eMedicine Specialties > Endocrinology > Thyroid

Thyroiditis, Subacute

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

Updated: Feb 7, 2007

Introduction

Background

Thyroiditis refers to inflammation of the thyroid gland. Subacute thyroiditis (SAT) is a self-limited condition characterized by a triphasic course of hyperthyroidism followed by hypothyroidism and ending with euthyroidism. Subacute thyroiditis may account for 15-20% of thyrotoxicosis presentations and 10% of hypothyroidism presentations. The thyrotoxicosis results from release of preformed thyroid hormone. This phase lasts 4-10 weeks. The disease undergoes remission in 2-4 months. At this time, the thyroid is depleted of colloid and is now incapable of producing thyroid hormone, resulting in hypothyroidism. The hypothyroidism may be mild and not requiring any therapy. As the follicles regenerate, the euthyroid state is restored. Up to 95% of patients return to this normal thyroid state. 

The term subacute thyroiditis (SAT) conventionally has been used interchangeably with subacute granulomatous (de Quervain) thyroiditis, which was the first syndrome described as causing inflammation and release of preformed hormone from the gland.

Pathophysiology

Subacute thyroiditis has been thought to have viral origins. Most patients have a history of an upper respiratory infection 2-8 weeks prior to the onset of thyroiditis. Therefore, more cases occur in the summer. The search for a viral cause is often unrewarding. A few cases appear to be associated with the mumps virus. High titers of mumps antibodies have been found in some patients with subacute thyroiditis, and, occasionally, parotitis or orchitis is associated with thyroiditis. The mumps virus has been cultured directly from thyroid tissue involved with subacute thyroiditis. The disease has also been reported in association with other viral conditions, including measles, influenza, adenovirus, infectious mononucleosis, myocarditis, cat scratch fever, and coxsackievirus. 

Numerous attempts to culture viruses from cases not associated with mumps have failed. However, viral antibody titers to common respiratory tract pathogens often are elevated in these patients. Because the titers fall promptly and multiple viral antibodies may appear in the same patient, the elevation probably is an anamnestic response to the inflammatory condition.

An autoimmune reaction is unlikely. During the illness, the development of cell-mediated immunity against various thyroid cell particulate fractions or crude antigens appears to be related to the release of these materials during tissue destruction. Data on the mechanism of inflammation and the pathogenesis of subacute thyroiditis at the cellular level are sparse.

The role of growth factors has received some attention. In the granulomatous stage of subacute thyroiditis, growth factor–rich monocytes and/or macrophages infiltrating into follicle lumina are thought to trigger the granulomatous reaction, and vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), platelet-derived growth factor (PDGF), and transforming growth factor beta 1 (TGF-β1) produced by the stromal cells probably mediate the reaction. In the regenerative phase, endothelial growth factor (EGF) mediates follicle regeneration through its mitogenic effect on thyrocytes, along with cofactors. In addition, the decreased expression of TGF-β1, a fibrogenic factor, contributes to thyroid tissue repair. VEGF and bFGF may be responsible for angiogenesis in both stages.

Frequency

United States

Subacute thyroiditis is uncommon. The reported incidence is 1 case in 10,000. The presence of the HLA-Bw35 haplotype confers a greater predilection for subacute thyroiditis by 6-fold, when compared to the general population.

Sex

A female preponderance exists, with a female-to-male ratio of 3-5:1.

Age

The disease has been reported in persons of all ages. Subacute thyroiditis is more common between the third and fifth decades of life. It is uncommon in childhood.

Clinical

History

• Pain is the predominant symptom. While the pain may be limited to the region of the thyroid, it may also involve the upper neck, throat, jaw or ears.  Some patients may first consult an otolaryngologist. The pain may be so severe that the patient cannot tolerate palpation of the neck.  The pain is most commonly bilateral.  Occasionally, the pain may be unilateral, beginning in one lobe and spreading to the opposite side (creeping thyroiditis). Coughing, swallowing, or even tightening a necktie aggravates pain.
• Systemic symptoms, including fatigue, malaise, and myalgia, are common. Fever (up to 104ºF) may also be present.
• Thyrotoxic symptoms may be absent, mild, or moderate but rarely are severe. Up to 50% of the patients present with hyperthyroidism. Patients may complain of nervousness, heat intolerance, palpitations, tremulousness, and increased sweating.

