Diffuse Toxic Goiter (Graves Disease) 

Updated: Jul 27, 2015
Author: Bernard Corenblum, MD, FRCPC; Chief Editor: George T Griffing, MD 



Diffuse toxic goiter, first described by the English physician Caleb H. Parry (1755-1822), is also known as Graves disease (after Robert J. Graves) in the English-speaking world and as Basedow disease (after Karl A. von Basedow) in the rest of Europe.

In diffuse toxic goiter, the thyroid gland is diffusely hyperplastic and excessively overproduces thyroid hormone. This results in accelerated metabolism in most body organs. The clinical response and its manifestations are variable in intensity, distribution, and are modified by age, gender, and associated premorbid medical problems. When diffuse toxic goiter is associated with clinical evidence of oculopathy, or rarely with dermopathy/acropachy, the term Graves disease is often applied. Awareness is needed regarding atypical clinical presentations.


The thyroid gland is usually enlarged to a variable degree and is vascular and diffusely affected. This results in a smooth, rubbery-firm consistency, and often a bruit is heard on auscultation. Microscopically, the thyroid follicular cells are hypertrophic and hyperplastic, and they contain little colloid (stored hormone) and show evidence of hypersecretion. Lymphocytes and plasma cells infiltrate into the thyroid gland and may aggregate into lymphoid follicles.

This condition is an autoimmune disorder whereby the thyroid gland is overstimulated by antibodies directed to the thyroid-stimulating hormone (TSH) receptor on the thyroid follicular cells. This antibody stimulates iodine uptake, thyroid hormonogenesis and release, and thyroid gland growth. Although mainly produced within the thyroid gland, these antibodies reach the circulation and can be measured by various assays in most, but not all, cases.

The association with another autoimmune thyroid disease, Hashimoto thyroiditis, and to a lesser degree, with other autoimmune diseases in other endocrine glands and other systems in the same person is high. A strong familial association exists with the same diffuse toxic goiter or the associated disorders, especially Hashimoto thyroiditis. The presence of Hashimoto thyroiditis, which has more of a destructive effect on the thyroid gland, or the presence of another antibody, TSH-receptor blocking antibody, results in a variable natural history of the course of diffuse toxic goiter.



United States

Diffuse toxic goiter is the most common cause of spontaneous hyperthyroidism. A Minnesota study found 0.3 new cases per 1000 per year.

In late childhood, the incidence rate is 3 per 100,000 in girls and 0.5 per 100,000 in boys. Prevalence studies show a rate of 2.7% in women and 0.23% in men.

A marked increase in familial incidence is noted.


Prewar Copenhagen found 0.2 new cases per 1000 per year.

British studies found 0.08-0.2 new cases per 1000 per year.


No racial predilection exists.


Diffuse toxic goiter is 7-10 times more common in women than in men. It is often associated with or following pregnancy.


Diffuse toxic goiter can occur in persons of all ages, but it is rare in children younger than 10 years and unusual in elderly persons. The peak incidence is in third and fourth decades of life.

Incidence is increased in postpartum women, when the first presentation of disease often occurs.


The natural history is usually of a benign course, which may vary in intensity of the symptoms and even spontaneously remit. The intensity of the symptoms and effect on quality of life are variable from person to person and are affected by age and gender.

Mortality is rare, but when it occurs, it is due to cardiovascular problems such as heart failure, arrhythmias, or myocardial infarction.

Therapy may be needed for myocardial ischemia, congestive failure, or atrial arrhythmias, which may require anticoagulation.

Debility and infection may occur. Thyroid storm is rare but may be fatal from dehydration, hyperthermia, and organ failure.

Morbidity may result from increased bone turnover and osteoporosis, especially in postmenopausal women, or from atrial fibrillation and its sequelae, such as thromboembolism, especially in older men. Personality changes and psychopathology, muscular weakness, and systemic symptoms all lead to quality of life changes. Associated oculopathy may be symptomatic, especially with double vision. Rarely it may progress to affect the integrity of the cornea and may even endanger vision.

