Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Hyperthyroidism Medication

  • Author: Stephanie L Lee, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
 
Updated: Jul 13, 2016
 

Medication Summary

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 of radioactive iodine (131I).

In some cases 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.

Patients with other forms of hyperthyroidism, including toxic multinodular goiter and toxic adenoma, continue to be thyrotoxic indefinitely. Remissions with antithyroid medications are not expected.

Next

Antithyroid Agents

Class Summary

Antithyroid agents inhibit the synthesis of thyroxine (T4) and triiodothyronine (T3).

Methimazole (Northyx, Tapazole)

 

With few exceptions, methimazole should be used in every patient who needs antithyroid drug therapy for hyperthyroidism. The exceptions are women in the first trimester of pregnancy, patients in thyroid storm, and patients with methimazole allergy or intolerance. Methimazole is avoided in early pregnancy because of increased placental transfer and risk of a rare fetal condition (cutis aplasia). Compared with propylthiouracil, it has a higher transfer rate into the milk of lactating women.

Methimazole inhibits thyroid hormone by blocking oxidation of iodine in the thyroid gland. However, it is not known to inhibit peripheral conversion of thyroid hormone. The drug is available as 5-mg or 10-mg tablets. It is readily absorbed and has a serum half-life of 6-8 hours. Methimazole is less protein-bound than propylthiouracil is.

Methimazole's duration of action is longer than its half-life, and the drug should be dosed every 12-24 hours. 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, the dose must be decreased or the patient will become hypothyroid.

Propylthiouracil (PropylThyracil, PTU)

 

Propylthiouracil is a derivative of thiourea that inhibits organification of iodine by the thyroid gland. It blocks oxidation of iodine in the thyroid gland, thereby inhibiting thyroid hormone synthesis; the drug inhibits T4 -to-T3 conversion (and thus has an advantage over other agents).

Propylthiouracil remains the drug of choice in uncommon situations of life-threatening severe thyrotoxicosis. It may be preferable during and before the first trimester of pregnancy.

In 2010, the US Food and Drug Administration (FDA) added a boxed warning to the prescribing information for propylthiouracil, emphasizing the risk for severe liver injury and acute liver failure, some cases of which have been fatal.

Propylthiouracil is available as a 50-mg tablet. It is readily absorbed and has a serum half-life of 1-2 hours. It is highly protein-bound in the serum. The drug's duration of action is longer than its half-life, and propylthiouracil generally should be dosed every 6-8 hours (though it can also be administered twice daily). If patient compliance is an issue, methimazole may be a better choice because it can be given as a single daily dose in many cases.

Thyroid hormone levels (thyroid-stimulating hormone [TSH], T4, free thyroxine index [FTI] or free T4, and T3) should be reassessed in 4-6 weeks after starting propylthiouracil. The dosage is increased if thyroid hormone levels have not significantly fallen or decreased if thyroid hormone levels have fallen by 50% or more (even if the patient is still thyrotoxic).

Usually, after thyroid function improves, the dosage should be gradually decreased to 50-150 mg/day in divided doses. Otherwise, the patient will become hypothyroid.

Potassium iodide (SSKI, ThyroSafe, ThyroShield, iOSAT)

 

Potassium iodide inhibits thyroid hormone secretion. Iodide therapy is primarily used for the treatment of thyroid storm or given preoperatively, 10-14 days before surgical procedures (including thyroidectomy).

Until high levels of iodine build up in the thyroid follicular cell, however, administration of iodine can increase thyroid hormone synthesis and lead to higher serum levels of thyroid hormone. Thus, it is usually recommended that iodine not be started until after antithyroid drug therapy has been initiated. In thyroid storm, iodine should be administered at least 1 hour after methimazole or propylthiouracil.

Potassium iodide and iodine (Lugol's solution)

 

Lugol's solution is primarily administered for 10 days before thyroidectomy or during thyrotoxic crisis because high levels of iodine in the follicular thyroid cell temporarily inhibit thyroid hormone synthesis and secretion. T4 and T3 concentrations can be reduced for several weeks.

Until high levels of iodine build up in the thyroid follicular cell, however, administration of iodine can increase thyroid hormone synthesis and lead to higher serum levels of thyroid hormone. Thus, it is usually recommended that iodine not be started until after antithyroid drug therapy has been initiated.

