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Subacute Thyroiditis Medication

  • Author: Stephanie L Lee, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP  more...
 
Updated: Nov 02, 2015
 

Medication Summary

Medical treatment for subacute thyroiditis is supportive in general. Thyrotoxicosis can be extreme but temporary (eg, 6-8 wk). The subsequent hypothyroid phase is usually mild and lasts 2-4 months. Therapy is directed toward reducing the signs and symptoms of the hyperthyroidism with beta blockers or iodine agents. Pain is treated with nonsteroidal anti-inflammatory agents (NSAIDs). Rarely, high-dose steroids and narcotic analgesic agents are used for extremely painful or recurrent life-threatening hyperthyroidism.

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Salicylates

Class Summary

Salicylates are used for symptomatic treatment. They aid in the relief of mild to moderate pain by inhibiting inflammatory reactions and pain. Patients should avoid high-dose aspirin because it can increase free thyroid hormone levels by displacing thyroid hormone from its protein-binding sites.

Aspirin (Anacin, Ascriptin, Bayer Aspirin, Bayer Buffered)

 

Aspirin treats mild to moderate pain. It inhibits prostaglandin synthesis, which prevents the formation of platelet-aggregating thromboxane A2.

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Nonsteroidal Anti-Inflammatory Drugs

Class Summary

Anti-inflammatory agents are administered to patients with subacute granulomatous thyroiditis. Narcotic analgesics can be administered if the pain is extreme and prevents oral hydration. In rare cases, high-dose steroids (eg, prednisone 40-60 mg/day PO for 4-6 wk) may be used to decrease the pain.

Ibuprofen (Advil, Motrin)

 

Ibuprofen is the drug of choice for patients with mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Naproxen (Aleve, Naprosyn, Naprelan)

 

Naproxen is used for the relief of mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing the activity of cyclo-oxygenase, which results in a decrease of prostaglandin synthesis.

Indomethacin (Indocin)

 

Indomethacin, which is rapidly absorbed, inhibits prostaglandin synthesis. The drug is metabolized in the liver by demethylation, deacetylation, and glucuronide conjugation.

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Iodinated Contrast Agents

Class Summary

High iodine levels inhibit the peripheral conversion of T4 to T3. The most effective agents are the iodinated contrast agents, but high levels of iodine provided by saturated solution of potassium iodide (SSKI; 2 drops in full glass of water PO tid) can be substituted.

Iopanoic acid (Telepaque)

 

This is an oral contrast agent used for the rapid and significant inhibition of the peripheral conversion of T4 to T3. Inorganic iodide also blocks the release of thyroid hormones. Reduction in the conversion of T4 to T3 can greatly reduce T3 levels and thyrotoxic symptoms.

Ipodate (Oragrafin)

 

Ipodate is one of the most effective inhibitors of deiodinase, which converts T4 to the more biologically active T3. Reduction in the conversion of T4 to T3 can greatly reduce T3 levels and thyrotoxic symptoms.

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Thyroid Products

Class Summary

Most patients with subacute thyroiditis experience a hypothyroid phase following thyrotoxicosis. Asymptomatic patients do not need to be treated if the TSH level is mildly elevated (< 15 µIU/mL), but they should be tested every 4 weeks to confirm that hypothyroidism is not worsening or becoming permanent.

Thyroid hormone is generally administered (usually 50 mcg/day) to normalize TSH. After 6 months, when 90-95% of patients have returned to normal thyroid function, thyroid hormone is discontinued; the TSH level is checked 4 weeks after discontinuation of therapy. If the TSH level is within the reference range, no further treatment is necessary. If the level is elevated, however, the patient has permanent hypothyroidism, and therapy should be continued indefinitely.

Levothyroxine (Levoxyl, Synthroid, Tirosint)

 

Levothyroxine is used for supplementation during the hypothyroid phase of subacute thyroiditis. The goal of levothyroxine therapy is to keep the TSH level within the reference range for 6 months; therapy is then discontinued. The TSH level should be checked 4 weeks later; if the level is elevated, levothyroxine therapy must be reinstituted and continued indefinitely.

