(See also Overview of Thyroid Function Overview of Thyroid Function The thyroid gland, located in the anterior neck just below the cricoid cartilage, consists of 2 lobes connected by an isthmus. Follicular cells in the gland produce the 2 main thyroid hormones... read more .)
Hyperthyroidism can be classified on the basis of thyroid radioactive iodine uptake and the presence or absence of circulating thyroid stimulators (see table ).
Etiology of Hyperthyroidism
Hyperthyroidism may result from increased synthesis and secretion of thyroid hormones Synthesis and Release of Thyroid Hormones The thyroid gland, located in the anterior neck just below the cricoid cartilage, consists of 2 lobes connected by an isthmus. Follicular cells in the gland produce the 2 main thyroid hormones... read more (thyroxine [T4] and triiodothyronine [T3]) from the thyroid, caused by thyroid stimulators in the blood or by autonomous thyroid hyperfunction. It can also result from excessive release of thyroid hormone from the thyroid without increased synthesis. Such release is commonly caused by the destructive changes of various types of thyroiditis.
The most common causes overall include
Graves disease
Multinodular goiter
Thyroiditis
Single, autonomous, hyperfunctioning "hot" nodule
Graves disease (toxic diffuse goiter), the most common cause of hyperthyroidism, is characterized by hyperthyroidism and one or more of the following:
Goiter
Infiltrative dermopathy
Graves disease is caused by an autoantibody against the thyroid receptor for thyroid-stimulating hormone (TSH); unlike most autoantibodies, which are inhibitory, this autoantibody is stimulatory, thus causing continuous synthesis and secretion of excess T4 and T3. Graves disease (like Hashimoto thyroiditis Hashimoto Thyroiditis Hashimoto thyroiditis is chronic autoimmune inflammation of the thyroid with lymphocytic infiltration. Findings include painless thyroid enlargement and symptoms of hypothyroidism. Diagnosis... read more ) sometimes occurs with other autoimmune disorders, including type 1 diabetes mellitus Diabetes Mellitus (DM) Diabetes mellitus is impaired insulin secretion and variable degrees of peripheral insulin resistance leading to hyperglycemia. Early symptoms are related to hyperglycemia and include polydipsia... read more , vitiligo Vitiligo Vitiligo is a loss of skin melanocytes that causes areas of skin depigmentation of varying sizes. Cause is unknown, but genetic and autoimmune factors are likely. Diagnosis is usually clear... read more 
, premature graying of hair, pernicious anemia, connective tissue disorders, and polyglandular deficiency syndrome Polyglandular Deficiency Syndromes Polyglandular deficiency syndromes are characterized by sequential or concurrent deficiencies in the function of several endocrine glands that have a common cause. Etiology is most often autoimmune... read more . Heredity increases the risk of Graves disease, although the genes involved are unknown.
The pathogenesis of infiltrative ophthalmopathy (responsible for the exophthalmos in Graves disease) is poorly understood but may result from immunoglobulins directed to the TSH receptors in the orbital fibroblasts and fat that result in release of proinflammatory cytokines, inflammation, and accumulation of glycosaminoglycans. Ophthalmopathy may also occur before the onset of hyperthyroidism or as late as 20 years afterward and frequently worsens or abates independently of the clinical course of hyperthyroidism. Typical ophthalmopathy in the presence of normal thyroid function is called euthyroid Graves disease.
Toxic solitary or multinodular goiter (Plummer disease) sometimes results from TSH receptor gene mutations causing continuous thyroid activation. Patients with toxic nodular goiter have none of the autoimmune manifestations or circulating antibodies observed in patients with Graves disease. Also, in contrast to Graves disease, toxic solitary and multinodular goiters usually do not remit.
