eMedicine Specialties > Endocrinology > Thyroid

Hyperthyroidism: Treatment & Medication

Author: Stephanie L Lee, MD, PhD, Fellow, Association of Clinical Endocrinology; Director of Thyroid Nodule and Cancer Center, Associate Chief, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Associate Professor, Department of Medicine, Boston University School of Medicine
Coauthor(s): Sonia Ananthakrishnan, MD, Attending Physician, Department of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine/Boston Medical Center
Contributor Information and Disclosures

Updated: Jun 8, 2009

Treatment

Medical Care

With the exception of low–123 I uptake hyperthyroidism (eg, subacute thyroiditis; see the eMedicine topics Subacute Thyroiditis; Thyrotoxicosis), the treatment of hyperthyroidism includes symptom relief and therapy with antithyroid medications, therapy with radioactive iodine131 I, or thyroidectomy.

  • Symptom relief - Many of the neurologic and cardiovascular symptoms of thyrotoxicosis are relieved by beta-blocker therapy. Prior to therapy, examine the patient for signs and symptoms of dehydration that often occur with hyperthyroidism. After oral rehydration, beta-blocker therapy can be started. Do not administer beta-blocker therapy to a patient with a significant history of asthma. Calcium-channel blockers can be used for the same purposes when beta blockers are contraindicated or poorly tolerated.
  • Antithyroid drugs - Antithyroid drugs (eg, methimazole, propylthiouracil) have been used for hyperthyroidism since their introduction in the 1940s. These drugs inhibit multiple steps in the synthesis of T4 and T3, leading to a gradual reduction in thyroid hormone levels over 2-8 weeks or longer. Titrate the antithyroid drug dose every 4 weeks until thyroid functions normalize. Some patients with Graves disease go into a remission after treatment for 12-18 months, and the drug can be discontinued. Notably, half the patients who go into remission have a recurrence of hyperthyroidism within the following year. Nodular forms of hyperthyroidism (toxic multinodular goiter and toxic adenoma) are permanent conditions and will not go into remission.
    • Antithyroid medications inhibit formation and coupling of iodotyrosines in thyroglobulin, which are necessary for thyroid hormone synthesis.
    • A second therapeutic action of propylthiouracil, but not methimazole, is the inhibition of conversion of T4 to T3. T3 is a more biologically active form of thyroid hormone. A quick reduction in T3 is associated with a clinically significant improvement in thyrotoxic symptoms.
    • The antithyroid medications are used for the long-term control of hyperthyroidism in children, adolescents, and pregnant women (propylthiouracil only for pregnancy). In women who are not pregnant, the medications are used to control hyperthyroidism prior to definitive therapy with radioactive iodine. In surveys of thyroid specialists in the United States, the preferred treatment of hyperthyroidism is radioactive iodine therapy.
    • The choice between propylthiouracil and methimazole is somewhat arbitrary. Methimazole is a more potent and longer-acting drug. Often, patient compliance is better with methimazole taken once or twice daily than with propylthiouracil given 3 or 4 times daily. Propylthiouracil often is the drug of choice in severe thyrotoxicosis because of the additional benefit of inhibition of T4 -to-T3 conversion. Administer propylthiouracil every 6-8 hours. The reduction in T3, which is 20-100 times more potent than T4, theoretically helps to reduce the thyrotoxic symptoms more quickly than does methimazole.
    • Adverse effects of antithyroid medications - The most common effects are allergic reactions of fever, rash, urticaria, and arthralgia, which occur in 1-5% of patients, usually within the first few weeks of treatment. Serious adverse effects include agranulocytosis, aplastic anemia, hepatitis, polyarthritis, and a lupuslike vasculitis. All of these adverse effects, except agranulocytosis, occur more frequently with propylthiouracil. Agranulocytosis occurs in 0.2-0.5% of patients, with an equal frequency for both drugs. Patients with agranulocytosis usually present with fever and pharyngitis. After the drug is stopped, granulocyte counts usually start to rise within several days but may not normalize for 10-14 days. Granulocyte colony-stimulating factor (G-CSF) appears to accelerate recovery in patients with a bone marrow aspiration showing a granulocyte-to-erythrocyte (G:E) ratio of 1:2 or greater than 0.5.
    • The US Food and Drug Administration (FDA) has identified 32 cases (22 adult and 10 pediatric) of serious liver injury associated with propylthiouracil. Of the adults, 12 deaths and 5 liver transplants occurred, and among the pediatric patients, 1 death and 6 liver transplants occurred. Propylthiouracil is indicated for hyperthyroidism due to Graves disease. These reports suggest an increased risk for liver toxicity with propylthiouracil compared with methimazole. Serious liver injury has been identified with methimazole in 5 cases (3 resulting in death).

