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Pediatric Graves Disease Medication

  • Author: Lynne Lipton Levitsky, MD; Chief Editor: Stephen Kemp, MD, PhD  more...
 
Updated: Oct 08, 2013
 

Medication Summary

Drugs used in the treatment of Graves disease include thiourea antithyroid medications, iodide or iodine preparations, beta-blocking agents, and thyroid hormone.

Treat all symptomatic patients with beta-adrenergic blocking agents unless an exacerbation of severe bronchospastic disease is a strong concern even with a selective beta1 antagonist. Other treatment plans depend on the therapeutic approach chosen.

Begin antithyroid drug therapy with methimazole or PTU promptly and carefully monitor. L-T4 can be added to the regimen when the dose of methimazole or PTU decreases and the thyroid gland is still large and firm, in order to establish an equilibrium during therapy. This addition of T4 does not enhance the rapidity of remission and is generally not required.

Discontinue antithyroid drugs 4 days before RAI therapy. Antithyroid drugs can be restarted 1 week after treatment or, alternatively, iodine drops can be administered until remission. In most cases, L-T4 therapy is started within 4-7 days after subtotal thyroidectomy.

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Thiourea Antithyroid Agents

Class Summary

Drugs used in the treatment of Graves disease include thiourea antithyroid medications, iodide or iodine preparations, beta-blocking agents, and thyroid hormone.

Treat all symptomatic patients with beta-adrenergic blocking agents unless an exacerbation of severe bronchospastic disease is a strong concern even with a selective beta1 antagonist. Other treatment plans depend on the therapeutic approach chosen.

Begin antithyroid drug therapy with methimazole or PTU promptly and carefully monitor. L-T 4 can be added to the regimen when the dose of methimazole or PTU decreases and the thyroid gland is still large and firm, in order to establish an equilibrium during therapy. This addition of T 4 does not enhance the rapidity of remission.

Discontinue antithyroid drugs 4 days before RAI therapy. Antithyroid drugs can be restarted 1 week after treatment or, alternatively, iodine drops can be administered until remission. In most cases, L-T 4 therapy is started within 4-7 days after subtotal thyroidectomy.

Methimazole (Tapazole)

 

Methimazole is typically the drug of choice except in thyroid storm and in pregnant women. It does not inhibit peripheral conversion of T4 to T3; thus, it does not have an immediate needed effect in the most severely thyrotoxic individuals. Methimazole possesses a longer half-life than PTU does, allowing daily or twice-daily administration. Methimazole has never been associated with life-threatening hepatitis. It is weakly associated with neonatal aplasia cutis following in utero exposure.

Propylthiouracil (PTU)

 

This is the drug of choice for thyroid storm, because it inhibits peripheral conversion of T4 to T3. It is also the drug of choice in lactation or pregnancy, because it does not cross the placenta to the extent that methimazole does and has not been associated with cutis aplasia in the fetus.

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Iodides

Class Summary

These agents decrease iodide transport, iodide oxidation, and organification and suppress thyroid hormone release from the thyroid. Various iodide preparations, including strong iodine solution (ie, Lugol 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 T 4 to T 3 . Sodium iodide may be intravenously administered if oral intake is compromised. It must be specially prepared by a pharmacy with that capability. Damaged or immature thyroid glands (eg, post-RAI treatment, thyrotoxic neonate) are particularly susceptible to the suppressive effects of iodides and are less likely to rebound from these effects.

Strong iodine solution (Lugol solution)

 

Lugol solution contains 100 mg KI and 50 mg elemental iodine per 1 mL, or approximately 8 mg iodine per drop. It is usually administered preoperatively to reduce gland vascularity or after RAI therapy to induce a more rapid remission.

Lugol solution may be used as part of the initial therapy of thyroid storm. It may also be used as monotherapy in children with neonatal Graves disease because of transplacental passage of maternal antibodies. Breakthrough from iodide suppression and intensification of Graves disease symptoms may occur; thus, do not use Lugol solution as monotherapy in older children except in the mildest cases of thyrotoxicosis. The salty metallic taste may be masked by orange juice or tomato juice.

Potassium iodide (SSKI)

 

SSKI is equally effective as Lugol solution, and it may be used in the same manner. One mL of SSKI contains 750 mg of iodide (ie, 35-50 mg per drop). The taste can be partially disguised by mixing in orange or tomato juice.

Sodium iodide

 

Acquire sodium iodide from a sterile compounding pharmacy.

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Beta-blocking agents

Class Summary

These agents rapidly decrease tachycardia, palpitations, tremor, and widened pulse pressure. Children feel better after starting a beta-blocking agent despite the minimal effect on thyroid hormone levels. Weight loss is not affected, nor is thyroid size. Central nervous system (CNS) effects are related to the lipid solubility of the agent. Use beta1 selective agents in children with asthma.