Associated dermopathy is uncommon and is usually minimally symptomatic, but it may be symptomatic to become debilitating.

Associated hypokalemic periodic paralysis, most commonly seen in Asian males, may be sudden, dramatic, and concerning but usually runs a benign course of recovery after a few hours of skeletal muscle paralysis.

A higher risk of associated immunologic diseases, such as adrenal insufficiency, each has their own associated morbidity and mortality, especially if undiagnosed.




Symptoms of hyperthyroidism, the goiter itself, and of comorbid conditions are present. The symptoms may be present for weeks, months, or even years before diagnosis.

The hyperthyroid symptoms may be multisystemic or predominate in a single organ system and mask the correct diagnosis in this manner. Many symptoms are adrenergic in origin and may be misdiagnosed as an anxiety disorder.

Elderly patients may have no adrenergic symptoms and present with weight loss (malignancy), atrial fibrillation (cardiac), or apathy (depression). The latter presentation is referred to as apathetic thyrotoxicosis.

The presenting symptoms may be modified by preexisting medical or psychiatric disorders, which may be modified or worsened. Symptoms are described below.

  • Hypermetabolism with heat generation and protein catabolism - Weight loss with good appetite, heat intolerance, sweating, muscle weakness (proximal more than distal), osteoporosis

  • Adrenergic - Palpitations, tremor, emotional lability, insomnia, restlessness, hyperdefecation

  • Other - Gynecomastia, lighter menses, insomnia, decreased concentration, fatigue, shortness of breath on exertion, and decreased exercise tolerance

  • Goiter - May be mildly tender, may have difficulty swallowing if large

  • Associated oculopathy (clinically present in about 25% of cases) - Tearing, pain, puffiness, grittiness, double vision, prominent appearance, rarely visual loss


General physical examination findings may include restless appearance, evidence of weight loss, pruritus, palmar erythema, and onycholysis of the finger nails.

  • Hypermetabolism with protein catabolism - Warm hands, often with heat radiation, velvety skin, proximal muscle weakness in the arms and legs compared with distal muscle strength

  • Hyperadrenergic - Bounding and fast pulse, wide pulse pressure with higher systolic and lower diastolic blood pressure, active precordium and abdominal aorta to palpation; lid retraction (upper eyelid more than halfway from pupil to top of iris) and lid lag or globe lag, tremor of fingers, brisk reflexes

  • Organ decompensation - Atrial fibrillation, congestive heart failure, jaundice

  • Oculopathy - Periorbital puffiness, chemosis, conjunctival redness, proptosis (sclera visible below iris), double vision with eye movements, loss of color vision (rare), or papilledema (rare)

  • Thyroid gland - Mildly enlarged (but may be normal in size, many times normal in size, or difficult to palpate); smooth, rubbery firm in texture; nontender or mildly tender; systolic bruit on auscultation

  • Miscellaneous - Pretibial myxedema (uncommon), rare may be finger clubbing, diffuse lymphadenopathy, and splenomegaly


Diffuse toxic goiter and its hyperthyroidism are caused by TSH-receptor stimulating antibodies. Although the exact cause is not understood, it has been suggested that there is a genetic lack of suppressor T cells that results in the unregulated production of the antibody, resulting in the autoimmune disease. The antibody may pass the placenta and result in fetal and neonatal hyperthyroidism.

As with most such disorders, usually a combination of genetic and environmental factors is present. The familial association indicates a strong genetic factor. Predisposing factors include genetic susceptibility (including HLA factors); female gender; mental stress; viral infection; surgery; postpartum state; iodine administration; drugs such as lithium and iodine-containing agents, such as amiodarone, interferons and interleukins, and antiretroviral agents.

Associated ophthalmopathy is not well understood, but it is a related but separate autoimmune disorder directed toward the extraocular muscles. It may run a course similar to or different from the hyperthyroidism. Smoking is an environmental aggravating factor. The presence and degree of clinical ophthalmopathy does correlate with the degree of elevation of the anti-TSH receptor antibodies.