      Propylthiouracil 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 propylthiouracil (for more information see the FDA Safety Alert)3 :
      • Reserve propylthiouracil use during first trimester of pregnancy or in patients who are allergic to or intolerant of methimazole
      • Closely monitor propylthiouracil therapy for signs and symptoms of liver injury, especially during the first 6 months after initiation of therapy
      • For suspected liver injury, promptly discontinue propylthiouracil therapy, evaluate the patient for evidence of liver injury, and provide supportive care
      • Propylthiouracil 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.
  • Other drugs - In severe thyrotoxicosis from Graves disease or subacute thyroiditis, iodine or iodinated contrast agents have been administered to block T4 conversion to T3 and the release of thyroid hormone from the gland. This therapy is reserved for severe thyrotoxicosis, because its use prevents definitive therapy of Graves thyrotoxicosis with radioactive iodine for many weeks. Either a saturated solution of potassium iodide (SSKI) at 10 gtt twice daily or iopanoic acid/ipodate (1 g/d) can be administered with rapid reduction in T3 levels. Take care to not administer these drugs to patients with toxic multinodular goiter or toxic adenomas. The autonomous nature of these conditions can lead to worsening of the thyrotoxicosis in the presence of pharmacologic levels of iodide, a substrate in thyroid hormone synthesis.
  • Radioactive iodine therapy4 - Radioactive iodine therapy is the most common treatment for hyperthyroidism in adults in the United States. Although the effect is less rapid than it is in antithyroid medication or thyroidectomy, it is effective and safe and does not require hospitalization. It is administered orally as a single dose, in capsule or liquid form. The radioactive iodine is quickly absorbed and taken up by the thyroid. No other tissue or organ in the body is capable of retaining the radioactive iodine and, therefore, very few adverse effects are associated with this therapy.
    • The treatment results in a thyroid-specific inflammatory response, causing fibrosis and destruction of the thyroid over weeks to many months.
    • Generally, the dose of131 I administered is 75-200 µCi/g of estimated thyroid tissue divided by the percent of123 I uptake in 24 hours. This dose is intended to render the patient hypothyroid. Lithium used in the weeks following radioactive iodine therapy may extend the retention of radioactive iodine and result in increased efficacy. However, studies looking at this are inconsistent, and the benefits of lithium used with radioactive iodine must be weighed against the toxicities associated with lithium.
    • Hypothyroidism is considered by many experts to be the expected goal of radioactive iodine therapy. In several large epidemiologic studies of radioactive iodine therapy in patients with Graves disease, no evidence indicated that radioactive iodine therapy caused the development of thyroid carcinoma. No evidence of increased mortality exists for any other form of cancer, including leukemia, with radioactive iodine therapy of hyperthyroidism.
    • Long-term follow-up data of children and adolescents treated with radioactive iodine are lacking. Consequently, long-term antithyroid medications, rather than radioiodine therapy, usually are recommended in children.
    • Radioactive iodine is never administered to pregnant or lactating women; it can cross the placenta and can be excreted into milk, which can ablate the infant's thyroid and result in hypothyroidism. Checking for pregnancy prior to radioactive iodine therapy and suggesting that the patient not become pregnant for at least 3-6 months after the treatment and until thyroid functions are normal are standard practice.
    • Retrospective reviews have demonstrated no excess in fetal malformations or miscarriage rates in women previously treated with radioactive iodine for hyperthyroidism.
    • Radioactive iodine usually is not administered to patients with severe ophthalmopathy, because clinical evidence suggests that usually mild, but occasionally severe, worsening of thyroid eye disease occurs after radioactive iodine therapy. The risk of ophthalmopathy is worse in patients who smoke cigarettes, but apparently it can be reduced by glucocorticoid therapy (prednisone 0.4 mg/kg for 1 mo with subsequent taper) after the radioactive iodine therapy.

