eMedicine Specialties > Pediatrics: General Medicine > Endocrinology

Hyperthyroidism: Treatment & Medication

Author: Robert J Ferry Jr, MD, Chief, Division of Pediatric Endocrinology and Metabolism, Le Bonheur Children's Medical Center, University of Tennessee Health Science Center at Memphis, and St Jude Children's Research Hospital; Field Surgeon (Medical Corps), 162nd Area Support Medical Company, Army National Guard
Coauthor(s): Jonathan G Gold, MD, Assistant Professor, Department of Pediatrics and Human Development, College of Human Medicine, Michigan State University
Contributor Information and Disclosures

Updated: Jun 4, 2009

Treatment

Medical Care

  • Self-limited causes of hyperthyroidism, such as subacute thyroiditis, iodine-induced hyperthyroidism, and exogenous administration of T4, can be treated symptomatically. For more significant cardiovascular symptoms, beta-adrenergic blockade with propranolol can be helpful.
  • To date, no treatments can correct the underlying immune dysfunction in Graves disease. Treatment is directed at correcting the clinical and biochemical abnormalities. Because each of the following 3 treatments currently used has advantages and disadvantages, the therapeutic choice must be individualized.
    • Medical therapy with antithyroid drugs
    • Ablation of the thyroid gland with radioactive iodine
    • Subtotal thyroidectomy
  • The US Preventative Services Task Force has released guidelines regarding screening for thyroid disease.4

Surgical Care

  • Surgery is the oldest treatment for Graves disease and is quite effective. Generally, patients are initially treated with antithyroid medications. Iodide then is added before surgery to decrease the vascularity of the thyroid gland. To minimize risk of recurrence, most of the gland is removed. Consequently, the risk of permanent hypothyroidism is high. Patients may require lifelong T4 replacement.
  • Surgical complications can include hypoparathyroidism and damage to the recurrent laryngeal nerve. In the hands of an experienced surgeon, these risks are 1-3%. The surgical mortality rate is very low.

Consultations

  • A pediatric endocrinologist should monitor patients with hyperthyroidism.
  • Ophthalmologic evaluation is necessary in patients with significant ophthalmopathy.
  • Consultation with a competent neck surgeon is required if a subtotal thyroidectomy is contemplated.
  • A nuclear radiologist should be consulted for radioactive iodine therapy.

Diet

  • No special diet is required.

Activity

  • Patients with symptomatic hyperthyroidism may present with restlessness or fatigue and decreased exercise tolerance. Generally, these symptoms resolve with therapy.
  • Activity may be guided by tolerance and should be limited until the hyperthyroidism is controlled.

Medication

Antithyroid medications

Two antithyroid medications currently used in the United States are propylthiouracil (PTU) and methimazole. A third medication, carbimazole, is similar in action to methimazole and is primarily used in Europe and Asia. All 3 antithyroid medications belong to the class of compounds known as thionamides and have been used for more than 50 years.

These medications inhibit thyroid hormone biosynthesis by decreasing the oxidation of iodide and iodination of tyrosine. In addition, PTU diminishes the peripheral conversion of T4 into T3. Some evidence suggests that antithyroid drugs modify the immune response and decrease circulating levels of thyroid autoantibodies; however, whether this is a direct effect of these medications or simply a fortuitous side effect of the reduction of circulating thyroid hormone levels is unclear.

Dosage and frequency of administration have not been well established for these medications. The usual pediatric dose of PTU is 5-7 mg/kg/d. Its serum half-life is 75 minutes. The more potent methimazole is administered at 0.5-0.7 mg/kg/d. Its half-life is 4-6 hours. Pharmacokinetically, it would seem that neither of these should be effective as once-daily therapy; however, because the thyroid accumulates the drugs, methimazole given once daily is clinically effective. PTU, on the other hand, should be administered 3 times a day.

Lower per-kilogram doses of methimazole (<0.5 mg/kg/d) have been shown to prolong the free T4 elevations for almost 3 times as long as the higher per-kilogram doses (>0.5 mg/kg/d).

Because antithyroid medications affect the thyroid principally at the level of hormone biosynthesis, patients may continue to secrete preformed hormone for 6-12 weeks after initiation of therapy. In patients with marked cardiac manifestations of hyperthyroidism, a beta-blocker (eg, propranolol, 80 mg/m2/d) is added to the regimen until hyperthyroidism is under control.

