H, Tuttle RM, Baskin HJ, Fish LH, Singer PA, McDermott MT. Joint statement
on management from the AACE, ATA, and ES. Subclinical thyroid dysfunction

(http://jcem.endojournals.org/content/90/1/581.full). J Clin Endocrinol Metabol. 2005;90:581-85

The American Thyroid Association (http://www.thyroid.org/)has produced the following:

Cooper DS, Doherty GM, Haugen BR et al; ATA Guidelines Taskforce. Management

guidelines for patients with thyroid nodules and differentiated thyroid cancer (http://www.thyroid.org
/professionals/publications/documents/Guidelinesthy2006.pdf). Thyroid. 2006;16:109-142

The U.S. Preventive Services Task Force (http://www.uspreventiveservicestaskforce.org/)has produced

the following:
Berg AO, Allan JD, Frame P, et al. Recommendation statement. Screening for Thyroid
Disease (http://www.uspreventiveservicestaskforce.org/3rduspstf/thyroid/thyrrs.htm). Ann Intern
Med. 2004;140:125-27

The Endocrine Society (http://www.endo-society.org/)has produced the following:

Abalovich M, Amino N, Barbour LA, et al. Clinical practice guideline. Management of

thyroid dysfunction during pregnancy and postpartum (http://www.endo-society.org/guidelines/final

/upload/Clinical-Guideline-Management-of-Thyroid-Dysfunction-during-Pregnancy-Postpartum.pdf). J

Clin Endocrinol Metabol. 2007;92:S1-47

Additional guidance material includes the following:

Surks MI, Ortiz E, Daniels GH, et al. Subclinical thyroid disease: scientific review and guidelines
for diagnosis and management (http://jama.ama-assn.org/cgi/content/full/291/2/228). JAMA.
2004;291:228-38

Further reading

Nayak B, Hodak SP. Hyperthyroidism. Endocrinol Metab Clin North Am.

2007;36:617-56

Pearce EN. Diagnosis and management of thyrotoxicosis. BMJ. 2006;332:1369-73

Nayak B, Burman K. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North
Am. 2006;35:663-86
McKeown NJ, Tews MC, Gossain VV, Shah SM. Hyperthyroidism. Emerg Med Clin North
Am. 2005;23:669-85

Brent GA. Clinical practice. Graves' disease. N Engl J Med. 2008;358:2594-605

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Pearce EN, Braverman LE. Hyperthyroidism: advantages and disadvantages of medical

therapy. Surg Clin North Am. 2004;84:833-47

LeBeau SO, Mandel SJ. Thyroid disorders during pregnancy. Endocrinol Metab Clin
North Am. 2006;35:117-36

Kung AW. Clinical review: Thyrotoxic periodic paralysis: a diagnostic challenge. J Clin
Endocrinol Metab. 2006;91:2490-95

Chattaway JM, Klepser TB. Propylthiouracil versus methimazole in treatment of Graves'

disease during pregnancy. Ann Pharmacother. 2007;41:1018-22

Salvi M, Vannucchi G, Campi I, et al. Treatment of Graves' disease and associated

ophthalmopathy with the anti-CD20 monoclonal antibody rituximab: an open study. Eur
J Endocrinol. 2007;156:33-40

Bartalena L, Tanda ML. Clinical practice. Graves ophthalmopathy. N Engl J Med.

2009;360:994-1001

Bahn R. Graves' ophthalmopathy. N Engl J Med. 2010;362:726-38

Basaria S, Cooper DS. Amiodarone and the thyroid. Am J Med. 2005;118:706-14
Okosieme OE, Chan D, Price SA, et al. The utility of radioiodine uptake and thyroid

scintigraphy in the diagnosis and management of hyperthyroidism. Clin Endocrinol

(Oxf). 2010;72:122-27
Abraham P, Avenell A, McGeoch SC, et al. Antithyroid drug regimen for treating Graves'
hyperthyroidism. Cochrane Database Syst Rev 2010:CD003420

Pearce EN, Farwell AP, Braverman LE. Thyroiditis. N Engl J Med. 2003;348:2646-55
Cooper DS. Antithyroid drugs. N Engl J Med. 2005;352:905-17
Bahn RS, Burch HS, Cooper DS, et al. The role of propylthiouracil in the management of