Inflammatory thyroid disease (thyroiditis) includes subacute granulomatous thyroiditis, Hashimoto thyroiditis Hashimoto Thyroiditis Hashimoto thyroiditis is chronic autoimmune inflammation of the thyroid with lymphocytic infiltration. Findings include painless thyroid enlargement and symptoms of hypothyroidism. Diagnosis... read more , and silent lymphocytic thyroiditis Silent Lymphocytic Thyroiditis Silent lymphocytic thyroiditis is a self-limited, subacute disorder occurring most commonly in women during the postpartum period. Symptoms are initially of hyperthyroidism, then hypothyroidism... read more , a variant of Hashimoto thyroiditis. Hyperthyroidism is more common in subacute granulomatous thyroiditis Subacute Thyroiditis Subacute thyroiditis is an acute inflammatory disease of the thyroid probably caused by a virus. Symptoms include fever and thyroid tenderness. Initial hyperthyroidism is common, sometimes followed... read more and results from destructive changes in the gland and release of stored hormone, not from increased synthesis. Hypothyroidism may follow.
Inappropriate TSH secretion is a rare cause. Patients with hyperthyroidism have essentially undetectable TSH except for those with a TSH-secreting anterior pituitary adenoma or pituitary resistance to thyroid hormone. TSH levels are high, and the TSH produced in both disorders is biologically more active than normal TSH. An increase in the alpha-subunit of TSH in the blood (helpful in differential diagnosis) occurs in patients with a TSH-secreting pituitary adenoma.
Drug-induced hyperthyroidism can result from amiodarone, checkpoint inhibitors used in cancer therapy, alemtuzumab used in treatment of multiple sclerosis, or interferon-alfa, which may induce thyroiditis with hyperthyroidism and other thyroid disorders. Although more commonly causing hypothyroidism, lithium can rarely cause hyperthyroidism. Patients receiving these drugs should be closely monitored.
Thyrotoxicosis factitia is hyperthyroidism resulting from intentional or accidental overingestion of thyroid hormone.
Excess iodine ingestion causes hyperthyroidism with a low thyroid radioactive iodine uptake. It most often occurs in patients with underlying nontoxic nodular goiter (especially older patients) who are given drugs that contain iodine (eg, amiodarone) or who undergo radiologic studies using iodine-rich contrast agents. The etiology may be that the excess iodine provides substrate for functionally autonomous (ie, not under TSH regulation) areas of the thyroid to produce hormone. Hyperthyroidism usually persists as long as excess iodine remains in the circulation.
Hydatidiform mole Gestational Trophoblastic Disease Gestational trophoblastic disease is proliferation of trophoblastic tissue in pregnant or recently pregnant women. Manifestations may include excessive uterine enlargement, vomiting, vaginal... read more 
(molar pregnancy) and choriocarcinoma produce high levels of serum human chorionic gonadotropin (hCG), a weak thyroid stimulator. Levels of hCG are highest during the 1st trimester of pregnancy and result in the decrease in serum TSH and mild increase in serum free T4 sometimes observed at that time. The increased thyroid stimulation may be caused by increased levels of partially desialated hCG, an hCG variant that appears to be a more potent thyroid stimulator than more sialated hCG. Hyperthyroidism in molar pregnancy, choriocarcinoma, and hyperemesis gravidarum is transient; normal thyroid function resumes when the molar pregnancy is evacuated, the choriocarcinoma is appropriately treated, or the hyperemesis gravidarum abates.
Nonautoimmune autosomal dominant hyperthyroidism manifests during infancy. It results from mutations in the TSH receptor gene that produce continuous thyroid stimulation.
Metastatic thyroid cancer is a possible cause. Overproduction of thyroid hormone occurs rarely from functioning metastatic follicular carcinoma, especially in pulmonary metastases.
Struma ovarii develops when ovarian teratomas contain enough thyroid tissue to cause true hyperthyroidism. Radioactive iodine uptake occurs in the pelvis, and uptake by the thyroid is usually suppressed.
Pathophysiology of Hyperthyroidism
In hyperthyroidism, serum T3 usually increases more than does T4, probably because of increased secretion of T3 as well as conversion of T4 to T3 in peripheral tissues. In some patients, only T3 is elevated (T3 toxicosis).
T3 toxicosis may occur in any of the common disorders that cause hyperthyroidism, including Graves disease, multinodular goiter, and the autonomously functioning solitary thyroid nodule. If T3 toxicosis is untreated, the patient usually also develops laboratory abnormalities typical of hyperthyroidism (ie, elevated T4 and iodine-123 uptake). The various forms of thyroiditis commonly have a hyperthyroid phase followed by a hypothyroid phase.