Sodium iodide 131I (Iodotope, Hicon)

 

Radioactive iodine is approved by the FDA for treatment of hyperthyroidism in adults. It can also be used with a radioactive uptake test to evaluate thyroid function. The agent is 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.

Previous
Next

Beta Blockers, Nonselective

Class Summary

Nonselective beta blockers reduce many of the symptoms of thyrotoxicosis, including tachycardia, tremor, and anxiety. Usually, propranolol is recommended because of central nervous system (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 are sometimes used when beta blockers are contraindicated or not tolerated.

Propranolol (Inderal, Inderal LA, InnoPran XL)

 

Propranolol is the drug of choice for treating cardiac arrhythmias resulting from hyperthyroidism. It controls cardiac and psychomotor manifestations within minutes.

Previous
Next

Beta Blockers, Beta1-Selective

Class Summary

Beta blockers diminish hyperthyroid symptoms, such as tachycardia, tremor, and anxiety. Beta1 -selective drugs may be tolerated better in patients who have relative beta-blockade contraindications.

Atenolol (Tenormin)

 

Atenolol selectively blocks beta1 receptors, with little or no effect on beta2 types. It is a longer-acting drug that can be more useful than propranolol for intraoperative and postoperative control.

Previous
 
Contributor Information and Disclosures
Author

Stephanie L Lee, MD, PhD Associate Professor, Department of Medicine, Boston University School of Medicine; Director of Thyroid Health Center, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Fellow, Association of Clinical Endocrinology

Stephanie L Lee, MD, PhD is a member of the following medical societies: American College of Endocrinology, American Thyroid Association, Endocrine Society

Disclosure: Nothing to disclose.

Coauthor(s)

Sonia Ananthakrishnan, MD Assistant Professor of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center, Boston University School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Romesh Khardori, MD, PhD, FACP Professor of Endocrinology, Director of Training Program, Division of Endocrinology, Diabetes and Metabolism, Strelitz Diabetes and Endocrine Disorders Institute, Department of Internal Medicine, Eastern Virginia Medical School

Romesh Khardori, MD, PhD, FACP is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians, American Diabetes Association, Endocrine Society

Disclosure: Nothing to disclose.

Acknowledgements

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Frederick H Ziel, MD Associate Professor of Medicine, University of California, Los Angeles, David Geffen School of Medicine; 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, andInternational Society for Clinical Densitometry

Disclosure: Nothing to disclose.

References
  1. Frost L, Vestergaard P, Mosekilde L. Hyperthyroidism and risk of atrial fibrillation or flutter: a population-based study. Arch Intern Med. 2004 Aug 9-23. 164(15):1675-8. [Medline].

  2. [Guideline] Bahn Chair RS, Burch HB, Cooper DS, 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].

  3. Lumbroso S, Paris F, Sultan C. Activating Gsalpha mutations: analysis of 113 patients with signs of McCune-Albright syndrome--a European Collaborative Study. J Clin Endocrinol Metab. 2004 May. 89(5):2107-13. [Medline].

  4. Betterle C, Dal Pra C, Mantero F, Zanchetta R. Autoimmune adrenal insufficiency and autoimmune polyendocrine syndromes: autoantibodies, autoantigens, and their applicability in diagnosis and disease prediction. Endocr Rev. 2002 Jun. 23(3):327-64. [Medline].

  5. Plagnol V, Howson JM, Smyth DJ, Walker N, Hafler JP, Wallace C, et al. Genome-wide association analysis of autoantibody positivity in type 1 diabetes cases. PLoS Genet. 2011 Aug. 7(8):e1002216. [Medline]. [Full Text].

  6. Chu X, Pan CM, Zhao SX, Liang J, Gao GQ, Zhang XM, et al. A genome-wide association study identifies two new risk loci for Graves' disease. Nat Genet. 2011 Aug 14. 43(9):897-901. [Medline].

  7. Simmonds MJ, Brand OJ, Barrett JC, Newby PR, Franklyn JA, Gough SC. Association of Fc receptor-like 5 (FCRL5) with Graves' disease is secondary to the effect of FCRL3. Clin Endocrinol (Oxf). 2010 Nov. 73(5):654-60. [Medline]. [Full Text].

  8. Newby PR, Pickles OJ, Mazumdar S, Brand OJ, Carr-Smith JD, Pearce SH, et al. Follow-up of potential novel Graves' disease susceptibility loci, identified in the UK WTCCC genome-wide nonsynonymous SNP study. Eur J Hum Genet. 2010 Sep. 18(9):1021-6. [Medline]. [Full Text].