Graves' disease in adults: report of a meeting jointly sponsored by the American Thyroid
Association and the Food and Drug Administration. Thyroid. 2009;19:673-74
Rivkees SA, Mattison DR. Propylthiouracil (PTU) hepatotoxicity in children and
recommendations for discontinuation of use. Int J Pediatr Endocrinol.
2009;2009:1320-41
Rivkees SA. The treatment of Graves' disease in children. J Pediatr Endocrinol Metab.
2006;19:1095-111
Cohen-Lehman J, Dahl P, Danzi S, Klein I. Effects of amiodarone therapy on thyroid
function. Nat Rev Endocrinol. 2010;6:34-41
Bogazzi F, Bartalena L, Martino E. Approach to the patient with amiodarone-induced
thyrotoxicosis. J Clin Endocrinol Metab. 2010;95:2529-35
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Reid JR, Wheeler SF. Hyperthyroidism: diagnosis and treatment. Am Fam Physician.
2005,72:623-30,635-6

Welker MJ, Orlov D. Thyroid nodules. Am Fam Physician. 2003;67:559-66

Wilson GR, Curry RW Jr. Subclinical thyroid disease. Am Fam Physician.
2005;72:1517-24

Codes

Shrier DK, Burman KD. Subclinical hyperthyroidism: controversies in management. Am

Fam Physician. 2002,65:431-38

ICD-9 code

242.00 Toxic diffuse goiter, without mention of thyrotoxic crisis or storm

242.01 Toxic diffuse goiter, with mention of thyrotoxic crisis or storm
242.10 Toxic uninodular goiter, without mention of thyrotoxic crisis or storm
242.11 Toxic uninodular goiter, with mention of thyrotoxic crisis or storm
242.30 Toxic nodular goiter, unspecified, without mention of thyrotoxic crisis or storm
242.31 Toxic nodular goiter, unspecified, with mention of thyrotoxic crisis or storm
242.90 Thyrotoxicosis without mention of goiter or other cause, without mention of
thyrotoxic crisis or storm
242.91 Thyrotoxicosis without mention of goiter or other cause, with mention of
thyrotoxic crisis or storm

245.1 Thyroiditis, subacute

FAQ

245.9 Thyroiditis, unspecified

What is the natural history of subacute thyroiditis? Initial phase of thyrotoxicosis is
observed due to release of thyroid hormone from damaged thyroid cells, which is
accompanied by thyroid pain. Initial phase is followed by a hypothyroid phase and then by
return to euthyroidism. Disease runs its course over 2 to 3 months

What is postpartum thyroiditis? Autoimmune thyroiditis that occurs in approximately

5% of women after delivery. Clinical course similar to subacute thyroiditis but it is painless.
May have thyrotoxic phase and can lead to development of hypothyroidism. Should be
differentiated from postpartum depression

What is the role of nuclear scanning/uptake study? Radioiodine imaging is not

required in patients with clear stigmata of Graves disease. However, when etiology of
hyperthyroidism is unclear, radioactive iodine uptake and scan can differentiate between
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different forms. In addition, radioactive iodine scan/uptake is done to evaluate activity of

goiter and calculate I-131 dose to be given to patients undergoing radioactive iodine therapy
In which order are treatments for Graves disease generally recommended?

There is a substantial amount of regional variation in the choice of initial therapy for Graves
disease. It is important for clinicians to be guided by patient preference. Radioactive iodine
ablation is often recommended as first-line treatment because it is generally easiest and
most efficacious therapy; however, it is contraindicated in patients with significant eye

disease as worsening of eye-findings can be seen after iodine ablation. Also, many patients
do not like idea of taking radiation internally. Antithyroid medications work well and are
generally well tolerated. They can be used as long as there are no adverse effects. Surgery
may be best option if patient has severe compressive symptoms or severe ophthalmopathy

Contributors

Elizabeth Pearce, MD
David W. Toth, MD
Kathleen M. O'Hanlon, MD

Copyright 2016 Elsevier, Inc. All rights reserved.

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