eMedicine Specialties > Endocrinology > Thyroid

Thyroiditis, Subacute: Differential Diagnoses & Workup

Author: Mark R Allee, MD, Assistant Professor, Department of Medicine, University of Oklahoma Health Sciences Center
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
Contributor Information and Disclosures

Updated: Feb 7, 2007

Differential Diagnoses

Graves Disease
Thyroid, Anaplastic Carcinoma
Hashimoto Thyroiditis
Thyroid, Papillary Carcinoma
Riedel Thyroiditis
Thyroid Lymphoma
Thyroid Nodule

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.

More on Thyroiditis, Subacute

Overview: Thyroiditis, Subacute
Differential Diagnoses & Workup: Thyroiditis, Subacute
Treatment & Medication: Thyroiditis, Subacute
Follow-up: Thyroiditis, Subacute
References
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References

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Further Reading

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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

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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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