  9. Nakabayashi K, Shirasawa S. Recent advances in the association studies of autoimmune thyroid disease and the functional characterization of AITD-related transcription factor ZFAT. Nihon Rinsho Meneki Gakkai Kaishi. 2010. 33(2):66-72. [Medline].

  10. Chu X, Dong Y, Shen M, Sun L, Dong C, Wang Y, et al. Polymorphisms in the ADRB2 gene and Graves disease: a case-control study and a meta-analysis of available evidence. BMC Med Genet. 2009 Mar 13. 10:26. [Medline]. [Full Text].

  11. Gabriel EM, Bergert ER, Grant CS, van Heerden JA, Thompson GB, Morris JC. Germline polymorphism of codon 727 of human thyroid-stimulating hormone receptor is associated with toxic multinodular goiter. J Clin Endocrinol Metab. 1999 Sep. 84(9):3328-35. [Medline].

  12. Mittra ES, Niederkohr RD, Rodriguez C, El-Maghraby T, McDougall IR. Uncommon causes of thyrotoxicosis. J Nucl Med. 2008 Feb. 49(2):265-78. [Medline].

  13. Davies TF, Larsen PR. Thyrotoxicosis. Larsen PR et al, eds. Williams Textbook of Endocrinology. 10th ed. Philadelphia: Saunders; 2003. 374-421.

  14. Dahl P, Danzi S, Klein I. Thyrotoxic cardiac disease. Curr Heart Fail Rep. 2008 Sep. 5(3):170-6. [Medline].

  15. Zhyzhneuskaya S, Addison C, Tsatlidis V, Weaver JU, Razvi S. The Natural History of Subclinical Hyperthyroidism in Graves' Disease: The Rule of Thirds. Thyroid. 2016 Jun. 26(6):765-9. [Medline].

  16. Heeringa J, Hoogendoorn EH, van der Deure WM, et al. High-normal thyroid function and risk of atrial fibrillation: the Rotterdam study. Arch Intern Med. 2008 Nov 10. 168(20):2219-24. [Medline].

  17. Hollowell JG, Staehling NW, Flanders WD, Hannon WH, Gunter EW, Spencer CA, et al. Serum TSH, T(4), and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). J Clin Endocrinol Metab. 2002 Feb. 87(2):489-99. [Medline]. [Full Text].

  18. Porterfield JR Jr, Thompson GB, Farley DR, Grant CS, Richards ML. Evidence-based management of toxic multinodular goiter (Plummer's Disease). World J Surg. 2008 Jul. 32(7):1278-84. [Medline].

  19. [Guideline] De Groot L, Abalovich M, Alexander EK, Amino N, Barbour L, Cobin RH, et al. Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2012 Aug. 97(8):2543-65. [Medline].

  20. FDA MedWatch Safety Alerts for Human Medical Products. Propylthiouracil (PTU). US Food and Drug Administration. Accessed: June 3, 2009. Available at http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm164162.htm.

  21. Stalberg P, Svensson A, Hessman O, et al. Surgical treatment of Graves' disease: evidence-based approach. World J Surg. 2008 Jul. 32(7):1269-77. [Medline].

  22. Wang J, Qin L. Radioiodine therapy versus antithyroid drugs in Graves' disease: a meta-analysis of randomized controlled trials. Br J Radiol. 2016 Jun 27. [Medline].

  23. Sisson JC, Freitas J, McDougall IR, Dauer LT, Hurley JR, Brierley JD, 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].

  24. Shindo M. Surgery for hyperthyroidism. ORL J Otorhinolaryngol Relat Spec. 2008. 70(5):298-304. [Medline].

  25. Worni M, Schudel HH, Seifert E, Inglin R, Hagemann M, Vorburger SA, et al. Randomized controlled trial on single dose steroid before thyroidectomy for benign disease to improve postoperative nausea, pain, and vocal function. Ann Surg. 2008 Dec. 248(6):1060-6. [Medline].

  26. FDA Drug Safety Communication: New Boxed Warning on severe liver injury with propylthiouracil. US Food and Drug Administration, April 21, 2010. Available at http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm209023.htm. Accessed: March 6, 2012.

  27. Yalamanchi S, Cooper DS. Thyroid disorders in pregnancy. Curr Opin Obstet Gynecol. 2015 Oct 19. [Medline].

  28. Burches-Feliciano MJ, Argente-Pla M, Garcia-Malpartida K, Rubio-Almanza M, Merino-Torres JF. Hyperthyroidism induced by topical iodine. Endocrinol Nutr. 2015 Aug 12. [Medline].