Physical

• The thyroid is mildly to moderately enlarged, usually 2-3 times its normal size. It is exquisitely tender to palpation.
• Rarely, the patient may present with a solitary nodule and tenderness.
• The gland is firm to hard in consistency. The swelling is diffuse and involves the entire gland but may involve one lobe.
• The presentation of hyperthyroidism may manifest with fever, tachycardia, and hyperreflexia.
• Orbitopathy and dermopathy, which are characteristic of Graves disease, are absent.

Causes

While most cases of subacute thyroiditis are secondary to a viral illness, other causes of subacute thyroiditis (SAT) exist and include the following:

• Subacute thyroiditis has been described in patients receiving interferon-alpha for chronic hepatitis.
• Radioiodine therapy for Graves disease can result in transient thyroidal inflammation, causing thyroiditis.
• Subacute thyroiditis also has been described following external radiation to the neck.
• Subacute thyroiditis has presented as a paraneoplastic manifestation of renal cell carcinoma.
• An association between subacute thyroiditis and febrile neutrophilic dermatoses (Sweet syndrome) has been reported.
• Concurrence of giant cell arteritis has been reported in patients with classic de Quervain thyroiditis.
• Subacute thyroiditis has been described after bone marrow transplantation for chronic granulocytic leukemia.
• Amiodarone may produce a painful thyroiditis with thyrotoxicosis.² While the major cause of amiodarone-induced thyrotoxicosis is iodine overload in a gland with underlying abnormalities, a direct toxic effect is observed in some patients.

Differential Diagnoses

Workup

Laboratory Studies

• Thyroid function testing will help to indicate disease as well as determine its phase. 
• The most reliable measure of thyroid function is thyroid-stimulating hormone (TSH). In hyperthyroidism, the TSH is typically suppressed to levels that are not measurable (<0.05 μ IU/mL).
• The active hormones in the circulation are represented by triiodothyronine (T3) and thyroxine (T4). During the initial phase of the illness, serum thyroxine and free T4 concentrations are elevated in almost all patients. Due to the concomitant release of nonhydrolyzed iodoproteins from the inflamed tissue, the serum T3 level is also high. The total T3:T4 ratio usually is less than 20, in contrast to patients with Graves disease.
• As the subacute thyroiditis evolves into the second phase, the serum T3 and T4 levels decline, and the serum TSH level remains suppressed.
• Serum thyroglobulin (TG) levels are elevated. The elevation may persist for well over a year after the initial diagnosis, indicating that disordered follicular architecture, low-grade inflammation, or both can persist for a relatively long period. TG in patients with subacute thyroiditis is heterogenous with respect to sedimentation properties and structural integrity. The presence of serum TG with hormone residue is a common and distinctive feature of subacute thyroiditis.
• The erythrocyte sedimentation rate (ESR) is elevated and is usually greater than 50 mm/h, often exceeding 100 mm/h. An elevated ESR is diagnostic in this setting.
• C-reactive protein (CRP) may also be elevated.
• Laboratory examination may reveal anemia, hyperglobulinemia, and leukocytosis.
• Serum alkaline phosphatase levels may be elevated in as many as 60% of patients; less commonly, other liver function test results may be elevated. Mild increases in pancreatic enzymes have also been reported.³
• Serum IL-6 levels are increased, probably reflecting ongoing inflammation. While other parameters, such as ESR and CRP, decrease during corticosteroid therapy, IL-6 levels continue to increase (up to 17 days in some patients). This probably reflects dissociation between persistent release of IL-6 from the damaged thyroid cells and immediate inhibition of secondary inflammatory reactions by corticosteroids.