Dermopathy (pretibial myxedema) may be brought on or aggravated by local trauma.



Diagnostic Considerations

If an associated ophthalmopathy is present, the diagnosis of diffuse toxic goiter is obvious.

Other common causes of hyperthyroidism include various forms of thyroiditis, hyperfunctioning (hot) nodule, multinodular goiter, iatrogenic (thyroxin and/or triiodothyronine ingestion). Iodine administration, such as drugs or contrast media, may precipitate hyperthyroidism in underlying nodular thyroid disease. Palpation of the thyroid gland gives useful clinical information in the separation of these entities.

Rare causes include TSH-secreting pituitary tumors, ectopic thyroxin production (struma ovarii), human chorionic gonadotropin (HCG) hypersecretion (trophoblastic disease, ectopic secretion), exogenous source (eg, hamburger thyrotoxicosis), and malingering (thyroxin ingestion). Peripheral resistance to thyroid hormone (receptor defect) may result in a complicated similar clinical picture.

Anxiety/psychotic state, pheochromocytoma, pregnancy and hyperemesis gravidarum, menopause, carcinoid syndrome, cocaine and other drug use are possible.

Primary systemic or organ diseases, such as atrial fibrillation, weight loss, or myopathy, require hyperthyroidism to be considered as an underlying cause.



Laboratory Studies

If hyperthyroidism due to diffuse toxic goiter is suspected after history and physical examination, the following should be performed:

  • Serum TSH (sensitive or third-generation assay): Levels suppressed below normal indicate the need for more tests. Normal serum TSH level rules out this diagnosis.

  • Serum free thyroxin (T4), or equivalent test, that compensates for any changes in thyroid-binding globulin. If levels are elevated, then hyperthyroidism is diagnosed. Levels will be in the normal range in about 5% of cases.

  • If free thyroxin is normal, then obtain total or free serum triiodothyronine (T3) level. If levels are elevated, then hyperthyroidism is diagnosed. If levels are normal, then subclinical hyperthyroidism is present.

  • The presence of ophthalmopathy indicates the diagnosis, and no more diagnostic testing is needed regarding the cause of the hyperthyroidism.

  • Serum anti-TSH receptor antibodies measurements can be obtained. These antibodies are present in more than 90% of cases of diffuse toxic goiter, depending on the assay.

  • An alternative test is radioiodine uptake. It will separate diffuse toxic goiter (elevated or normal uptake) from the hyperthyroid phase of thyroiditis (suppressed uptake). If the hyperthyroid symptoms have been present for more than 4 months, then thyroiditis is not the cause. This test is contraindicated in women who are pregnant or breastfeeding.

  • An elevated or normal uptake may be found with a single nodular goiter and a multinodular goiter. These may be separated from diffuse toxic goiter by the absence of anti-TSH receptor antibodies, clinical examination, or thyroid scan (technetium-99m or I-123) or ultrasonography.

  • Concomitant presence of Hashimoto thyroiditis may be detected by serum antithyroid antibodies (anti-TPO or thyroperoxidase).

  • If confirmation of oculopathy is needed, then orbital CT or MRI may be performed.

Diffuse toxic goiter would have a suppressed serum TSH level, elevated serum free thyroxin level (or T3 if needed), elevated titer of anti-TSH receptor antibodies, or elevated radioiodine uptake. No further testing is needed.

Consideration of complications: ECG should be performed if arrhythmia is suspected; liver function tests may be indicated.

Consideration of associated disorders: If clinical suspicion, screen for adrenal insufficiency, type 1 diabetes, gonadal failure, other autoimmune disease (eg, pernicious anemia, rheumatoid arthritis, immune thrombocytopenic purpura). Concomitant Hashimoto thyroiditis may have an effect on spontaneous resolution or progression to a hypothyroid state.

Drugs that may alter T4 laboratory results include anabolic steroids, androgens, estrogens, heparin, iodine, phenytoin, rifampin, salicylates, and thyroxine/triiodothyronine.