Surgical Care

Subtotal thyroidectomy is the oldest form of treatment for hyperthyroidism. Total thyroidectomy and combinations of hemithyroidectomies and contralateral subtotal thyroidectomies also have been used.4,5

  • Because of excellent effectiveness in regulating thyroid function with antithyroid medications and radioactive iodine, thyroidectomy is reserved for special circumstances, including the following:
    • Severe hyperthyroidism in children
    • Pregnant women who are noncompliant or intolerant of antithyroid medication
    • Patients with very large goiters or severe ophthalmopathy
    • Patients who refuse radioactive iodine therapy
    • Refractory amiodarone-induced hyperthyroidism
    • Patients who require normalization of thyroid functions quickly, such as pregnant women, women who desire pregnancy in the next 6 months, or patients with unstable cardiac conditions
  • With current operative techniques, bilateral subtotal thyroidectomy should have a mortality rate approaching zero in patients who are properly prepared. Historically, the most common cause of thyroid storm, a physiologic decompensation in patients who are severely thyrotoxic, with a mortality rate of 50-100%, is operative stress.
  • Preoperative preparation includes antithyroid medication, stable (cold) iodine treatment (to decrease gland vascularity), and beta-blocker therapy.5
    • Generally, antithyroid drug therapy should be administered until thyroid functions normalize (4-8 wk).
    • Titrate propranolol until the resting pulse rate is less than 80 bpm.
    • Finally, administer iodide as SSKI (1-2 drops bid for 10-14 d) before surgery.
    • An additional benefit from stable iodide therapy, besides the reduction in thyroid hormone excretion, is a demonstrated decrease in thyroid blood flow and possible reduction in blood loss during surgery.
  • Adverse effects of therapy include recurrent laryngeal nerve damage and hypoparathyroidism due to damage of local structures during surgery. (A Swiss study indicated that a single dose of steroid administered prior to thyroidectomy can reduce nausea, pain, and vomiting associated with the procedure, as well as improve voice function.)6

Consultations

  • Generally, thyrotoxicosis should be evaluated and treated by an endocrinologist.
  • Therapy including radioactive iodine and antithyroid medication requires careful follow-up, which is best performed by a specialist.
  • Generally, after definitive therapy is completed with radioactive iodine or surgical thyroidectomy, the patient can be cared for by the primary care doctor (with thyroid hormone replacement therapy if necessary).
  • Patients with Graves thyrotoxicosis should be examined by an ophthalmologist for thyroid eye disease, which occurs in some form in 50% of patients. Often, the eye disease is subclinical and remits with time. The eye disease usually occurs within 1 year before or after the diagnosis of hyperthyroidism, but new-onset has been detected decades later. Graves eye disease also can occur without the patient ever having developed hyperthyroidism.

Diet

  • No special diet must be followed by patients with thyroid disease.
  • Notably, excess amounts of iodide found in some expectorants, radiographic contrast dyes, seaweed tablets, and health food supplements should be avoided, because the iodide interferes with or complicates the management of antithyroid and radioactive iodine therapies.

Activity

  • In otherwise healthy patients with hyperthyroidism, exercise tolerance often is not significantly affected. For these people, no reduction in physical activity is necessary. For elderly patients or for persons with cardiopulmonary comorbidities, a decrease in activity is prudent until hyperthyroidism is medically controlled.
  • With severe thyrotoxicosis, systolic and diastolic cardiac dysfunction are often manifested by dyspnea upon exertion.
  • In many cases, beta-blocker therapy greatly improves exercise tolerance until thyroid hormones levels are reduced by other therapies.

Medication

Drug therapy includes medications that reduce the symptoms of thyrotoxicosis and decrease the synthesis and release of thyroid hormone. In the United States, the most common definitive therapy for hyperthyroidism is ablation of the hyperactive thyroid with an oral dose of131 I. Sometimes, the patient is treated with antithyroid medication to return thyroid hormone levels to normal. When that is accomplished, some patients (eg, those with a toxic multinodular goiter or toxic adenoma) are treated immediately with radioactive iodine, while patients with autoimmune Graves disease may be treated for 12-18 months with antithyroid medications because of the possibility that the patient will go into remission.7

Nevertheless, the most common treatment for these patients in the United States is to receive131 I as their first and only medication. Patients with other forms of hyperthyroidism, including toxic multinodular goiter and toxic adenoma, continue indefinitely to be thyrotoxic, and remissions with antithyroid medications are not expected.