Imaging Studies

• In subacute thyroiditis, radioiodine uptake is low, often less than 1%, reflecting thyrotoxicosis due to a discharge of preformed stores of thyroid hormone and not due to an increase in synthesis. Administration of TSH usually fails to produce normal increase in uptake, probably because thyroid cell damage reduces the ability of the cell to respond to TSH. In the later phases of subacute thyroiditis, scintigraphy reveals virtually no uptake of isotope in the thyroid. Less dramatic presentations may demonstrate patchy uptake. If only one part of the thyroid gland is involved, the radioactive iodine uptake (RAIU) may be within the reference range.
• Thyroid ultrasonography reveals an enlarged thyroid that is diffusely or focally hypoechoic. Doppler ultrasonography shows low echogenicity without increased tissue vascularity in the affected swollen thyroid. Isoechogenicity and slightly increased vascularization characterize the recovery phase. Abnormalities in vascularization resolve in 1 year.
• On CT scan, the normal thyroid has a high attenuation (80-100 HU). The enlarged gland with subacute thyroiditis shows low attenuation (45 HU) due to follicular cell destruction and loss of iodine concentration within the thyroid gland. After the administration of contrast material, the normal thyroid gland has marked enhancement, which is attributed to its vascularity. Moderate enhancement is seen in contrast-enhanced scans in patients with subacute thyroiditis, correlating with the diffuse inflammatory nature of the disease process.
• In MRIs, the normal thyroid gland shows homogeneous T1-weighted signal intensity that is slightly greater than that of skeletal muscle. On T2-weighted sequences, the normal thyroid gland is hyperintense to the neck muscles. After the administration of contrast material, the normal gland enhances diffusely and homogeneously. Thyroid glands with subacute thyroiditis have slightly irregular margins and higher than normal T1- and T2-weighted signal intensity.

Procedures

In cases of goiter, fine-needle aspiration of the thyroid may be necessary to make a diagnosis, especially in a solitary painful nodule.

Histologic Findings

Fine-needle aspiration of the thyroid reveals multinucleated giant cells, which have angulated shapes, dense foamy cytoplasm, and a high number of nuclei. Cytologic findings of certain cells in the same aspirate include (1) follicular cells with intravacuolar granules and/or plump transformed follicular cells, (2) epithelioid granulomas, and (3) multinucleated giant cells. The background pattern is one of acute and chronic inflammation revealing hypertrophic follicular cells, oncocytic cells, and transformed lymphocytes.

Treatment

Medical Care

• Analgesia is the initial focus of therapy for the pain seen in subacute thyroiditis. Nonsteroidal anti-inflammatory drugs (NSAIDs) are the first-line agents used to treat the pain. Large dosages are typically needed. Most NSAIDs provide comparable efficacy of pain relief. Corticosteroids can be used with patients who fail NSAIDs or who have severe pain.
• Corticosteroids are highly effective, and relief of pain is quick and dramatic. If pain and tenderness do not disappear within 72 hours of the start of therapy, the diagnosis of subacute thyroiditis should be questioned. Prednisone is administered in dosages of 40-60 mg per day. After 1-2 weeks, the steroids are tapered slowly. Symptoms of thyrotoxicosis are also alleviated with glucocorticoids.
• Beta-blockers may be used if symptoms of adrenergic stimulation are troublesome. Propranolol has the theoretical advantage of inhibiting conversion of T4 to T3 at higher doses. Beta 1 selective agents (metoprolol or atenolol) have more convenient dosing and are better tolerated.
• Thionamides are not indicated because the mechanism of thyrotoxicosis is leakage of hormone from damaged thyroid follicles not overproduction of the hormones.
• When thyrotoxic symptoms are severe or if the patient cannot tolerate beta-blockers, ipodate or iopanoic acid can be used. They are potent blockers of conversion of T4 to T3. At a dose of 500 mg twice a day, these drugs rapidly normalize T3 levels and ameliorate the hyperthyroid symptoms.
• The hypothyroid phase does not require treatment; however, if the patient is symptomatic, levothyroxine may be initiated with successful discontinuation after an arbitrary time of approximately 6 months.