Imaging Studies

Radiological studies are useful. The radioiodine uptake is elevated or normal with diffuse toxic goiter, functioning nodule, and multinodular goiter. It is low with thyroiditis (all causes), exogenous thyroid administration, and ectopic sources such as struma ovarii.

The thyroid scan is useful but more expensive and with greater radiation exposure. It shows a diffuse uptake with diffuse toxic goiter, a single area of uptake over a functioning nodule, and several areas of uptake over a multinodular goiter. It is best used if nodularity is suspected.

Ultrasound is a sensitive and inexpensive test, without radiation exposure, if Doppler is used to assess vascularity. The vascularity accurately distinguishes diffuse toxic goiter from thyroiditis, the most common clinical problem in the differential diagnosis of hyperthyroidism.[1]



Medical Care

Even though the natural history of diffuse toxic goiter is to possibly spontaneously remit (and perhaps later relapse), or even progress into hypothyroidism, observation without intervention, even in minimally symptomatic people, is not recommended. The risk of bone loss and atrial fibrillation occur, especially in older women and men, even in subclinical cases.

The goals of therapy are to resolve hyperthyroid symptoms and to restore the euthyroid state.

Each therapeutic choice has advantages and disadvantages, so treatment should be individualized. Patient input into the treatment choice is important and must be discussed and considered. The American Thyroid Association and American Association of Clinical Endocrinologists have released guidelines for the management of hyperthyroid and other causes of thyrotoxicosis, including the use of radioactive iodine or surgery to treat toxic multinodular goiter.[1]

Therapy may be by subtotal thyroidectomy, administration of radioiodine, antithyroid drugs, or a combination of these. In North America, radioiodine is the most common treatment and is available for all ages. Adjunctive symptomatic therapy, such as beta-blockers, may help adrenergic symptoms. Nonsurgical therapy occurs in the outpatient setting. Surgical therapy requires first normalization of the hyperthyroid state by medication.

Cardiac decompensation or arrhythmias may require hospitalization.

Thyroid storm is a rare emergency requiring intensive care support and therapy.

Surgical Care

Subtotal thyroidectomy may be considered if it is the choice of the patient, second trimester of pregnancy, failure (resistance or intolerance) of drug therapy, or poor compliance to drug therapy. Risks are low with experienced surgeons but include anesthetic risks, hemorrhage, hypoparathyroidism, and vocal cord paralysis. Patients should be made euthyroid prior to surgery to minimize anesthetic risks, cardiovascular/hemodynamic complications, and risk of thyroid storm. If normalizing with antithyroid drugs is not possible, then beta-blockers and potassium iodide 4 drops/day for 10 days will decrease vascularity of the thyroid gland.


Oculopathy usually requires ophthalmologic consultation, and dermopathy may require dermatologic consultation.


Diet must include caloric intake to meet the energy expenditure of the hypermetabolism. High iodine-containing substances, such as kelp, should be avoided.


Physical activity is limited by the presence of symptoms, until recovery occurs. Usually, shortness of breath on exertion, fatigue, and palpitations are the limiting symptoms.



Medication Summary

No standard treatment protocols exist; individualization of treatment based on clinical experience is protocol. Patient preference after informed consent affects all therapeutic decisions. The long-term quality of life following treatment is the same in patients randomly allocated to each of the 3 treatment options.[2]


Beta-blockers should be considered for patients with resting heart rates over 90 bpm or coexistent cardiovascular disease.[1] In symptomatic patients, they decrease the heart rate, systolic blood pressure, muscle weakness, and tremor and improve emotional irritability.[1] Beta-blockers may be used during lactation.

Beta-blockers are used if symptomatic tremor or palpitations require their use. They may be used even as investigation is ongoing because they have no effect on thyroid gland function, but they block the beta-adrenergic peripheral manifestations of the hyperthyroid state. Propranolol has an effect in decreasing the peripheral conversion of T4 to T3, but this is of unknown clinical significance with the usual doses. The dose may be decreased and then stopped when the euthyroid state occurs. They should not be used in the presence of bronchospasm, even the beta1-selective agents. Calcium channel blockers may be substituted.