Symptoms and Signs of Hyperthyroidism
Most symptoms and signs are the same regardless of the cause. Exceptions include infiltrative ophthalmopathy and dermopathy, which occur only in Graves disease.
The clinical presentation may be dramatic or subtle. A goiter or nodule may be present.
Many common symptoms of hyperthyroidism are due to enhanced sensitivity to adrenergic hormones, such as nervousness, palpitations, hyperactivity, increased sweating, heat hypersensitivity, fatigue, increased appetite, weight loss, insomnia, weakness, and frequent bowel movements (occasionally diarrhea). Hypomenorrhea may be present.
Signs may include warm, moist skin, tremor, tachycardia, widened pulse pressure, and atrial fibrillation.
Older patients, particularly those with toxic nodular goiter, may present atypically (apathetic or masked hyperthyroidism) with symptoms more akin to depression Symptoms and Signs Depressive disorders are characterized by sadness severe enough or persistent enough to interfere with function and often by decreased interest or pleasure in activities. Exact cause is unknown... read more or dementia Symptoms and Signs Dementia is chronic, global, usually irreversible deterioration of cognition. Diagnosis is clinical; laboratory and imaging tests are usually used to identify treatable causes. Treatment is... read more . Most do not have exophthalmos or tremor. Atrial fibrillation Atrial Fibrillation Atrial fibrillation is a rapid, irregularly irregular atrial rhythm. Symptoms include palpitations and sometimes weakness, effort intolerance, dyspnea, and presyncope. Atrial thrombi may form... read more , syncope, altered sensorium, heart failure Heart Failure (HF) Heart failure (HF) is a syndrome of ventricular dysfunction. Left ventricular (LV) failure causes shortness of breath and fatigue, and right ventricular (RV) failure causes peripheral and abdominal... read more 
, and weakness are more likely. Symptoms and signs may involve only a single organ system.
Eye signs include stare, eyelid lag, eyelid retraction, and mild conjunctival injection and are largely due to excessive adrenergic stimulation. They usually remit with successful treatment. Infiltrative ophthalmopathy, a more serious development, is specific to Graves disease and can occur years before or after hyperthyroidism. It is characterized by orbital pain, lacrimation, irritation, photophobia, increased retro-orbital tissue, exophthalmos, and lymphocytic infiltration of the extraocular muscles, causing ocular muscle weakness that frequently leads to double vision.
© Springer Science+Business Media
© Springer Science+Business Media
© Springer Science+Business Media
© Springer Science+Business Media
A patient with Graves disease manifests ocular signs, including widened palpebral fissures, lid retraction, strabismus, and exophthalmos.
By permission of the publisher. From Mulligan M, Cousins M. In Atlas of Anesthesia: Preoperative Preparation and Intraoperative Monitoring. Edited by R Miller (series editor) and JL Lichtor. Philadelphia, Current Medicine, 1998.
Infiltrative dermopathy, also called pretibial myxedema (a confusing term, because myxedema suggests hypothyroidism), is characterized by nonpitting infiltration by proteinaceous ground substance, usually in the pretibial area. It rarely occurs in the absence of Graves ophthalmopathy. The lesion is often pruritic and erythematous in its early stages and subsequently becomes brawny. Infiltrative dermopathy may appear years before or after hyperthyroidism.
Thyroid storm
Thyroid storm is an acute form of hyperthyroidism that results from untreated or inadequately treated severe hyperthyroidism. It is rare, occurring in patients with Graves disease or toxic multinodular goiter (a solitary toxic nodule is a less common cause and generally causes less severe manifestations). It may be precipitated by infection, trauma, surgery, embolism, diabetic ketoacidosis, or preeclampsia.
Thyroid storm causes abrupt florid symptoms of hyperthyroidism with one or more of the following: fever, marked weakness and muscle wasting, extreme restlessness with wide emotional swings, confusion, psychosis, coma, nausea, vomiting, diarrhea, and hepatomegaly with mild jaundice. The patient may present with cardiovascular collapse and shock. Thyroid storm is a life-threatening emergency requiring prompt treatment.