Dosage of PTU or methimazole is titrated to maintain T4 concentration within the normal range. As the disease comes under control and thyroid-stimulating hormone (TSH) levels rise, the dose is decreased and eventually discontinued. An alternative approach is to give a larger dose of medication to induce hypothyroidism, and exogenous T4 is added to the regimen to correct the hypothyroidism. The addition of T4 has been suggested to result in a higher rate of remission, although studies are conflicting. This approach requires administration of 2 drugs and, because of the higher dose of antithyroid drugs, may increase the risk of adverse effects.

Remission is defined as persistent euthyroidism after discontinuation of therapy. The reported remission rate with medical therapy is 34-64%. In the first 24-48 months of therapy, the remission rate increases with the duration of therapy. After the first few years, however, spontaneous remission is less likely. Patients may have a relapse weeks or years after discontinuation of therapy. Variation in the reported relapse rate is, in part, related to differences in the length of follow-up.

Adverse effects of these medications are relatively common and may be dose-related. Approximately 1-9% of patients develop a drug-induced rash that resolves with discontinuation of therapy. Drug cross-reactivity between PTU and methimazole may be as high as 50%. Other minor adverse effects include a bitter taste, nausea, and headache. An asymptomatic, mild, transient granulocytopenia is observed in as many as 12% of patients; however, patients can generally continue on the medication, provided that the WBC is closely monitored.

More severe adverse effects are less common. Arthritis, fever, and mucosal ulcerations are observed in a small number of patients. Other serious adverse effects include agranulocytosis, hepatitis, glomerulonephritis, arthritis, and a lupuslike syndrome. These effects, thought to be idiosyncratic reactions, can occur at any time during the course of therapy. Medication should be stopped immediately. Reactions usually resolve within a few weeks.

The US Food and Drug Administration (FDA) has identified 32 cases (22 adult and 10 pediatric) of serious liver injury associated with propylthiouracil (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 as second-line drug therapy, except in patients who are allergic or intolerant to methimazole, or for 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.5
  • 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 and evaluate 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.

For neonatal Graves disease, various approaches may be used. In mild cases, symptomatic treatment with a beta-blocker (eg, propranolol) may be tried. In some cases, this is adequate because the disease is usually transient. In more severe cases, antithyroid medications are necessary. In very severe cases, iodides in the form of Lugol iodine solution or saturated solution of potassium iodide (SSKI) are used.

Iodide inhibits the release of preformed T4 and T3 from the thyroid gland and therefore has a more rapid onset of action than the thionamides. Glucocorticoids may be necessary in severe cases. These inhibit the peripheral conversion of T4 to T3 and protect the infant against adrenal insufficiency, which can occur because T4 increases the metabolism of cortisol. Note that iodide or thionamide therapy may render the neonate hypothyroid, which is clearly not desirable. Therefore, thyroid function tests must be monitored very closely, and the dose of thionamide reduced or T4 must be added if the infant becomes hypothyroid. In rare cases of congestive heart failure (CHF), digoxin is a useful adjunct.

Medical treatment of maternal hyperthyroidism is not a contraindication to breastfeeding. In this case, the drug of choice is propylthiouracil because it is bound mostly to plasma proteins and does not cross the blood-milk barrier to a significant degree.

Overall, treatment with antithyroid medications is a relatively safe option provided that patients are willing to participate in prolonged therapy. Currently, this is considered to be the treatment of choice in children and adolescents.

Radioiodine

Ablation of the thyroid gland with radioiodine is the treatment of choice for most adults. Pregnancy is the sole contraindication to this therapy. After more than 50 years of widespread use, no evidence of an increased risk of malignancy or genetic damage is noted. Nonetheless, because of the theoretical risk, frequency of radioiodine therapy is much lower in pediatric patients.

131 I is administered orally in 1-2 doses. Ablation may take several weeks to months, and hyperthyroid symptoms may continue until that time. Propranolol may be used to ameliorate these symptoms.

The major undesirable effect of radioiodine ablation is hypothyroidism. Most patients eventually become hypothyroid regardless of the radiation dose. Patients treated with this method should expect to require lifelong thyroid replacement with T4.

Long-term follow-up (36 y) of approximately 100 children who were treated with radioactive iodine prior to age 20 years revealed no increase in the rates of thyroid cancer or birth defects in offspring of these children.

Thionamides

These agents block the synthesis of thyroid hormone.


Propylthiouracil (PTU)

In addition to inhibiting thyroid hormone biosynthesis by decreasing the oxidation of iodide and iodination of tyrosine, diminishes peripheral conversion of T4 into T3.