Consultations

Consultation with an endocrinologist may be beneficial.

Medication

Glucocorticoids

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

Prednisone (Deltasone, Sterapred, Orasone)

Reduces inflammation and controls pain.

Dosing

Adult

5-60 mg/d PO depending on patient's response, taper over 2 wk as symptoms resolve
Physiologic replacement: 4-5 mg/m²/d PO

Pediatric

Anti-inflammatory or immunosuppressive dose: 0.05-2 mg/kg/d PO divided bid/qid, taper over 2 wk as symptoms resolve

Interactions

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics; decreases effectiveness of salicylates, vaccines, and toxoids

Contraindications

Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease; diabetes mellitus

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use; caution in elderly patients

Beta-adrenergic Blocker

These agents inhibit chronotropic, inotropic, and vasodilatory response to beta-adrenergic stimulation.

Propranolol (Inderal)

Drug of choice in treating cardiac arrhythmias resulting from hyperthyroidism. Controls cardiac and psychomotor manifestations within minutes.

Dosing

Adult

10-40 mg PO
1-3 mg slow IV push as a single dose in a monitored setting; continue until hyperadrenergic state resolves

Pediatric

Not established

Interactions

Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease propranolol effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity of propranolol; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase with propranolol

Contraindications

Documented hypersensitivity; uncompensated congestive heart failure; cardiogenic shock; bradycardia; AV conduction abnormalities; heart block; pulmonary edema; severe hyperactive airway disease; chronic obstructive lung disease; Raynaud disease

Precautions

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

Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely; caution in CHF, asthma

Atenolol (Tenormin)

Useful in treating cardiac arrhythmias resulting from hyperthyroidism. Controls cardiac and psychomotor manifestations within min.

Dosing

Adult

25-100 mg PO qd; higher doses sometimes may be necessary to control symptoms

Pediatric

1-2 mg/kg/dose PO qd

Interactions

Coadministration with aluminum salts, barbiturates, calcium salts, cholestyramine, NSAIDs, penicillins, and rifampin may decrease effects; haloperidol, hydralazine, loop diuretics, and MAOIs may increase toxicity of atenolol

Contraindications

Documented hypersensitivity; congestive heart failure; pulmonary edema; cardiogenic shock; AV conduction abnormalities; heart block (without a pacemaker)

Precautions

Pregnancy

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

Precautions

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; monitor patients closely and withdraw drug slowly; during an IV, carefully monitor BP, heart rate, and ECG

Metoprolol (Lopressor, Toprol XL)

Selective beta1-adrenergic receptor blocker that decreases automaticity of contractions. Helps treat cardiac arrhythmias resulting from hyperthyroidism. Controls cardiac and psychomotor manifestations within min.

Dosing

Adult

50-100 mg PO bid

Pediatric

1-5 mg/kg/24 h PO divided bid

Interactions

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels of metoprolol, possibly resulting in decreased pharmacologic effects; toxicity of metoprolol may increase with coadministration of sparfloxacin, phenothiazines, astemizole, calcium channel blockers, quinidine, flecainide, and contraceptives; metoprolol may increase toxicity of digoxin, flecainide, clonidine, epinephrine, nifedipine, prazosin, verapamil, and lidocaine

Contraindications

Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; asthma; cardiogenic shock; AV conduction abnormalities

Precautions

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

Beta-adrenergic blockade may reduce signs and symptoms of acute hypoglycemia and may decrease clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; monitor patient closely and withdraw the drug slowly; during IV administration, carefully monitor blood pressure, heart rate, and ECG

Analgesic Nonsteroidal Anti-inflammatory Drug

These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

Ibuprofen (Motrin, Ibuprin)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Dosing

Adult

200-400 mg q6h while symptoms persist; not to exceed 3.2 g/d

Pediatric

<6 months: Not established
6 months to 12 years: 4-10 mg/kg/dose PO tid/qid
>12 years: Administer as in adults

Interactions

Coadministration with aspirin increases risk of inducing serious NSAID-related side effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT in patients taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Contraindications

Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

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

Precautions

Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy

Thyroid products

These agents are used for replacement therapy during hypothyroid phase when the patient becomes symptomatic.