Beta-blocking agents are used for initial treatment before antithyroid drugs are administered or in patients awaiting remission after receiving RAI. They are used for primary management in neonatal Graves disease or during subtotal thyroidectomy without other preparation; however, these 2 indications are not recommended. All of the symptoms and signs of hyperthyroidism are not masked.

Propranolol (Inderal)

 

This is the drug of choice in children who do not have asthma. It is a nonselective beta-adrenergic antagonist.

Atenolol (Tenormin)

 

Atenolol is a selective beta1-receptor blocking agent recommended for children with a history of asthma. Because of its decreased lipid solubility, this agent does not cross the blood-brain barrier as well as propranolol does; thus, some of the CNS effects of thyrotoxicosis (eg, irritability, sleeplessness) may not respond as well to atenolol as they do to propranolol.

Esmolol (Brevibloc)

 

This is a very short-acting, intravenous (IV) beta1-specific blocking drug. It should be reserved for use to treat tachycardia or atrial fibrillation in severe Graves disease or thyroid storm or during surgery and anesthesia in an individual discovered to have active thyrotoxicosis. Dilute the concentrated preparation in IV fluid before administration.

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Thyroid hormones

Class Summary

Hypothyroidism is readily treated by lifelong replacement therapy with levothyroxine.

Levothyroxine (T4, Synthroid, Levothroid, Levoxyl)

 

Levothyroxine is the drug of choice for thyroid hormone replacement after the treatment of Graves disease with RAI or surgery or during long-term maintenance on a balanced regimen of antithyroid drug and thyroid hormone.

Levothyroxine is metabolized in the periphery by outer ring deiodinases to T3, the active form of thyroid hormone. Therefore, T4 and T3 preparations or T3 alone are not needed. These preparations provide T3 peaks and produce levels of T4 and T3 that are less smooth than those that result when the levothyroxine product is administered alone.

Patients with thyrotoxicosis may need a smaller dose than the recommended dose of 0.1-0.2 mg/d, because they do not readily suppress the remaining endogenous thyroid function.

Reevaluate thyroid tests 4-6 weeks after starting T4. TSH may not be an adequate means of assessment if the patient has had a suppressed TSH level for a long time. Rarely, the TSH level may stay suppressed and not rise adequately until the axis recovers; therefore, FT4 or the FT4 index (FT4I) may provide more accurate monitoring.

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Contributor Information and Disclosures
Author

Lynne Lipton Levitsky, MD Chief, Pediatric Endocrine Unit, Massachusetts General Hospital; Associate Professor of Pediatrics, Harvard Medical School

Lynne Lipton Levitsky, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Diabetes Association, American Pediatric Society, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research

Disclosure: Received grant/research funds from Eli Lilly for pi; Received grant/research funds from NovoNordisk for pi; Received consulting fee from NovoNordisk for consulting; Partner received consulting fee from Onyx Heart Valve for consulting.

Coauthor(s)

Sunil Sinha, MD Assistant Professor, Division of Pediatric Endocrinology and Metabolism, Department of Pediatrics, University of Tennessee Health Science Center

Sunil Sinha, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, Endocrine Society, Pediatric Endocrine Society

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD Former Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, 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, Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Acknowledgements

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; UNESCO Chair on Adolescent Health Care, University of Athens, 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, Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Robert J Ferry Jr, MD Le Bonheur Chair of Excellence in Endocrinology, Professor and Chief, Division of Pediatric Endocrinology and Metabolism, Department of Pediatrics, University of Tennessee Health Science Center

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, Pediatric Endocrine Society, Society for Pediatric Research, and Texas Pediatric Society

Disclosure: Eli Lilly & Co Grant/research funds Investigator; MacroGenics, Inc Grant/research funds Investigator; Ipsen, SA (formerly Tercica, Inc) Grant/research funds Investigator; NovoNordisk SA Grant/research funds Investigator; Diamyd Grant/research funds Investigator; Bristol-Myers-Squibb Grant/research funds Other; Amylin Other; Pfizer Grant/research funds Other; Takeda Grant/research funds Other

Thomas A Wilson, MD Professor of Clinical Pediatrics, Chief and Program Director, Division of Pediatric Endocrinology, Department of Pediatrics, The School of Medicine at Stony Brook University Medical Center

Thomas A Wilson, MD is a member of the following medical societies: Endocrine Society, Pediatric Endocrine Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Lynne L. Levitsky, MD, to the original writing and development of this article.

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A 16-year-old girl with thyrotoxicosis for 3 years is shown. Note her thyrotoxic stare (infrequent blinking with exophthalmos) and enlarged thyroid gland (goiter).
Neonate with thyrotoxicosis secondary to transplacental passage of maternal thyroid-stimulating immunoglobulins (TSI). The baby has a noteworthy stare. Upon examination, a small goiter and a rapid heart rate could be appreciated.
 
 
 
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