eMedicine Specialties > Endocrinology > Thyroid

De Quervain Thyroiditis: Differential Diagnoses & Workup

Author: Ildiko Lingvay, MD, MPH, Assistant Professor, Department of Internal Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Texas Southwestern Medical Center at Dallas
Coauthor(s): Daniel Matei Brailita, MD, Chief of Infectious Diseases, Mary Lanning Memorial Hospital; Joseph E Loewenstein, MD, Retired; James Burks, MD, FACP, FACE, Professor of Medicine, Program Director, Department of Medicine, Texas Tech University Health Sciences Center; KoKo Aung, MD, MPH, FACP, Associate Professor, Department of Medicine, University of Texas Health Science Center; Adjunct Assistant Professor of Public Health, University of Texas School of Public Health
Contributor Information and Disclosures

Updated: Dec 16, 2008

Differential Diagnoses

Autoimmune Thyroid Disease and Pregnancy
Cellulitis
Hashimoto Thyroiditis
Pharyngitis, Viral
Thyroid Lymphoma
Thyroid Nodule

Other Problems to Be Considered

Acute hemorrhage into a thyroid cyst, nodule, or neoplasm
Acute suppurative (pyogenic) thyroiditis

Workup

Laboratory Studies

  • Usually, the diagnosis is made on clinical grounds, and the only laboratory studies needed initially are those to determine whether hyperthyroidism is present, including TSH and free T4.
  • If any doubt exists as to whether de Quervain thyroiditis is the correct diagnosis, 2 other tests may be helpful.
    • Serum thyroglobulin is almost always markedly elevated.
    • Erythrocyte sedimentation rate (ESR) is usually higher than 50 mm/h in the initial phase. A normal or slightly elevated ESR makes the diagnosis of de Quervain thyroiditis relatively unlikely. ESR falls as the inflammatory process resolves, but following the ESR provides no useful information beyond what clinical observation yields.
  • After the initial inflammatory phase subsides, TSH should be monitored at intervals of 4-6 weeks for a few months to determine whether hypothyroidism occurs.
  • Antibodies to TGB, thyroid peroxidase, and TSH receptor are usually absent in de Quervain thyroiditis and need not be sought unless the clinical differential diagnosis includes immune thyroid disease (Graves disease, chronic lymphocytic [Hashimoto] thyroiditis).
  • In rare cases with systemic multiorgan involvement, elevation of serum alkaline phosphatase, gamma-glutamyl transpeptidase, aminotransferases, and pancreatic enzymes may occur. Glucose intolerance has been reported.

Imaging Studies

  • Ultrasonography of the thyroid gland5,6,7,8
    • Ultrasonography provides no additional information and is rarely indicated for diagnostic purposes.
    • In the first 3 phases of the disease, the thyroid gland is enlarged, shows unclear contour, and is diffusely or focally hypoechogenic.
    • In the recovery phase, the thyroid structure and dimensions return to normal.
    • Fibrosis is observed in some patients as hyperechogenicity and may occur as a form of healing. Extensive fibrosis is a predictor of hypothyroid state.
    • Doppler ultrasonography shows a near absence of vascularization in the acute phase and slightly increased vascularization in the recovery phase. During the acute phase, the more affected areas in the thyroid gland show the greatest decrease in vascularization, with the echogenically healthy-appearing regions of the thyroid showing normal or slightly increased vascularization.9
    • Ultrasonographic abnormalities are not correlated with the intensity of the inflammatory syndrome and/or thyroid function status. Recurrence can be seen as a new thyroid enlargement and an extension of hypoechoic regions. Risk of recurrence is not correlated with the initial ultrasonographic aspect, and there are no significant differences between patients with and without recurrence concerning the initial thyroid volume or echogenicity.
    • One study noted that thyroid volume is much smaller during the acute phase of the disease, and end-stage mean thyroid volume is significantly lower in patients who develop persistent hypothyroidism compared to patients with final normal thyroid function.
  • CT scanning of the neck
    • CT scanning of the neck is not indicated for the diagnosis of thyroiditis. Consider that the administration of iodinated contrast material before measuring radioiodine uptake may result in a falsely decreased iodine uptake. If CT scanning is planned, it should be performed after any radioiodine uptake studies are completed.
    • The normal thyroid gland has a high attenuation (80-100 HU) because the normal thyroid gland concentrates iodine almost 100 times more than does the serum. In subacute thyroiditis, a diffusely swollen thyroid gland is observed, with a low attenuation corresponding to 45 HU. There is also moderate enhancement of the thyroid gland on contrast-enhanced scanning, suggesting the diffuse inflammatory nature of the disease process.
  • Magnetic resonance imaging: MRI is not indicated for the diagnosis or evaluation of subacute granulomatous thyroiditis. If one is performed during the acute phase, the thyroid gland shows irregular margins and a higher than normal T1-weighted signal intensity and a much higher than normal T2-weighted signal intensity.10,11