Levothyroxine (Synthroid, Levoxyl, Levothroid)

DOC, rapidly inhibits the release of thyroid hormones via a direct effect on the thyroid gland and inhibits the synthesis of thyroid hormones. Iodide also appears to attenuate the cAMP-mediated effects of thyrotropin. In active form, influences growth and maturation of tissues. Involved in normal growth, metabolism, and development.

Dosing

Adult

12.5-50 mcg/d PO; may increase by 25-50 mcg/d q2-4wk, not to exceed 100-200 mcg/d

Pediatric

Neonate to 6 months: 25-50 mcg/d PO
6-12 months: 50-75 mcg/d PO
1-5 years: 75-100 mcg/d PO
6-12 years: 100-150 mcg/d PO
>12 years: 150 mcg/d PO

Interactions

Cholestyramine may decrease liothyronine absorption; estrogens may decrease response to thyroid hormone therapy in patients with nonfunctioning thyroid glands; effect of anticoagulants increased when administered with liothyronine; activity of some beta-blockers may decrease when hypothyroid patient is converted to a euthyroid state

Contraindications

Documented hypersensitivity; uncorrected adrenal insufficiency

Precautions

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Caution in angina pectoris or cardiovascular disease; monitor thyroid status periodically

Follow-up

Further Outpatient Care

• Periodic thyroid function testing is needed to establish the phase of illness and to evaluate the restoration of the euthyroid state.
• Patients who develop permanent hypothyroidism require periodic thyroid function testing with TSH to monitor the supplementation of thyroid hormone.
• No consensus exists regarding the need for periodic testing in patients whose thyroid function has recovered.

Complications

Extensive fibrosis of the gland will result in permanent hypothyroidism in 1-5% of patients with subacute thyroiditis.

Patient Education

For patient education resources, visit eMedicine's Endocrine System Center. Also, see eMedicine's patient education article Thyroid Problems.

Miscellaneous

Medicolegal Pitfalls

• Patients presenting with a solitary nodule should undergo workup for the possibility of thyroid malignancy.
• Another rare cause of low radioactive iodine uptake is struma ovarii. Some malignant ovarian neoplasms present with thyrotoxicosis.

References

1. Ohsako N, Tamai H, Sudo T. Clinical characteristics of subacute thyroiditis classified according to human leukocyte antigen typing. J Clin Endocrinol Metab. Dec 1995;80(12):3653-6. [Medline].

2. Basaria S, Cooper DS. Amiodarone and the thyroid. Am J Med. Jul 2005;118(7):706-14.

3. Salvi A, Spandrio S, Tosoni M. Liver enzyme abnormalities in subacute thyroiditis. Recenti Prog Med. Nov 1990;81(11):686-8. [Medline].

4. Bianda T, Schmid C. De Quervain's subacute thyroiditis presenting as a painless solitary thyroid nodule. Postgrad Med J. Oct 1998;74(876):602-3. [Medline].

5. Bindra A, Braunstein GD. Thyroiditis. Am Fam Physician. May 15 2006;73(10):1769-76.

6. Chopra IJ, van Herle AJ, Korenman SG. Use of sodium ipodate in management of hyperthyroidism in subacute thyroiditis. J Clin Endocrinol Metab. Jul 1995;80(7):2178-80. [Medline].

7. Garcia Solano J, Gimenez Bascunana A, Sola Perez J. Fine-needle aspiration of subacute granulomatous thyroiditis (De Quervain's thyroiditis): a clinico-cytologic review of 36 cases. Diagn Cytopathol. Mar 1997;16(3):214-20. [Medline].