Thionamide drugs, propylthiouracil (PTU) and methimazole (MTZ), inhibit hormonogenesis within the thyroid gland. PTU has an effect in decreasing the peripheral conversion of T4 to T3, but this is of unknown added clinical significance. Other than in pregnancy and breastfeeding, MTZ has advantages over PTU by a longer half-life with once-a-day dosing, and possibly more rapid return to the euthyroid state. Although rare, agranulocytosis, lupuslike vasculitis, and hepatitis are more commonly associated with PTU than with MTZ. Agranulocytosis occurs in less that 0.1% of cases but is unpredictable; it may occur at any time. Routine monitoring of WBC count is not useful. Should any infection occur, such as a sore throat, the WBC count should then be measured. Discontinuation of the drug results in a rise of WBC within a few days.

Hyperthyroidism itself can result in abnormal liver function tests, so a baseline is measured before medication is started. A rise to 3 times above normal dictates discontinuation of the drug.

Minor skin itch or rash may be managed by an antihistamine, without discontinuation of the drug. More marked reactions require discontinuation of that drug.

Granulocyte colony-stimulating factor may need to be administered. Skin rash may perhaps be more common with MTZ; incidence is about 3%, and it usually occurs within the first few weeks of therapy. Methimazole is the drug of choice.[3]

The US Food and Drug Administration (FDA) added a boxed warning, the strongest warning issued by the FDA, to the prescribing information for PTU. The boxed warning emphasizes the risk for severe liver injury and acute liver failure, some of which have been fatal. The boxed warning also states that PTU should be reserved for use in patients who cannot tolerate other treatments, such as methimazole, radioactive iodine, or surgery.

The decision to include a boxed warning was based on the FDA's review of postmarketing safety reports and on meetings held with the American Thyroid Association, the National Institute of Child Health and Human Development, and the pediatric endocrine clinical community.

The FDA has identified 32 cases (22 adult and 10 pediatric) of serious liver injury associated with PTU. Of the adults, 12 deaths and 5 liver transplants occurred, and among the pediatric patients, 1 death and 6 liver transplants occurred. PTU is indicated for hyperthyroidism due to Graves disease. These reports suggest an increased risk for liver toxicity with PTU compared with methimazole. Serious liver injury has been identified with methimazole in 5 cases (3 resulting in death).

PTU is considered to be a second-line drug therapy, except in patients who are allergic to or intolerant of methimazole, or in women who are in the first trimester of pregnancy. Rare cases of embryopathy, including aplasia cutis, have been reported with methimazole during pregnancy. The FDA recommends the following criteria be considered for prescribing PTU (for more information, see the FDA Safety Alert)[4] :

  • Reserve PTU use during first trimester of pregnancy, or in patients who are allergic to or intolerant of methimazole.

  • Closely monitor PTU therapy for signs and symptoms of liver injury, especially during the first 6 months after initiation of therapy.

  • For suspected liver injury, promptly discontinue PTU therapy, evaluate the patient for evidence of liver injury, and provide supportive care.

  • PTU should not be used in pediatric patients unless the patient is allergic to or intolerant of methimazole and no other treatment options are available.

  • Counsel patients to promptly contact their health care provider for the following signs or symptoms: fatigue, weakness, vague abdominal pain, loss of appetite, itching, easy bruising, or yellowing of the eyes or skin.

Monitor the serum thyroid indices monthly until euthyroid, and then the dose of the drug may be decreased for maintenance. The lowest dose needed to maintain the euthyroid state is then used for long-term therapy.

Normalization of thyroid function with these drugs must occur for some time, at least 6 months and perhaps for 1-2 years, to maximize the remission rate after drug discontinuation. Despite this, the relapse rate is 50-70%, usually within the first few weeks or months, but occasionally after a few years. Remission is weakly predicted by a short duration of symptoms, age younger than 40 years, minimal enlargement of the thyroid gland, and concomitant presence of Hashimoto thyroiditis.

