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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvOTIxNzA3LXRyZWF0bWVudA==\nDrugs & Diseases > Pediatrics: General Medicine\nPediatric Hyperthyroidism Treatment & Management\nAuthor: Sunil Kumar Sinha, MD; Chief Editor: Stephen Kemp, MD, PhD more...\nPediatric Hyperthyroidism\nSections Pediatric Hyperthyroidism\nComplete Blood Cell Count\nSymptomatic Treatment\nAntithyroid Agents\nRadioactive Iodine Ablation of the Thyroid Gland\nThionamides\nIodide Agents\nBeta-Adrenergic Blocking Agents\nThe treatment administered for pediatric hyperthyroidism depends on the child's age and severity of their disease. Treatment approaches include antithyroid medications, radioiodine ablation, and thyroidectomy [6] ; because each of these treatments has advantages and disadvantages, the therapeutic choice must be individualized.\nOnce treatment is initiated, careful monitoring is essential because patients are at risk for either recurrent thyrotoxic symptoms or hypothyroidism. Patients who receive inadequate treatment may have bone demineralization and subsequently be at increased risk for osteoporosis and fractures.\nInpatient care is rarely required in children with hyperthyroidism, and serious complications of medical therapy (eg, agranulocytosis, hepatitis, lupuslike syndrome) are quite rare. Nonetheless, patients should be carefully monitored for complications.\nSurgery is the oldest treatment for Graves disease and is quite effective. [7] 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.\nSurgical complications can include hypoparathyroidism and damage to the recurrent laryngeal nerve. In a recent study, incidental parathyroid excision was reported in 19.4% of pediatric thyroidectomies. [8] Transient hypocalcemia is another potential complication, even without incidental parathyroid excision. In the hands of an experienced surgeon, these risks are 1-3%. The surgical mortality rate is very low, but referring patients to experienced surgeons who report both their case volumes and complication rates is prudent.\nRemission, which can takes months to years, is defined as persistent euthyroidism after discontinuation of therapy. The reported remission rate with medical therapy is 34-64% within 5 years of diagnosis. 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.\nAttempts to define positive prognostic indicators of long-term remission have not been successful thus far.\nPatients treated medically should have thyroid function tests (T 4 , T 3 , thyroid-stimulating hormone [TSH]) every 2-3 months. TSH levels are suppressed for several months after the initiation of therapy; therefore, T 3 and T 4 levels are better initial chemical markers of the euthyroid state.\nBesides thyroid function tests, routine laboratory evaluation is generally not required. Although hepatitis, thrombocytopenia, and agranulocytosis are known side effects of propylthiouracil (PTU) and methimazole, they are rare enough and of such sudden onset that routine laboratory screening is rarely helpful.\nGhrelin and insulinlike growth factor – binding protein-1 (IGFBP-1) levels may have a role in the hunger-satiety signal pathway in patients with Graves thyrotoxicosis. Ghrelin levels in untreated patients are low and increase with medical therapy, whereas fasting IGFBP-1 levels, which are initially elevated, fall.\nGlucocorticoid therapy should be considered in patients (both adults and children) with severe ophthalmopathy. Pulse therapy may provide a favorable response in up to 88% of patients.\nPatients treated with radioiodine or surgery should have thyroid function tests annually.\nSelf-limited causes of hyperthyroidism, such as subacute thyroiditis, iodine-induced hyperthyroidism, and exogenous administration of T 4 , can be treated symptomatically. For more significant cardiovascular symptoms, beta-adrenergic blockade with propranolol can be helpful.\nInitial response to antithyroid medications depends on the level of preformed thyroid hormone. Because antithyroid medications do not block the release of preformed hormone, patients may need 3-12 weeks on therapy before they become clinically and chemically euthyroid. Propranolol can be a useful adjunct during this period. See Antithyroid Agents.\nNeonatal Graves disease\nTo date, no treatments can correct the underlying immune dysfunction in Graves disease. Treatment is directed at correcting the clinical and biochemical abnormalities.\nFor 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.\nIodide inhibits the release of preformed T 4 and T 3 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 T 4 to T 3 and protect the infant against adrenal insufficiency, which can occur because T 4 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 T 4 must be added if the infant becomes hypothyroid. In rare cases of congestive heart failure (CHF), digoxin is a useful adjunct.\nMaternal hyperthyroidism and breastfeeding\nMedical treatment of maternal hyperthyroidism is not a contraindication to breastfeeding. In this case, the drug of choice is propylthiouracil (PTU), because it is bound mostly to plasma proteins and does not cross the blood-milk barrier to a significant degree.\nTreatment with antithyroid medications is considered to be the treatment of choice in children and adolescents. This treatment is a relatively safe option, provided that patients are willing to participate in prolonged therapy.