Diagnosis of Hyperthyroidism
TSH
Free T4, plus either free T3 or total T3
Sometimes radioactive iodine uptake
Diagnosis of hyperthyroidism is based on history, physical examination, and thyroid function tests. Serum TSH measurement is the best test because TSH is suppressed in hyperthyroid patients except in the rare instance when the etiology is a TSH-secreting pituitary adenoma or pituitary resistance to the normal inhibition by thyroid hormone.
Free T4 is increased in hyperthyroidism. However, T4 can be falsely normal in true hyperthyroidism in patients with a severe systemic illness (similar to the falsely low levels that occur in euthyroid sick syndrome Euthyroid Sick Syndrome Euthyroid sick syndrome is a condition in which serum levels of thyroid hormones are low in patients who have nonthyroidal systemic illness but who are actually euthyroid. Diagnosis is based... read more ) and in T3 toxicosis. If free T4 level is normal and TSH is low in a patient with subtle symptoms and signs of hyperthyroidism, then serum T3 should be measured to detect T3 toxicosis; an elevated level confirms that diagnosis.
The cause can often be diagnosed clinically (eg, the presence of signs specific to Graves disease). If not, radioactive iodine uptake by the thyroid may be measured by using iodine-123. When hyperthyroidism is due to hormone overproduction, radioactive iodine uptake by the thyroid is usually elevated. When hyperthyroidism is due to thyroiditis, iodine ingestion, or overtreatment with thyroid hormones, radioactive iodine uptake is low.
TSH receptor antibodies can be measured to evaluate for Graves disease. Measurement is done in pregnant women with a history of Graves disease during the 3rd trimester of pregnancy to assess the risk of neonatal Graves disease Hyperthyroidism in Infants and Children Hyperthyroidism is excessive thyroid hormone production. Diagnosis is by thyroid function testing (eg, free serum thyroxine, thyroid-stimulating hormone). Treatment is with methimazole and sometimes... read more ; TSH receptor antibodies readily cross the placenta to stimulate the fetal thyroid. Most patients with Graves disease have circulating antithyroid peroxidase antibodies, and fewer have antithyroglobulin antibodies.
Inappropriate TSH secretion is uncommon. The diagnosis is confirmed when hyperthyroidism occurs with elevated circulating free T4 and T3 concentrations and normal or elevated serum TSH.
If thyrotoxicosis factitia is suspected, serum thyroglobulin can be measured; it is usually low or low-normal—unlike in all other causes of hyperthyroidism.
Subclinical hyperthyroidism
Subclinical hyperthyroidism is low serum TSH in patients with normal serum free T4 and T3 and absent or minimal symptoms of hyperthyroidism.
Subclinical hyperthyroidism is far less common than subclinical hypothyroidism Subclinical hypothyroidism Hypothyroidism is thyroid hormone deficiency. Symptoms include cold intolerance, fatigue, and weight gain. Signs may include a typical facial appearance, hoarse slow speech, and dry skin. Diagnosis... read more 
.
Many patients with subclinical hyperthyroidism are taking levothyroxine. The other causes of subclinical hyperthyroidism are the same as those for clinically apparent hyperthyroidism Etiology Hyperthyroidism is characterized by hypermetabolism and elevated serum levels of free thyroid hormones. Symptoms include palpitations, fatigue, weight loss, heat intolerance, anxiety, and tremor... read more 
.
Patients with serum TSH < 0.1 microU/mL (0.1 mU/L) have an increased incidence of atrial fibrillation (particularly older patients), reduced bone mineral density, increased fractures, and increased mortality. Patients with serum TSH that is only slightly below normal are less likely to have these features.
Treatment of Hyperthyroidism
Treatment of hyperthyroidism depends on cause (1 Treatment references Hyperthyroidism is characterized by hypermetabolism and elevated serum levels of free thyroid hormones. Symptoms include palpitations, fatigue, weight loss, heat intolerance, anxiety, and tremor... read more ) but may include
Radioactive iodine
Methimazole or propylthiouracil
Beta-blockers
Iodine
Surgery
Radioactive sodium iodine (iodine-131, radioiodine)
In the United States, iodine-131 is the most common treatment for hyperthyroidism. Radioiodine is often recommended as the treatment of choice for Graves disease and toxic nodular goiter in all patients, including children. Dosage of iodine-131 is difficult to adjust because the response of the gland cannot be predicted; some physicians give a standard dose of 8 to 15 millicurie. Others adjust the dose based on estimated thyroid size and the 24-hour uptake to provide a dose of 80 to 120 microcurie/g thyroid tissue.