Relapse after discontinuation of the drug requires a decision regarding radioiodine therapy or surgery for more definitive therapy, or return to the antithyroid drug. Although general practice is not to use these drugs long-term, there is no reason why this cannot occur, if that is what the patient chooses.


In severe cases, such as thyroid storm, iodine in the form of potassium iodide (SSKI) 10 drops twice a day or iopanoic acid 1-3 g/d may be given. They inhibit the release of thyroxin from the gland and inhibit peripheral conversion of T4 to T3. They help render a euthyroid state more rapidly in response to antithyroid drugs, or prepare for surgery, but will eliminate the use of radioiodine for many months due to expansion of the iodine pool and thus decrease the delivery of radioiodine to the thyroid gland.


Oral administration of I 131 is incorporated into the thyroid follicular cells, and the beta emission results in cell destruction and glandular fibrosis. The effect is seen in 1 and a half to 4 months. Off medications, the thyroid hormone levels become normal (requiring continued monitoring), fall below normal (requiring thyroid hormone replacement therapy, likely for life), or remain elevated (requiring another administration of radioiodine). In those becoming euthyroid, the chance every year of becoming hypothyroid due to ongoing disease in the gland is 5%; occasionally, hyperthyroidism may reoccur. The usual dose is 6-8 mCi. The dose is adjusted based on size of the thyroid gland, age of the patient, and severity of the clinical picture. Resistance is increased by age older than 40 years, large goiters, prior therapy with PTU, and nodularity (not seen with diffuse toxic goiter). Recent reviews confirm the safety of the use of radioiodine.[5]

Radioiodine therapy is not used in clinically severe hyperthyroidism or thyroid storm until the hyperthyroid state is medically controlled.

Because of transplacental transfer and lactation transfer, it is contraindicated in women who are pregnant or breastfeeding. For the theoretical ovarian exposure, conception in treated women is empirically discouraged for 3-6 months.

It may be administered to children, if clinically indicated. Long-term safety data in children are not available.

Worsening of the hyperthyroid state may occur after radioiodine therapy due to release of prestored hormone. Gland tenderness and swelling is uncommon and may be treated with nonsteroidal anti-inflammatory drugs (NSAIDs) (not aspirin), and they rarely require steroid administration.

Radioiodine administration has been associated with worsening or progression of symptomatic ophthalmopathy. Either radioiodine is avoided in very symptomatic individuals or corticosteroids (prednisone 0.5 mg/kg) are used beginning the day after the radioiodine administration for 1-3 months, or they are administered if any worsening of the ophthalmopathy occurs after radioiodine administration. Cessation of smoking and avoidance of hypothyroidism also help the course of ophthalmopathy.

The return to the euthyroid state, regardless of therapy, is best monitored by serum free thyroxin, or its equivalent, because the pituitary is suppressed and TSH secretion may remain low for some time after a normal or hypothyroid state occurs. Relapse from a euthyroid state to hyperthyroidism is first monitored by new suppression of the serum TSH, and often the serum T3 then increases above normal before the serum T4 increases above normal.

Pregnancy and breastfeeding

Pregnancy often has an effect on improving the immunologic disease state during the pregnancy and then often relapses following delivery. The treatment of choice is PTU, which has less placental transfer than MTZ. Rare congenital anomalies reported with MTX (eg, aplasia cutis) are even less associated with PTU. Overall, the congenital abnormality rate with these drugs is similar to background normal rate. MTZ may be used if a problem exists with PTU.

The goal is to keep the free thyroxin in the upper part of normal to minimize fetal drug exposure. Monthly monitoring of serum free thyroxin usually allows the dose of PTU to be decreased and often discontinued in the third trimester. Both PTU and MTZ may be used in breastfeeding mothers. A small amount of drug does enter the milk, but neonatal thyroid levels generally remain normal. PTU and MTZ are not contraindicated in pregnancy or lactation.