\nIn the United States, methimazole is the only antithyroid medication currently used. [9] A third medication, carbimazole, is similar in action to methimazole and is primarily used in Europe and Asia. PTU has been discouraged as routine practice due to its more adverse risk profile. These antithyroid medications belong to the thionamides class and have been used for more than 60 years.\nDosage and frequency of administration for these medications have not been well established. The usual pediatric dose of methimazole is 0.4-0.7 mg/kg/d, with a lower maintenance dose (one third to one half the starting dose). Its half-life is 4-6 hours. Pharmacokinetically, it would seem that neither methimazole nor PTU should be effective as once-daily therapy; yet, because the thyroid accumulates these drugs, methimazole given once daily is clinically effective. However, PTU is administered 3 times a day.\nLower 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).\nBecause 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 given once in the morning) is added to the regimen until hyperthyroidism is under control.\nThe dosage of PTU or methimazole is titrated to maintain free T4 and total T3 concentrations 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 obsolete approach was to give a larger dose of medication to induce hypothyroidism, then to add exogenous T4 to correct the hypothyroidism. Such rest of the thyroid by an addition of T4 appeared to result in a higher rate of remission, although the preponderance of evidence does not support this conclusion. Moreover, this complex approach requires administration of 2 drugs and, because of the higher dose of antithyroid drugs, could increase the risk of adverse effects.\nAdverse 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 receiving methimazole or PTU. However, these patients can generally continue on the medication, provided that the WBC count is closely monitored.\nMore 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.\nBoxed warning for PTU\nOn April 21, 2010, the US Food and Drug Administration (FDA) added a boxed warning to the prescribing information for PTU that emphasizes the risk for severe liver injury and acute liver failure, some of which have been fatal, in adult and pediatric patients receiving PTU. [10] The boxed warning also states that PTU should be reserved for use in those who cannot tolerate other treatments such as methimazole, radioactive iodine, or surgery.\nThe decision to include a boxed warning was based on the FDA's review of postmarketing safety reports and meetings held with the American Thyroid Association, the National Institute of Child Health and Human Development, and the pediatric endocrine clinical community.\nFor more information, see the FDA Safety Alert [10] as well as the Medication section. The FDA recommends the following criteria be considered for prescribing PTU [10] :\nReserve PTU use during first trimester of pregnancy, or in patients who are allergic to or intolerant of methimazole; the dose of PTU is 5-7 mg/kg/d, divided 3 times daily.\nClosely monitor PTU therapy for signs and symptoms of liver injury, especially during the first 6 months after initiation of therapy.\nFor suspected liver injury, promptly discontinue PTU therapy, and evaluate for evidence of liver injury and provide supportive care.\nPTU should not be used in pediatric patients unless the patient is allergic to or intolerant of methimazole, and no other treatment options are available.\nCounsel patients to promptly contact their healthcare 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.\nAblation 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 theoretic risk, frequency of radioiodine therapy is much lower in pediatric patients.\n131 I is administered orally in 1-2 doses by mouth in a controlled setting (ie, the hospital). Ablation may take about 2-3 months to achieve hypothyroid state, and hyperthyroid symptoms may continue until that time. Propranolol may be used to ameliorate these symptoms.\nThe 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.\nLong-term follow-up (36 y) of over 100 children who were treated with radioactive iodine before age 20 years revealed no increase in the rates of thyroid cancer or birth defects in offspring of these children. [11]\nConsultations with the following specialists may be necessary:\nA pediatric endocrinologist should monitor patients with hyperthyroidism\nOphthalmologic evaluation is necessary in patients with significant ophthalmopathy\nA nuclear radiologist should be consulted for radionuclide studies or radioactive iodine therapy\nConsultation with a competent neck surgeon is required if a subtotal thyroidectomy is contemplated\nPatients 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.\nConference Proceeding. Hepatic Toxicity Following Treatment for Pediatric Graves’ Disease Meeting. October 28, 2008. Available at http://bpca.nichd.nih.gov/collaborativeefforts/Documents/Hepatic_Toxicity_10-28-2008.pdf#search=graves.\nEmiliano AB, Governale L, Parks M, Cooper DS. Shifts in Propylthiouracil and Methimazole Prescribing Practices: Antithyroid Drug Use in the United States from 1991 to 2008. J Clin Endocrinol Metab. 2010 Mar 24. [Medline].\nBartalena L, Baldeschi L, Dickinson AJ, et al. Consensus statement of the European group on Graves' orbitopathy (EUGOGO) on management of Graves' orbitopathy. Thyroid. 