When sufficient iodine-131 is given to cause euthyroidism, about 25 to 50% of patients become hypothyroid 1 year later, and the incidence continues to increase yearly. Thus, most patients eventually become hypothyroid. However, if smaller doses are used, incidence of recurrence is higher. Larger doses, such as 10 to 20 millicurie, often cause hypothyroidism within 6 months, and thus ablative therapy (ie, iodine-131) has become the preferred approach.
Radioactive iodine is not used during lactation because it can enter breast milk and cause hypothyroidism in the infant. It is not used during pregnancy because it crosses the placenta and can cause severe fetal hypothyroidism. There is no proof that radioiodine increases the incidence of tumors, leukemia, thyroid cancer, or birth defects in children born to previously hyperthyroid women who become pregnant later in life.
Methimazole and propylthiouracil
These antithyroid drugs block thyroid peroxidase, decreasing the organification of iodide, and impair the coupling reaction. Propylthiouracil in high doses also inhibits the peripheral conversion of T4 to T3.
Methimazole is the preferred drug. The usual starting dosage of methimazole is 5 to 20 mg orally 2 or 3 times a day. Normalization of TSH lags normalization of T4 and T3 levels by one or more weeks. Therefore, when T4 and T3 levels normalize, the dosage is decreased to the lowest effective amount, usually methimazole 2.5 to 10 mg once a day in order to avoid inducing hypothyroidism. Control generally is achieved in 2 to 3 months. Maintenance doses of methimazole may be continued for one or many years depending on the clinical circumstances. Carbimazole, which is used widely in Europe but is unavailable in the US, is rapidly converted to methimazole. The usual starting dose is similar to that of methimazole; maintenance dosage is 2.5 to 10 mg orally once a day or 2.5 to 5 mg twice a day.
Because of severe liver failure in some patients < age 40, especially children, propylthiouracil is recommended only in special situations (eg, in the 1st trimester of pregnancy, in thyroid storm). The usual starting dose of propylthiouracil is 100 to 150 mg orally every 8 hours. Rapid control can be achieved by increasing the dosage of propylthiouracil to 150 to 200 mg every 8 hours. Such dosages or higher ones (up to 400 mg every 8 hours) are generally reserved for severely ill patients, including those with thyroid storm, to block the conversion of T4 to T3. Maintenance dosing with propylthiouracil is 50 mg twice a day or 3 times a day
About 20 to 50% of patients with Graves disease remain in remission after a 1- to 2-year course of either drug. The return to normal or a marked decrease in gland size, the restoration of a normal serum TSH level, and less severe hyperthyroidism before therapy are good prognostic signs of long-term remission. The concomitant use of antithyroid drug therapy and levothyroxine does not improve the remission rate in patients with Graves disease. Because toxic nodular goiter rarely goes into remission, antithyroid drug therapy is given only in preparation for surgical treatment or iodine-131 therapy.
Adverse effects include rash, allergic reactions, abnormal liver function (including hepatic failure with propylthiouracil), and, in about 0.1% of patients, reversible agranulocytosis. Patients allergic to one drug can be switched to the other, but cross-sensitivity may occur. If agranulocytosis occurs, the patient cannot be switched to the other drug; other therapy (eg, radioiodine, surgery) should be used.
Potential adverse effects or other characteristics vary between the two drugs and guide the indications for each. Methimazole need only be given once a day, which improves adherence. Furthermore, when methimazole is used in dosages of < 20 mg a day, agranulocytosis is less common; with propylthiouracil, agranulocytosis may occur at any dosage.
Methimazole has been used successfully in pregnant and nursing women without fetal or infant complications, but rarely methimazole has been associated with scalp and gastrointestinal defects in neonates and with a rare embryopathy. Because of these complications, propylthiouracil is used in the 1st trimester of pregnancy.
Propylthiouracil is preferred for the treatment of thyroid storm, because the high dosages used (over 800 mg a day) partially block the peripheral conversion of T4 to T3 in addition to decreasing production in the thyroid.