Antithyroid agents

Class Summary

These agents may either inhibit hormonogenesis within the thyroid gland or inhibit release of thyroid hormone from the gland.

Propylthiouracil (PTU)

Actively transported into the thyroid gland and inhibits incorporation of iodine to thyroid hormones, and inhibits peripheral conversion of T4 to T3. Drug recommended in pregnancy and lactation with dose adjustment to minimum needed. Laboratory monitoring of free T4 to adjust dose therapy. The serum TSH may lag behind the changes in free T4. Long-term experience with this drug.

Methimazole (Tapazole)

Actively transported in thyroid gland and inhibits thyroid synthesis by preventing oxidation of trapped iodine. Ten times more potent than PTU, and once-a-day dose is effective. Euthyroid state is achieved in 4-6 wk, and maintenance treatment continued for 12-24 mo. Relapse may be observed 1-6 mo after stopping therapy, occasionally later.

Less desirable than propylthiouracil in pregnancy and lactation but may be used if propylthiouracil cannot be used.

Potassium iodide (Pima, Thyro-Block)

Inhibits thyroid hormone secretion. Contains 8 mg of iodide per gtt. May be mixed with juice or water for intake.

May decrease thyroid gland secretion and vascularity for a short time, such as 2 wk; may be used in severe cases of hyperthyroidism, such as thyroid storm, or to prepare patient for thyroidectomy

Supersaturated potassium iodide (SSKI)

Contains 50 mg of iodide per drop. May be mixed with juice or water for ingestion. Inhibits thyroid hormone release.


Class Summary

These agents have profound and varied metabolic effects.

Dexamethasone (Decadron)

Steroids block peripheral conversion of T4 to T3. Used as adjunct in management of thyroid storm and symptomatic progressive Graves ophthalmopathy.


Class Summary

These agents are used to destroy thyroid cells.

Radioiodine (I-131)

Agent of choice because it is selectively taken up by the thyroid gland. Causes dysfunction or death of thyroid cells over time. Long-term experience suggests good safety profile.

Beta-adrenergic receptor blockers

Class Summary

Relief of adrenergic symptoms, especially cardiac and neurologic. Propranolol blocks peripheral conversion of T4 to T3, but this is of unknown clinical significance.

Propanolol (Inderal)

Nonselective beta-adrenergic receptor blocker. Also blocks peripheral conversion of T4 to T3. Used along with antithyroid drugs, before and after radioiodine treatment. Useful in thyroid crisis/storm, or in cardiac complications such as atrial fibrillation. Oral or intravenous use controls cardiac and psychomotor manifestations within minutes. Continue until euthyroid state is achieved.



Further Outpatient Care

Regardless of the therapy used, long-term follow-up is needed to monitor thyroid status, especially with a high risk of becoming hypothyroid in the near and distant future or relapse again into hyperthyroidism.

Ophthalmopathy runs its own course, independent of the thyroid course. Although generally benign, it may become symptomatic years after the thyroid status has been rendered normal.

Further Inpatient Care

Hospitalization is rarely necessary. Severe disease with cardiac or other organ compensation, or thyroid storm may require more intense and controlled therapy.

Complications, such as agranulocytosis, may need specialized hospital care.

Thyroidectomy, if uncomplicated, requires a short hospital stay from 1-3 days.


Cessation of smoking has a beneficial effect on the course of ophthalmopathy.

The strong familial nature dictates that first-degree relatives, especially siblings and children, be aware of the increased risk of developing this or associated disorders. Routine testing is not recommended, but consideration for this risk is needed with new symptom development.

Associated autoimmune disease in other glands is uncommon but is of increased incidence and may clinically occur at presentation or in the near or distant future. New symptoms dictate consideration for these.

Patient Education

For excellent patient education resources, visit eMedicineHealth's Thyroid and Metabolism Center. Also, see eMedicineHealth's patient education article Thyroid Problems.