Other Tests

  • Tests of research interest but seldom of clinical value include the following:
    • Sex hormone–binding globulin (SHBG) levels usually are within the reference range because of the short time of exposure to increased thyroid hormone levels. SHBG is usually elevated in chronic hyperthyroid conditions.
    • Acute phase reactants, including serum C-reactive protein (CRP), are elevated in the initial phase.
    • Test results for viral nucleic acid fragments by polymerase chain reaction in the thyroid tissue are negative.
    • Soluble interleukin-2 receptor concentrations, CD4+ cell count, cytotoxic T cell count, and gamma interferon–positive lymphocytes have been used to assess the role of the immune system in de Quervain thyroiditis. Increased levels of these markers support a viral etiology of the disease.
    • Intercellular adhesion molecules have been found to be increased in de Quervain thyroiditis and in other thyroid disorders (eg, Graves disease, Hashimoto thyroiditis), independent of the hypothyroid or hyperthyroid state, reflecting the degree of inflammatory activity in the thyroid gland.
    • Sialic acid level was studied as a marker of disease activity and was found to be a better indicator than ESR, TGB, or CRP levels for active disease or relapse.
    • Genetic studies show a high incidence of HLA-B35 antigen in patients with subacute granulomatous thyroiditis in selected populations.12
  • Neither radioiodine uptake (RAIU) nor thyroid scanning is indicated unless pain is mild or absent, in which case Graves disease might be considered in the differential diagnosis.
    • RAIU is very low in the initial phase of subacute thyroiditis (<1-2% at 24 h) but usually is elevated in Graves disease.
    • Technetium-99m-pertechnetate scintigraphy typically demonstrates markedly reduced uptake in the thyroid gland during the acute stage, but this finding is not present in all patients.
    • Technetium-99m-tetrafosmin uptake correlates with the stage of disease, particularly with inflammation, and shows increased uptake in the damaged area during the acute phase. However, this procedure is rarely used in the United States.
    • Technetium-99m-sestamibi scanning may show diffuse increased uptake in the region of the thyroid gland, suggesting increased perfusion. The clearance rate of Technetium-99m-sestamibi during the early phase (ie, from 10 min to 1 h) is decreased in the acute stage of subacute granulomatous thyroiditis.13

Procedures

  • Fine-needle aspiration of the thyroid14,15,16,17
    • Fine-needle aspiration (FNA) is rarely needed; most of the time, the diagnosis of de Quervain thyroiditis can be made solely on clinical grounds. Some authors advocate that FNA should be performed in all patients with a tender thyroid to avoid misdiagnosis and inappropriate management.
    • FNA is useful for diagnosis when atypical presentations of thyroid carcinoma and thyroid abscess are considered in the differential diagnoses.
    • It usually shows the specific histological features of de Quervain thyroiditis (see Histologic Findings).
    • FNA may provide unclear results in the acute stage when atypical follicular cells may appear in the aspirate, mimicking thyroid carcinoma.

Histologic Findings

Macroscopic

The thyroid gland is moderately enlarged and edematous in de Quervain thyroiditis. It may be unilaterally or bilaterally enlarged and has an intact capsule. Affected areas are firm and yellow-white and stand out from the more rubbery, normal, brown thyroid substance.

Microscopic

The changes are patchy and vary with the stage of the disease. The early phase is the active inflammatory phase and is characterized by areas of entirely disrupted follicles, which are replaced by neutrophils, forming microabscesses.

In a later phase, the classic changes of granulomatous thyroiditis develop. This is characterized by aggregations of lymphocytes, large histiocytes, and plasma cells among damaged thyroid follicles. Multinucleated giant cells enclose pools or fragments of colloid, from which stems the designation giant cell thyroiditis. Colloid is also found within the giant cells, following a process called colloidophagy. In the final stages, the areas of injury are replaced by a chronic inflammatory infiltrate and fibrosis. Different histologic stages sometimes are found in the same gland, suggesting waves of destruction over a period of time.

Under a scanning electron microscope, the cytomorphology of subacute granulomatous thyroiditis shows loss of a uniform honeycomb cellular arrangement, variation in size and decreased or shortened microvilli in follicular cells, and the appearance of round or ovoid giant cells.

The giant cells are closely associated with the granulomas, and are CD68+, thyroglobulin negative, and cytokeratin negative. The small lymphocytes in the granulomas are CD3+, CD8+, CD45RO+ cytotoxic T cells. In the nongranulomatous lesions, the follicles are infiltrated by CD8+ T lymphocytes, plasmacytoid monocytes, and histiocytes, resulting in disrupted basement membrane and rupture of the follicles. These findings suggest that cellular immune response may play an important role in the pathogenesis of subacute thyroiditis.

More on De Quervain Thyroiditis

Overview: De Quervain Thyroiditis
Differential Diagnoses & Workup: De Quervain Thyroiditis
Treatment & Medication: De Quervain Thyroiditis
Follow-up: De Quervain Thyroiditis
References
[ CLOSE WINDOW ]

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Further Reading

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Keywords

subacute nonsuppurative thyroiditis, subacute granulomatous thyroiditis, subacute thyroiditis, giant cell thyroiditis, subacute painful thyroiditis

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Contributor Information and Disclosures

Author

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.

Coauthor(s)

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.

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.

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.

KoKo Aung, MD, MPH, FACP, Associate Professor, Department of Medicine, University of Texas Health Science Center; Adjunct Assistant 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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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.

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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