Adult

Not first-line agent
100-150 mg/d PO divided q8h

Pediatric

Not first-line agent
5-7 mg/kg/d PO divided q8h

Has antivitamin K activity; may potentiate activity of oral anticoagulants

Documented hypersensitivity; agranulocytosis, arthritis, mucosal ulcerations, hepatitis, glomerulonephritis, lupuslike syndrome; pediatric patients (unless allergic or intolerant to methimazole and no other treatment is an option); transient granulocytopenia is not a contraindication to use

Pregnancy

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

Precautions

Drug doses must be titrated to maintain TSH and T4 in normal range; drug-induced rash is common; cross-reactivity with methimazole is up to 50%; perform thyroid function tests q2-3mo; 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)

Treatment of choice for fetal hyperthyroidism.

Adult

5-15 mg/d PO divided q8-24h

Pediatric

0.5-0.7 mg/kg/d PO divided q8-24h

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

Documented hypersensitivity; agranulocytosis, arthritis, mucosal ulcerations, hepatitis, glomerulonephritis, lupuslike syndrome; transient granulocytopenia is not a contraindication to use

Pregnancy

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

Precautions

Titrate dose to maintain TSH and T4 in normal range; drug-induced rash is common; cross-reactivity with propylthiouracil is up to 50%; perform thyroid function tests q2-3mo; readily crosses into placenta and breast milk

Iodide

This agent blocks iodide uptake by the thyroid, thereby transiently decreasing T4 synthesis. This effect lasts for about 2 weeks. Various iodide preparations, including strong iodine solution (ie, Lugol iodine solution), SSKI, and iodinated radiographic contrast agents (sodium ipodate) have been used. Radiographic contrast agents are effective, not only because they release iodide, but also because they inhibit conversion of T4 to T3. Sodium iodide may be administered intravenously if oral intake is compromised. Damaged or immature thyroid glands (eg, posttreatment with radioactive iodine, thyrotoxicosis in the neonate) are particularly susceptible to the suppressive effects of iodides and are less likely to rebound from these effects.


Iodide (Lugol Solution, SSKI)

Strong iodine solution (ie, Lugol iodine solution) contains about 6.3 mg iodine/gtt. Potassium iodide (ie, SSKI) contains about 38 mg/gtt.
Sodium ipodate and sodium iopanoic acid are iodinated contrast agents that act by liberating iodide. Sodium ipodate contains 308 mg iodine/cap, whereas sodium iopanoic acid contains 333 mg iodine/cap. Advantageous because also thought to inhibit extrathyroidal conversion of T4 to T3.

Adult

Lugol solution: 3-5 gtt PO tid
SSKI: 1-10 gtt PO tid

Pediatric

Neonatal Graves disease:
Lugol solution: 1 gtt PO tid
SSKI: 1-5 gtt PO tid
Sodium ipodate or iopanoic acid: 100-200 mg/d PO

Administer propylthiouracil before iodides in thyroid storm so that the effect of the propylthiouracil is manifested fully; iodides may inhibit the action of the thiourea drugs because iodine uptake may be increased initially with these drugs; increases lithium toxicity by inducing additive hypothyroid effects

Pregnancy

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

Precautions

Effect on decreasing T4 synthesis transient, although some mild cases may be treated for longer; crosses the placenta thereby blocking fetal T4 synthesis; irregular heart beat may occur with potassium iodide; may exacerbate acne or cause skin eruption and rash

Beta-adrenergic blocking agents

These agents are used for symptomatic treatment of cardiac complications of hyperthyroidism.


Propranolol (Inderal)

Cardiac symptoms can be alleviated with propranolol.

Adult

10-40 mg PO q6-8h; alternatively, 120-160 mg PO qd for long-acting preparation

Pediatric

2-4 mg/kg/d PO divided bid

Barbiturates, indomethacin, or rifampin may increase metabolism, lowering serum levels, whereas cimetidine, hydralazine, verapamil, or chlorpromazine may increase serum levels; bioavailability may be increased in Down syndrome, thus lower doses may be required; coadministration with catecholamine-depleting drugs such as reserpine may lead to hypotension, bradycardia, and vertigo; may decrease clearance of theophylline, antipyrine, and lidocaine

Documented hypersensitivity; uncompensated congestive heart failure; bradycardia, cardiogenic shock; AV conduction abnormalities bronchospastic disease because may increase bronchospasm; weakness, nausea, vomiting, depression, exacerbation of asthma, or heart block

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

Do not use in children with asthma; use in diabetes mellitus may mask symptoms of hypoglycemia; monitor pulse rate and BP; dose chosen should decrease pulse and BP only into the normal range; beta-adrenergic blockade may reduce symptoms of acute hypoglycemia and mask signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism and cause thyroid storm; closely monitor patients and slowly withdraw drug; carefully monitor BP, heart rate, and ECG during IV

Radioiodine (I 131)

This agent is used for radioablation as an alternative to medical or surgical therapy.