Tirosint is a preparation of T4 in a liquid form in a gelatin capsule. This form of thyroid hormone contains only T4, glycerol, and gelatin, with no other additives. This form may be preferred in patients on long-term proton pump inhibitors, a history of erratic T4 absorption, and reactions to the nonhormone content of other pills (eg, gluten, dyes).

T3, liothyronine (Cytomel, Triostat)

 

Liothyronine is a synthetic form of natural thyroid hormone T3 converted from T4. Its duration of activity is short, which allows for quick dosage adjustments in the event of overdosage. Liothyronine may need to be administered as often as 4 times daily. In its active form, the drug influences the growth and maturation of tissues.

Thyroid hormone replacement with T3 alone is not recommended because of the need for dosing at 2-3 times daily. The short half-life means there is significant fluctuation between too low and too high levels during the course of the day.

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Beta-Adrenergic Blocking Agents

Class Summary

Beta-blockers reduce many of the symptoms of thyrotoxicosis, including tachycardia, tremor, and anxiety. Propranolol is usually recommended because of its CNS penetration, but some patients prefer the longer-acting beta-blockers.

Propranolol (Inderal LA, InnoPran XL)

 

Propranolol is the drug of choice for treating cardiac arrhythmia resulting from hyperthyroidism. The drug effects cardiac and psychomotor manifestations within minutes.

Atenolol (Tenormin)

 

Atenolol selectively blocks beta1 receptors, with little or no effect on beta2 types. This agent is useful for treating cardiac arrhythmias resulting from hyperthyroidism. It effects cardiac and psychomotor manifestations within minutes.

Metoprolol (Lopressor, Toprol XL)

 

Metoprolol is a selective beta1-adrenergic receptor blocker that decreases the automaticity of contractions. It aids in the treatment of cardiac arrhythmias resulting from hyperthyroidism. The drug effects cardiac and psychomotor manifestations within minutes.

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Corticosteroids

Class Summary

If thyroid pain is extreme, high-dose steroids rapidly reduce thyroid hormone levels and swelling. Generally, therapy must be continued for 4-6 weeks before tapering.

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects, modifying the body's immune response to diverse stimuli.

Prednisone

 

Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear (PMN) cell activity.

Prednisolone (Millipred, Orapred, Orapred ODT, Prelone)

 

Corticosteroids act as potent inhibitors of inflammation. They may cause profound and varied metabolic effects, particularly in relation to salt, water, and glucose tolerance, in addition to their modification of the immune response of the body. Alternative corticosteroids may be used in equivalent dosages.

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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

Mark R Allee, MD Associate Professor, Department of Medicine, University of Oklahoma Health Sciences Center

Mark R Allee, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

KoKo Aung, MD, MPH, FACP Associate Professor, Department of Medicine, University of Texas Health Science Center at San Antonio; Adjunct Associate Professor of Public Health, University of Texas School of Public Health

KoKo Aung, MD, MPH, FACP is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Mary Zoe Baker, MD Professor, Department of Medicine, Section of Endocrinology, Metabolism and Hypertension, University of Oklahoma; Medical Director, University of Oklahoma Physicians, Medicine Specialty Clinic, General Medicine Clinic and Medicine Residents' Clinic

Mary Zoe Baker, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American Chemical Society, and American College of Physicians-American Society of Internal Medicine

Disclosure: Nothing to disclose.

Daniel Matei Brailita, MD Chief of Infectious Diseases, Mary Lanning Memorial Hospital

Daniel Matei Brailita, MD is a member of the following medical societies: HIV Medicine Association of America and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

James Burks, MD, FACP, FACE Professor of Medicine, Program Director, Department of Medicine, Texas Tech University Health Sciences Center

James Burks, MD, FACP, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists, American Diabetes Association, and Endocrine Society

Disclosure: Nothing to disclose.