The combination of high-dose propylthiouracil and dexamethasone, also a potent inhibitor of T4 to T3 conversion, can relieve symptoms of severe hyperthyroidism as seen in patients with thyroid storm and restore the serum T3 level to normal within a week.
Beta-blockers
Symptoms and signs of hyperthyroidism due to adrenergic stimulation may respond to beta-blockers; propranolol has had the greatest use, but atenolol or metoprolol may be preferable.
Other manifestations typically do not respond.
Manifestations typically responding to beta-blockers: Tachycardia, tremor, mental symptoms, eyelid lag; occasionally heat intolerance and sweating, diarrhea, proximal myopathy
Manifestations typically not responding to beta-blockers: goiter, exophthalmos, weight loss, bruit, increased oxygen consumption, and increased circulating thyroxine levels
Propranolol is indicated in thyroid storm (see table Treatment of Thyroid Storm Treatment of Thyroid Storm 
). It rapidly decreases heart rate, usually within 2 to 3 hours when given orally and within minutes when given intravenously. Esmolol should be used only in the intensive care unit because it requires careful titration and monitoring. Beta-blockers are also indicated for tachycardia with hyperthyroidism, especially in older patients, because antithyroid drugs usually take several weeks to become fully effective. Calcium channel blockers may control tachyarrhythmias in patients in whom beta-blockers are contraindicated.
Iodine
Iodine in pharmacologic doses inhibits the release of T3 and T4 within hours and inhibits the organification of iodine, a transitory effect lasting from a few days to a week, after which inhibition usually ceases. Iodine is used for emergency management of thyroid storm, for hyperthyroid patients undergoing emergency nonthyroid surgery, and (because it also decreases the vascularity of the thyroid) for preoperative preparation of hyperthyroid patients undergoing thyroidectomy. Iodine generally is not used for routine treatment of hyperthyroidism. The usual dosage is 2 to 3 drops (100 to 150 mg) of a saturated potassium iodide solution orally 3 times a day or 4 times a day or sodium iodide in 1 L 0.9% saline solution 0.5 to 1 g IV given slowly once a day.
Complications of iodine therapy include inflammation of the salivary glands, conjunctivitis, and rash.
Surgery
Surgery is indicated for patients with Graves disease whose hyperthyroidism has recurred after courses of antithyroid drugs and who refuse iodine-131 therapy, patients who cannot tolerate antithyroid drugs, patients with very large goiters, and in some younger patients with toxic adenoma and multinodular goiter. Surgery may be done in older patients with giant nodular goiters.
Surgery usually restores normal function. Postoperative recurrences vary between 2 and 16%; risk of hypothyroidism is directly related to the extent of surgery. Vocal cord paralysis and hypoparathyroidism are uncommon complications. Saturated solution of potassium iodide 3 drops (about 100 to 150 mg) orally 3 times a day should be given for 10 days before surgery to reduce the vascularity of the gland. Methimazole must be given first because the patient should be euthyroid before iodide is given. Dexamethasone can be added to rapidly restore euthyroidism. Surgical procedures on the anterior neck are more difficult in patients who previously underwent thyroidectomy or radioiodine therapy.
Treatment of thyroid storm
A treatment regimen for thyroid storm is shown in the table Treatment of Thyroid Storm Treatment of Thyroid Storm . The precipitating cause should also be addressed.
Treatment of infiltrative dermopathy and ophthalmopathy
In infiltrative dermopathy (in Graves disease), topical corticosteroids or corticosteroid injections into the lesions may decrease the dermopathy. Dermopathy sometimes remits spontaneously after months or years.
Ophthalmopathy should be treated jointly by the endocrinologist and ophthalmologist and may require selenium, corticosteroids, orbital radiation, and surgery. Surgical thyroidectomy may help resolve or prevent progression of ophthalmopathy. Teprotumumab, an insulin-like growth factor 1 (IGF-1) receptor inhibitor, is very effective therapy for moderately severe ophthalmopathy (2 Treatment references Hyperthyroidism is characterized by hypermetabolism and elevated serum levels of free thyroid hormones. Symptoms include palpitations, fatigue, weight loss, heat intolerance, anxiety, and tremor... read more ). Radioiodine therapy may accelerate progression of ophthalmopathy when ophthalmopathy is active, and is thus contraindicated in this active phase.