Radioiodine (I 131, Iodotope)

One to 2 doses sufficient. Some physicians give standard dose, but others calculate dose based on measured radioiodine uptake.

Adult

4-10 mCi

Pediatric

Administer as in adults

Increases lithium toxicity by producing additive hypothyroid effects; uptake affected by stable iodine, thyroid, and antithyroid agents

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Caution in breastfeeding women because drug may pass through placenta and is secreted into milk; may cause bone marrow depression, acute leukemia, anemia, blood dyscrasias, leukopenia, thrombocytopenia, radiation sickness, angina, sinus tachycardia, pruritus, rash, hives; high doses may cause radiation thyroiditis with painful thyroid or release of stored thyroid hormone causing temporary thyrotoxicosis

Glucocorticoids

Stress doses used primarily to treat thyroid storm. Effects are thought to be due to reduction in conversion of T4 to T3, reduction in autoantibody formation, and protection from adrenal insufficiency. High-dose glucocorticoids may also be used for severe sight-threatening ophthalmopathy.


Hydrocortisone (Hydrocortone, Cortef)

Elicits anti-inflammatory properties and causes profound and varied metabolic effects. Modify the body's immune response to diverse stimuli.

Adult

100 mg PO/IV qid

Pediatric

100-200 mg/m2/d PO/IV

Corticosteroid clearance may decrease with estrogens; may increase digitalis toxicity secondary to hypokalemia

Documented hypersensitivity; viral, fungal, or tubercular skin infections

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

Caution in hyperthyroidism, osteoporosis, peptic ulcer, cirrhosis, nonspecific ulcerative colitis, diabetes mellitus, and myasthenia gravis

More on Hyperthyroidism

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

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Further Reading

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Keywords

hyperthyroidism, thyrotoxicosis, Graves disease, Graves' disease, thyroid disease, thyroid gland, thyroid hormone, thyroid-stimulating hormone, TSH, thyrotropin-releasing hormone, TRH, triiodothyronine, T3, thyroxine, T4, diabetes mellitus, Addison disease, systemic lupus erythematosus, rheumatoid arthritis, myasthenia gravis, vitiligo, immune thrombocytopenic purpura, pernicious anemia, treatment, diagnosis, craniosynostosis, developmental delay, hypercalcemia, McCune-Albright syndrome, precocious puberty, attention deficit hyperactivity, disorder, insomnia, heat intolerance, diarrhea, menstrual irregularities, goiter, tachycardia, exophthalmos, toxic adenoma, toxic nodular goiter, subacute thyroiditis, chronic lymphocytic thyroiditis, pituitary adenoma, exogenous thyroid hormone, polyostotic fibrous dysplasia, café-au-lait spots, Jod-Basedow phenomenon

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Contributor Information and Disclosures

Author

Robert J Ferry Jr, MD, Chief, Division of Pediatric Endocrinology and Metabolism, Le Bonheur Children's Medical Center, University of Tennessee Health Science Center at Memphis, and St Jude Children's Research Hospital; Field Surgeon (Medical Corps), 162nd Area Support Medical Company, Army National Guard
Robert J Ferry Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, Society for Pediatric Research, and Texas Pediatric Society
Disclosure: Nutropin Speakers Bureau Honoraria Speaking and teaching; Genotropin Speakers Bureau Honoraria Speaking and teaching; Eli Lilly & Co. Grant/research funds Independent contractor; MacroGenics, Inc. Grant/research funds Independent contractor; Ipsen, S.A. (formerly Tercica, Inc.) Grant/research funds Independent contractor

Coauthor(s)

Jonathan G Gold, MD, Assistant Professor, Department of Pediatrics and Human Development, College of Human Medicine, Michigan State University
Jonathan G Gold, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Sigma Xi
Disclosure: Nothing to disclose.

Medical Editor

Thomas A Wilson, MD, Professor of Clinical Pediatrics, Department of Pediatrics; Director of Pediatric Endocrinology, Division of Pediatric Endocrinology, Department of Pediatrics, State University of New York at Stony Brook
Thomas A Wilson, MD is a member of the following medical societies: Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London), Professor and Chair, First Department of Pediatrics, Athens University Medical School, Aghia Sophia Children's Hospital, Greece
George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Endocrinology, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Merrily P M Poth, MD, Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences
Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD, Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas and Arkansas Children's Hospital
Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research
Disclosure: Genentech, Inc. Honoraria Speaking and teaching; Pfizer, Inc. Honoraria Consulting

 
 
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