  29. Brandt F. The long-term consequences of previous hyperthyroidism. A register-based study of singletons and twins. Dan Med J. 2015 Jun. 62 (6):[Medline].

  30. Srinivasan S, Misra M. Hyperthyroidism in children. Pediatr Rev. 2015 Jun. 36 (6):239-48. [Medline].

 
Previous
Next
 
Severe proptosis, periorbital edema, and eyelid retraction from thyroid-related orbitopathy. This patient also had optic nerve dysfunction and chemosis (conjunctival edema) from thyroid-related orbitopathy.
Color flow ultrasonogram in patient with Graves disease. Generalized hypervascularity is visible throughout gland (note red areas), which often can be heard as hum or bruit with stethoscope.
Absence of iodine 123 (123I) radioactive iodine uptake in patient with thyrotoxicosis and subacute painless or lymphocytic thyroiditis. Laboratory studies at time of scan demonstrated the following: thyroid-stimulating hormone (TSH), less than 0.06 mIU/mL; total thyroxine (T4), 21.2 µg/dL (reference range, 4.5-11); total triiodothyronine (T3), 213 ng/dL (reference range, 90-180); T3-to-T4 ratio, 10; and erythrocyte sedimentation rate (ESR), 10 mm/hr. Absence of thyroid uptake, low T3-to-T4 ratio, and low ESR confirm diagnosis of subacute painless thyroiditis.
Three multinuclear giant cell granulomas observed in fine-needle aspiration biopsy of thyroid from patient with thyrotoxicosis from subacute painful or granulomatous thyroiditis.
Scan in patient with toxic multinodular goiter. 5-Hour 123I-iodine uptake was elevated at 28% (normal 5-15%). Note multiple foci of variably increased tracer uptake.
Iodine 123 (123I) nuclear scintigraphy: 123I scans of normal thyroid gland (A) and common hyperthyroid conditions with elevated radioiodine uptake, including Graves disease (B), toxic multinodular goiter (C), and toxic adenoma (D).
Gross photo of subtotal thyroidectomy for diffuse toxic goiter (Graves Disease) showing homogenous enlargement without nodules.
Low-power photomicrograph showing diffuse papillary hyperplasia (hallmark histologic feature of Graves disease).
High-power photomicrograph showing papillary hyperplasia of follicular cells with increased nuclear size and small nucleoli.
Bilateral erythematous infiltrative plaques on lower extremities in 42-year-old man with Graves disease are consistent with pretibial myxedema. Myxedematous changes of skin usually occur in pretibial areas and resemble orange peel in color and texture.
Hypothalamic-pituitary-thyroid axis feedback. Schematic representation of negative feedback system that regulates thyroid hormone levels. TRH = thyrotropin-releasing hormone; TSH = thyroid-stimulating hormone.
Table 1. Thyrotoxicosis and Hyperthyroidism
Common Forms (85-90% of Cases) 24-Hour RAIU Over Neck*
Diffuse toxic goiter (Graves disease) Increased (moderate to high: 40-100%)
Toxic multinodular goiter (Plummer disease) Increased (mild to moderate: 25-60%)
Thyrotoxic phase of subacute thyroiditis Decreased (very low: < 2%)
Toxic adenoma Increased (mild to moderate: 25-60%)
Less Common Forms
Iodide-induced thyrotoxicosis Variable but usually low (< 25%)
Thyrotoxicosis factitia Decreased (very low: < 2%)
Uncommon Forms
Pituitary tumors producing TSH Increased (mild to moderate: 25-60%)
Excess human chorionic gonadotropin (molar pregnancy/choriocarcinoma) Increased (variable: 25-100%)
Pituitary resistance to thyroid hormone Increased (mild to moderate: 25-60%)
Metastatic thyroid carcinoma Decreased
Struma ovarii with thyrotoxicosis Decreased
RAIU = radioactive iodine uptake; TSH = thyroid-stimulating hormone.



* A normal 6-hour RAIU is approximately 2-16%; a 24-hour RAIU is about 8-25% but is modified according to the iodine content of the patient’s diet. RAIU or scanning should not be performed in a woman who is pregnant (with the exception of a molar pregnancy) or breastfeeding.



Previous
Next
 
 
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.