Antithyroid medications

Inhibit T4 and T3 synthesis.


Propylthiouracil

Derivative of thiourea that inhibits organification of iodine by the thyroid gland. Blocks oxidation of iodine in thyroid gland, thereby inhibiting thyroid hormone synthesis; inhibits T4 -to-T3 conversion (advantage over other agents). Available as a 50-mg tab. Readily absorbed and has a serum half-life of 1-2 h. Highly protein-bound in the serum. Duration of action is longer than half-life and should be dosed q6-8h (but can be administered bid). If patient compliance is an issue, methimazole is better choice because of qd dosing.
Thyroid hormone levels (TSH, T4, FTI or free T4, and T3) should be reassessed in 4 wk and increased if thyroid hormone levels have not significantly fallen or decreased if thyroid hormone levels have fallen by 50% or more (even if still thyrotoxic). Usually after thyroid function improves, gradually decrease the dose to 50-150 mg/d in divided doses (or the patient will become hypothyroid).

Adult

Not first-line agent
Initial dose: 100-150 mg PO tid (decrease in dose is virtually always required in 4-8 wk when using this starting dose)
Thyroid storm: 150-200 mg PO q4-6h

Pediatric

Not first-line agent
Neonates: 5-10 mg/kg/d PO divided tid
Children: 2-7 mg/kg/d PO divided tid
Because of neurological consequences of hypothyroidism, dose must be carefully monitored to prevent hypothyroidism

Antivitamin K activity; may potentiate activity of oral anticoagulants

Documented hypersensitivity, known liver disease; pediatric patients (unless allergic or intolerant to methimazole and no other treatment is an option)

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Monitor oral anticoagulant therapy closely because hyperthyroxinemia causes hypoprothrombinemia and reduces requirements for anticoagulant medication; as hyperthyroxinemia resolves, anticoagulant dose increases; once symptoms of hyperthyroidism have resolved, lower maintenance dose of PTU if serum TSH levels are elevated; caution in breastfeeding women (monitor infants for hypothyroidism); urticaria, pruritus, and arthralgias occur in 5%; agranulocytosis occurs in 0.2-0.5%; severe hepatitis is a rare complication
Risk of serious liver injury, including liver failure and death, has been reported in adults and children by the FDA (carefully consider drug therapy, and if PTU initiated, monitor for symptoms and signs of liver injury, especially during first 6 mo of therapy)


Methimazole (Tapazole)

Inhibits thyroid hormone by blocking oxidation of iodine in thyroid gland. However, not known to inhibit peripheral conversion of thyroid hormone.
Available as 5-mg or 10-mg tab. Readily absorbed and has serum half-life of 6-8 h. Less protein-bound than PTU and generally is not used in pregnancy because of increased placental transfer and risk of a rare fetal condition (cutis aplasia). Has higher transfer rate into the milk of lactating women. Duration of action is longer than half-life and should be dosed q12-24h.
Studies have shown that rectal suppositories or retention enemas can be used at the same dose as orally administered methimazole for patients who cannot take oral medications.
Usually after thyroid function improves, dose must be decreased or patient will become hypothyroid.

Adult

Initial dose: 20-40 mg/d PO or PR (suppository or retention enema) qd or divided bid
Usual maintenance dose: 2.5-15 mg/d PO or PR (suppository or retention enema)

Pediatric

0.2 mg/kg/d PO
Avoid hypothyroidism in children and infants

Inhibits vitamin K activity and may potentiate activity of oral anticoagulants; toxicity increased with coadministration of lithium and potassium iodide

Documented hypersensitivity; breastfeeding women; known liver disease

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Monitor oral anticoagulant therapy closely because hyperthyroxinemia causes hypoprothrombinemia and reduces requirements for anticoagulant medication; as hyperthyroxinemia resolves, anticoagulant dose increases; once symptoms of hyperthyroidism have resolved, lower maintenance dose if serum TSH levels are elevated; caution in breastfeeding women (monitor infants for hypothyroidism); urticaria, pruritus, and arthralgias occur in 5%; agranulocytosis occurs in 0.2-0.5%

Beta-adrenergic receptor blockers

Reduce many of the symptoms of thyrotoxicosis, including tachycardia, tremor, and anxiety. Usually, propranolol is recommended because of CNS penetration, but some patients prefer longer-acting beta blockers. Patients note an immediate improvement in tachycardia, anxiety, heat intolerance, and tremor. Calcium-channel blockers for tachycardia sometimes are used when beta blockers are contraindicated or not tolerated.