Management of subclinical hyperthyroidism
In patients with subclinical hyperthyroidism who are taking levothyroxine, reduction of the dose is the most appropriate management unless therapy is aimed at maintaining suppressed TSH levels in patients with thyroid cancer.
Therapy is indicated for patients with endogenous subclinical hyperthyroidism (serum TSH < 0.1 mU/L), especially those with atrial fibrillation or reduced bone mineral density. The usual treatment is iodine-131, but low doses of methimazole are also effective.
Treatment references
1. Ross DS, Burch HB, Cooper DS, et al: 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid 26(10):1343–1421, 2016. doi: 10.1089/thy.2016.0229
2. Douglas RS, Kahaly GJ, Patel A, et al: Teprotumumab for the treatment of active thyroid eye disease. N Engl J Med 382(4):341–352. 2020. doi: 10.1056/NEJMoa1910434
Key Points
Hyperthyroidism has many causes; the most common etiology is Graves disease, caused by excessive hormone synthesis by an abnormal thyroid.
Other causes of hyperthyroidism include excessive stimulation of a normal thyroid gland (eg, by thyroid-stimulating hormone [TSH], human chorionic gonadotrophin [hCG], ingestion of iodine or iodine-containing drugs), excessive hormone synthesis by an abnormal thyroid (eg, toxic nodular goiter), excessive release of thyroid hormones (eg, due to thyroiditis), or ingestion of excessive quantities of thyroid hormone.
Symptoms and signs are many but include tachycardia, fatigue, weight loss, nervousness, and tremor; patients with Graves disease may also have exophthalmos and infiltrative dermopathy.
Free thyroxine (T4), and/or free or total triiodothyronine (T3) are elevated, and TSH is suppressed (except in rarer cases of pituitary causes of hyperthyroidism).
Hormone synthesis can be suppressed with methimazole (or in certain cases, propylthiouracil) and adrenergic symptoms relieved with beta-blockers; long-term treatment may require thyroid ablation with radioactive iodine or surgery.
Thyroid storm—resulting from untreated or inadequately treated severe hyperthyroidism—is a life-threatening emergency that presents with severe symptoms of hyperthyroidism and may result in cardiovascular collapse or shock; it is treated with a regimen of antithyroid drugs, iodine, and hemodynamic support.
Drugs Mentioned In This Article
| Drug Name | Select Trade |
|---|---|
amiodarone |
Cordarone, Nexterone, Pacerone |
alemtuzumab |
Campath, LEMTRADA |
lithium |
Eskalith, Eskalith CR, Lithobid |
human chorionic gonadotropin |
Novarel, Ovidrel, Pregnyl |
levothyroxine |
Ermeza, Estre , Euthyrox, Levo-T, Levothroid, Levoxyl, Synthroid, Thyquidity, Thyro-Tabs, TIROSINT, TIROSINT-SOL, Unithroid |
methimazole |
Northyx, Tapazole |
propylthiouracil |
No brand name available |
dexamethasone |
AK-Dex, Baycadron, Dalalone, Dalalone D.P, Dalalone L.A, Decadron, Decadron-LA, Dexabliss, Dexacort PH Turbinaire, Dexacort Respihaler, DexPak Jr TaperPak, DexPak TaperPak, Dextenza, DEXYCU, DoubleDex, Dxevo, Hemady, HiDex, Maxidex, Ocu-Dex , Ozurdex, ReadySharp Dexamethasone, Simplist Dexamethasone, Solurex, TaperDex, ZCORT, Zema-Pak, ZoDex, ZonaCort 11 Day, ZonaCort 7 Day |
propranolol |
HEMANGEOL, Inderal, Inderal LA, Inderal XL, InnoPran XL |
atenolol |
Tenormin |
metoprolol |
KAPSPARGO, Lopressor, Toprol XL |
esmolol |
Brevibloc |
potassium iodide |
Pima, SSKI |
sodium iodide |
Iodopen |
selenium |
Selepen |
teprotumumab |
TEPEZZA |
insulin |
Afrezza, Exubera |