8. Hamburger JI. The various presentations of thyroiditis. Diagnostic considerations. Ann Intern Med. Feb 1986;104(2):219-24. [Medline].

9. Hay ID. Thyroiditis: a clinical update. Mayo Clin Proc. Dec 1985;60(12):836-43. [Medline].

10. Hiromatsu Y, Ishibashi M, Miyake I. Color Doppler ultrasonography in patients with subacute thyroiditis. Thyroid. Dec 1999;9(12):1189-93. [Medline].

11. Hiromatsu Y, Ishibashi M, Miyake I. Technetium-99m tetrofosmin imaging in patients with subacute thyroiditis. Eur J Nucl Med. Oct 1998;25(10):1448-52. [Medline].

12. Houghton DJ, Gray HW, MacKenzie K. The tender neck: thyroiditis or thyroid abscess?. Clin Endocrinol (Oxf). Apr 1998;48(4):521-4. [Medline].

13. Iitaka M, Momotani N, Ishii J. Incidence of subacute thyroiditis recurrences after a prolonged latency: 24-year survey. J Clin Endocrinol Metab. Feb 1996;81(2):466-9. [Medline].

14. Kannan CR, Seshadri KG. Thyrotoxicosis. Dis Mon. Sep 1997;43(9):601-77. [Medline].

15. Koga M, Hiromatsu Y, Jimi A. Immunohistochemical analysis of Bcl-2, Bax, and Bak expression in thyroid glands from patients with subacute thyroiditis. J Clin Endocrinol Metab. Jun 1999;84(6):2221-5. [Medline].

16. Lazarus JH. Silent thyroiditis and subacute thyroiditis. In: Braverman LE, Utiger RD, eds. The Thyroid: A fundamental and Clinical Text. Philadelphia, Pa:. JB Lippincott;1996:577.

17. Lio S, Pontecorvi A, Caruso M. Transitory subclinical and permanent hypothyroidism in the course of subacute thyroiditis (de Quervain). Acta Endocrinol (Copenh). May 1984;106(1):67-70. [Medline].

18. Mizukami Y, Michigishi T, Kawato M. Immunohistochemical and ultrastructural study of subacute thyroiditis, with special reference to multinucleated giant cells. Hum Pathol. Sep 1987;18(9):929-35. [Medline].

19. Ross DS. Syndromes of thyrotoxicosis with low radioactive iodine uptake. Endocrinol Metab Clin North Am. Mar 1998;27(1):169-85. [Medline].

20. Sakata S, Nagai K, Maekawa H. Serum ferritin concentration in subacute thyroiditis. Metabolism. Jul 1991;40(7):683-8. [Medline].

21. Shabb NS, Tawil A, Gergeos F. Multinucleated giant cells in fine-needle aspiration of thyroid nodules: their diagnostic significance. Diagn Cytopathol. Nov 1999;21(5):307-12. [Medline].

22. Watts NB, Sewell CW. Carcinomatous involvement of the thyroid presenting as subacute thyroiditis. Am J Med Sci. Aug 1988;296(2):126-8. [Medline].

Keywords

subacute thyroiditis, SAT, subacute granulomatous thyroiditis, de Quervain thyroiditis, de Quervain's thyroiditis, giant cell thyroiditis, pseudogranulomatous thyroiditis, pseudo-granulomatous thyroiditis, painless thyroiditis, lymphocytic thyroiditis, inflamed thyroid, inflammation of the thyroid gland, hyperthyroidism, hypothyroidism, euthyroidism, thyrotoxicosis, thyroid disease

Contributor Information and Disclosures

Author

Mark R Allee, MD, Assistant 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.

Coauthor(s)

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.

Medical Editor

Steven R Gambert, MD, Program Director, Physician-in-Chief, Professor, Department of Internal Medicine, Sinai Hospital, Johns Hopkins University School of Medicine
Steven R Gambert, MD is a member of the following medical societies: American College of Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

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