Propranolol (Inderal, Betachron E-R)

DOC in treating cardiac arrhythmias resulting from hyperthyroidism. Controls cardiac and psychomotor manifestations within minutes.

Adult

20-80 mg PO tid; 1-2 mg IV q4-8h

Pediatric

0.5-1 mg/kg/d PO divided tid/qid

Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase

Documented hypersensitivity; uncompensated CHF; bradycardia; cardiogenic shock; AV conduction abnormalities; reactive airway disease (COPD, asthma)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may cause angina and exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely


Atenolol (Tenormin)

Selectively blocks beta1 receptors with little or no effect on beta2 types.

Adult

50-100 mg/d PO

Pediatric

Not established

Coadministration with aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease effects; haloperidol, hydralazine, loop diuretics, and MAOIs may increase toxicity

Documented hypersensitivity; CHF; pulmonary edema; cardiogenic shock; AV conduction abnormalities; heart block (without a pacemaker), reactive airway disease (COPD, asthma)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and mask signs of hyperthyroidism; abrupt withdrawal may induce angina and exacerbate symptoms of hyperthyroidism and cause thyroid storm; monitor patients closely and withdraw drug slowly; during an IV, carefully monitor BP, heart rate, and ECG

Inorganic iodide or iodinated radiographic contrast agents

High intrathyroidal iodine levels in Graves thyrotoxicosis lead to an inhibition of iodine transport and thyroid hormone synthesis (Wolff-Chaikoff effect) and block the release of T4 and T3 from the thyroid. Excess iodide with toxic multinodular goiter or toxic adenoma may result in exacerbation of thyrotoxicosis. Administration of pharmacologic doses of iodide prevents radioactive iodine therapy for many weeks. Many patients unexpectedly escape from the inhibitory effects of iodide. Therefore, it is not used in long-term maintenance therapy of Graves thyrotoxicosis.


Iopanoic acid (Telepaque)

Oral contrast agent for rapid and significant inhibition of peripheral T4 -to-T3 conversion. Inorganic iodide released also blocks release of thyroid hormones. Quickly reduces levels of the biologically active form of thyroid hormone, T3, and decreases symptoms accordingly. Not available in the United States.

Adult

1-3 g PO as a single dose or 0.5 g PO bid continued

Pediatric

Not established

Coadministration with lithium may result in hypothyroid effects

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in hypersensitivity to iodinated products; possibility of hypotension increases with increased dosage; anuria may develop if agents are administered to patients with combined hepatic and renal disease or severe renal impairment; prolonged iodine storage in tissues may lead to rebound thyrotoxicosis with potential to cause thioamide resistance


Potassium iodide (Lugol solution, SSKI)

Inhibits thyroid hormone secretion. Lugol solution contains 8 mg of iodide per drop. SSKI contains approximately 35-50 mg of iodide per drop. Iodide treatment is reserved for the treatment of thyroid storm or for 10-14 d prior to surgical procedure, including thyroidectomy. Can be used with Graves thyrotoxicosis but exacerbates thyrotoxicosis from toxic multinodular goiter and toxic adenoma.

Adult

Lugol solution: 3-5 gtt in water PO tid
SSKI: 1-2 gtt in water PO bid

Pediatric

Administer as in adults

Increases lithium toxicity by inducing additive hypothyroid effects

Documented hypersensitivity; pulmonary edema; bronchitis; tuberculosis; hyperkalemia; toxic multinodular goiter or toxic adenoma; planned therapy with131 I within 3-6 mo

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Prolonged use may result in hypothyroidism; caution in renal failure or GI obstruction; long-term use of high-dose iodide during pregnancy may cause fatal fetal goiter and hypothyroidism


Sodium iodide131 I (Iodotope)

Most common treatment of hyperthyroidism in adults in the US. Quickly absorbed and taken up by the thyroid. No other tissue or organ in the body is capable of retaining radioactive iodine; therefore, few adverse effects develop.