2008. 18:333-46. [Medline].\nBahn R. The EUGOGO consensus statement on the management of Graves' orbitopathy: equally applicable to North American clinicians and patients. Thyroid. 2008. 18:281-2. [Medline].\nYoshimura Noh J, Miyazaki N, et al. Evaluation of a new rapid and fully automated electrochemiluminescence immunoassay for thyrotropin receptor autoantibodies. Thyroid. 2008. 18:1157-64. [Medline].\n[Guideline] US Preventative Services Task Force. Screening for thyroid disease: recommendation statement. Ann Intern Med. 2004 Jan 20. 140(2):125-7. [Medline].\nPeroni E, Angiolini MR, Vigone MC, Mari G, Chiumello G, Beretta E, et al. Surgical management of pediatric Graves' disease: an effective definitive treatment. Pediatr Surg Int. 2012 Jun. 28(6):609-14. [Medline].\nChen Y, Masiakos PT, Gaz RD, et al. Pediatric thyroidectomy in a high volume thyroid surgery center: Risk factors for postoperative hypocalcemia. Journal of Pediatric Surgery. 2015-08-01. Volume 50, Issue 8:1316-1319. [Medline].\nKlatka M, Grywalska E, Partyka M, Charytanowicz M, Rolinski J. Impact of methimazole treatment on magnesium concentration and lymphocytes activation in adolescents with graves' disease. Biol Trace Elem Res. 2013 Jun. 153(1-3):155-70. [Medline].\nFDA MedWatch Safety Alerts for Human Medical Products. Propylthiouracil (PTU). Accessed: June 3, 2009. US Food and Drug Administration. Available at http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm164162.htm.\nSisson JC, Freitas J, McDougall IR, et al. Radiation safety in the treatment of patients with thyroid diseases by radioiodine 131I : practice recommendations of the American Thyroid Association. Thyroid. 2011 Apr. 21(4):335-46. [Medline].\n[Guideline] Bahn Chair RS, Burch HB, et al. Hyperthyroidism and other causes of thyrotoxicosis: management guidelines of the American Thyroid Association and American Association of Clinical Endocrinologists. Thyroid. 2011 Jun. 21(6):593-646. [Medline].\n[Guideline] Kahaly GJ, Bartalena L, Hegedüs L. The American Thyroid Association/American Association of Clinical Endocrinologists guidelines for hyperthyroidism and other causes of thyrotoxicosis: a European perspective. Thyroid. 2011 Jun. 21(6):585-91. [Medline].\nSchematic representation of the negative/positive feedback system with respect to the hypothalamic-pituitary-thyroid axis. TRH = thyrotropin-releasing hormone; TSH = thyroid-stimulating hormone.\nSunil Kumar Sinha, MD Clinical Assistant Professor, Division of Pediatric Endocrinology, University of Arizona College of Medicine\nSunil Kumar Sinha, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, Endocrine Society, Pediatric Endocrine Society\nJonathan G Gold, MD Associate Professor, Department of Pediatrics and Human Development, College of Human Medicine, Michigan State University College of Human Medicine\nJonathan G Gold, MD is a member of the following medical societies: American Academy of Pediatrics, Council on Medical Student Education in Pediatrics\nStephen 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\nStephen 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\nGeorge 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\nGeorge 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\nCydney L Fenton, MD, FAAP Consulting Staff, Department of Pediatric Endocrinology, Children's Hospital Medical Center of Akron\nCydney L Fenton, MD, FAAP is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society\nRobert 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\nRobert 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\nDisclosure: 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\nAb Sadeghi-Nejad, MD Chief, Division of Pediatric Endocrinology and Metabolism, Tufts Medical Center; Professor of Pediatrics, Tufts University School of Medicine\nAb Sadeghi-Nejad, MD is a member of the following medical societies: American Academy of Pediatrics, American Association for the Advancement of Science, American Pediatric Society, Endocrine Society, Massachusetts Medical Society, Pediatric Endocrine Society, and Society for Pediatric Research\nThomas 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\nThomas A Wilson, MD is a member of the following medical societies: Endocrine Society, Pediatric Endocrine Society, and Phi Beta Kappa\nencoded search term (Pediatric Hyperthyroidism) and Pediatric Hyperthyroidism\nHyperthyroidism and Thyrotoxicosis\nHyperthyroidism, Thyroid Storm, and Graves Disease\nAutoimmune Thyroid Disease and Pregnancy\nToxic Nodular Goiter\nNeurological Manifestations of Thyroid Disease\nRadioiodine/Cancer Link in Hyperthyroidism Study Sparks Debate\nDon't Screen for Thyroid Problems in Asymptomatic Patients\nHypothyroidism Overtreatment Linked to Risk of Atrial Fibrillation\nNew Guidelines and Recommendations\nAccording to Endocrinologists\nIntermittent Fasting Promotes Weight Loss, Improves Lipids\nFDA Investigating Metformin for Possible Carcinogen\nMelatonin: Magic Potion or Unregulated Danger?\nHigh-Protein Diet Could Be Harmful, Even for Healthy Kidneys\nMediterranean Diet Repeats as Best Overall of 2020\nDiseases & Conditions Pediatric Hyperthyroidism\nNews Radioiodine/Cancer Link in Hyperthyroidism Study Sparks Debate\nDiseases & Conditions Hyperthyroidism and Thyrotoxicosis\n2010 hicon-sodium-iodide-i-131-999924 Drugs\nDrugs sodium iodide I-131"