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS Professor of Medicine (Endocrinology, Adj), Johns Hopkins School of Medicine; Affiliate Research Professor, Bioinformatics and Computational Biology Program, School of Computational Sciences, George Mason University; Principal, C/A Informatics, LLC

Arthur B Chausmer, MD, PhD, FACP, FACE, FACN, CNS is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Endocrinology, American College of Nutrition, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Informatics Association, American Society for Bone and Mineral Research, Endocrine Society, and International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

Steven R Gambert, MD, MACP Chairman, Department of Medicine, Physician-in-Chief, Sinai Hospital of Baltimore; Professor of Medicine, Program Director, Internal Medicine Program, Johns Hopkins University School of Medicine

Steven R Gambert, MD, MACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American Geriatrics Society, Association of Professors of Medicine, Endocrine Society, and Gerontological Society of America

Disclosure: Nothing to disclose.

Amir E Harari, MD Staff Physician, Endocrinology Division, Instructor, Department of Clinical Medicine, Naval Medical Center at San Diego

Amir E Harari, MD is a member of the following medical societies: Alpha Omega Alpha, American Association of Clinical Endocrinologists, American College of Physicians, and Endocrine Society

Disclosure: Nothing to disclose.

Ildiko Lingvay, MD, MPH Assistant Professor, Department of Internal Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Texas Southwestern Medical Center at Dallas

Ildiko Lingvay, MD, MPH is a member of the following medical societies: Endocrine Society and Texas Medical Association

Disclosure: Nothing to disclose.

Joseph E Loewenstein, MD Retired

Joseph E Loewenstein, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Diabetes Association, Endocrine Society, and Phi Beta Kappa

Disclosure: Nothing to disclose

Don S Schalch, MD Professor Emeritus, Department of Internal Medicine, Division of Endocrinology, University of Wisconsin Hospitals and Clinics

Don S Schalch, MD is a member of the following medical societies: American Diabetes Association, American Federation for Medical Research, Central Society for Clinical Research, and Endocrine Society

Disclosure: Nothing to disclose.

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

Stanley Wallach, MD Executive Director, American College of Nutrition; Clinical Professor, Department of Medicine, New York University School of Medicine

Stanley Wallach, MD is a member of the following medical societies: American College of Nutrition, American Society for Bone and Mineral Research, American Society for Clinical Investigation, American Society for Clinical Nutrition, American Society for Nutritional Sciences, Association of American Physicians, and Endocrine Society

Disclosure: Nothing to disclose.

Kent Wehmeier, MD Professor, Department of Internal Medicine, Division of Endocrinology, Diabetes, and Metabolism, St Louis University School of Medicine

Kent Wehmeier, MD is a member of the following medical societies: American Society of Hypertension, Endocrine Society, and International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

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Three multinucleated, giant cell granulomas observed in a fine-needle aspiration biopsy of the thyroid; from a patient with thyrotoxicosis resulting from subacute granulomatous thyroiditis.
Absence of iodine-123 (123I) radioactive iodine uptake in a patient with thyrotoxicosis and lymphocytic (subacute painless) thyroiditis. Laboratory studies at the time of the scan demonstrated the following: thyroid-stimulating hormone (TSH), less than 0.06 mIU/mL; total thyroxine (T4), 21.2 mcg/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/h. The absence of thyroid uptake, the low T3-to-T4 ratio, and the low ESR confirm the diagnosis of lymphocytic thyroiditis.
Example of laboratory values as they vary over the course of subacute granulomatous thyroiditis. The entire episode may evolve through all 3 phases of the disorder over a period of as long as 6 months.
Table. Characteristic Course of de Quervain Thyroiditis
Parameters Stage 1 Stage 2 Stage 3 Stage 4
Symptoms Hyperthyroid Euthyroid Hypothyroid Euthyroid (recovery)
T4, T3 Elevated Normal Decreased Normal
TSH Decreased Normal Elevated Normal
T4 = thyroxine



T3 = triiodothyronine



TSH = thyroid-stimulating hormone



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