Adult

75-200 µCi/g of thyroid multiplied by estimated thyroid gland size/24-h radioiodine uptake

Pediatric

Not established

Coadministration with lithium may result in hypothyroid effects

Documented hypersensitivity; pregnant or breastfeeding women

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Discontinue antithyroid therapy for 3-4 d before administration; not usually administered to patients with severe ophthalmopathy because good clinical evidence indicates that usually mild, but occasionally severe, worsening of thyroid eye disease occurs after radioactive iodine therapy

More on Hyperthyroidism

Overview: Hyperthyroidism
Differential Diagnoses & Workup: Hyperthyroidism
Treatment & Medication: Hyperthyroidism
Follow-up: Hyperthyroidism
Multimedia: Hyperthyroidism
References
Further Reading
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References

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Keywords

hyperthyroidism, thyroid, TSH, Graves disease, hyperthyroid, thyroiditis, thyroid hormone, thyroid nodule, thyroid function, thyroid treatment, thyroid goiter, thyroid medication, thyroid medicine, thyroid problem, thyroidectomy, enlarged thyroid, thyroid-stimulating hormone, thyroid problems symptoms, thyrotoxicosis, diffuse toxic goiter, Graves' disease, Hashimoto thyroiditis, toxic multinodular goiter, toxic multi-nodular goiter, Plummer disease, Plummer's disease, subacute thyroiditis, toxic adenoma, iodide-induced thyrotoxicosis, thyrotoxicosis factitia, thyroid-stimulating hormone, thyroid carcinoma, struma ovarii with thyrotoxicosis, antithyroid medication, anti-thyroid medication, radioactive iodine therapy, iodine radiotherapy, elevated levels of free thyroxine, elevated levels of free triiodothyronine, molar hydatidiform pregnancy, choriocarcinoma, pituitary tumors, metastatic thyroid carcinoma, heat intolerance, oligomenorrhea, unexplained weight loss, lid lag, sinus tachycardia, atrial fibrillation, high output failure, fine tremor, muscle weakness, anxiety, thyroid ophthalmopathy, pernicious anemia, periorbital edema, chemosis, conjunctival edema, conjunctival injection, proptosis, myasthenia gravis, vitiligo, adrenal insufficiency, type I diabetes mellitus, apathetic hyperthyroidism, follicular thyroid adenoma, toxic thyroid adenoma, Jod-Basedow syndrome, dermoid tumors, ovarian teratomas, congestive heart failure, CHF, left ventricular thickening, dermopathy, extraocular muscle dysfunction, diplopia, swelling of the pretibial area, tachycardia, atrial arrhythmia, systolic hypertension, rheumatoid arthritis, nontoxic goiter, thyroid autonomy, granulomatous thyroiditis, HLA-DRw3, HLA-B89, Hashimoto hypothyroidism

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Contributor Information and Disclosures

Author

Stephanie L Lee, MD, PhD, Fellow, Association of Clinical Endocrinology; Director of Thyroid Nodule and Cancer Center, Associate Chief, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Associate Professor, Department of Medicine, Boston University School of Medicine
Stephanie L Lee, MD, PhD is a member of the following medical societies: American College of Endocrinology, American Thyroid Association, and Endocrine Society
Disclosure: Nothing to disclose.

Coauthor(s)

Sonia Ananthakrishnan, MD, Attending Physician, Department of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine/Boston Medical Center
Disclosure: Nothing to disclose.

Medical Editor

Frederick H Ziel, MD, Associate Professor of Medicine, David Geffen School of Medicine at UCLA; Physician-In-Charge, Endocrinology/Diabetes Center, Director of Medical Education, Kaiser Permanente Woodland Hills; Chair of Endocrinology, Co-Chair of Diabetes Complete Care Program, Southern California Permanente Medical Group
Frederick H Ziel, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Federation for Medical Research, American Medical Association, American Society for Bone and Mineral Research, California Medical Association, Endocrine Society, and International Society for Clinical Densitometry
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Yoram Shenker, MD, Chief of Endocrinology Section, Veterans Affairs Medical Center of Madison; Interim Chief, Associate Professor, Department of Internal Medicine, Section of Endocrinology, Diabetes and Metabolism, University of Wisconsin at Madison
Yoram Shenker, MD is a member of the following medical societies: American Heart Association, Central Society for Clinical Research, and Endocrine Society
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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