eMedicine Specialties > Endocrinology > Thyroid

Subacute Thyroiditis: Differential Diagnoses & Workup

Author: Stephanie L Lee, MD, PhD, Fellow, Association of Clinical Endocrinology; Director of Thyroid Nodule and Cancer Center, Associate Chief, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Associate Professor, Department of Medicine, Boston University School of Medicine
Coauthor(s): Sonia Ananthakrishnan, MD, Attending Physician, Department of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine/Boston Medical Center
Contributor Information and Disclosures

Updated: Apr 27, 2009

Differential Diagnoses

Riedel Thyroiditis

Other Problems to Be Considered

Infectious thyroiditis
Radiation-induced thyroiditis
Trauma- or palpation-induced thyroiditis
Riedel or fibroid thyroiditis
Graves thyrotoxicosis
Toxic thyroid adenoma
Toxic multinodular goiter

Workup

Laboratory Studies

  • Thyroid-stimulating hormone (TSH) levels
    • The most reliable measure of thyroid function is a TSH level. TSH levels are usually suppressed to unmeasurable levels (<0.05 µIU/mL) in thyrotoxicosis.
    • The degree of thyrotoxicosis cannot be estimated with a TSH level and must be measured by the thyroid hormone levels in the plasma.
    • Thyroid hormone circulates as triiodothyronine (T3) and thyroxine (T4). T3 is 20-100 times more biologically active than T4. Five percent of patients with thyrotoxicosis have elevations only in T3; therefore, measuring an estimate of free T4 and free T3 is recommended.
    • Most laboratories use a calculation to estimate the free T4 levels (ie, total T4 x correction for thyroid hormone binding = free thyroxin index).
  • Thyroid autoantibodies
    • The most specific autoantibody for autoimmune thyroiditis is antithyroperoxidase (anti-TPO) antibody. Positive antithyroglobulin antibodies are not associated with autoimmune thyroid disease.
    • Antithyroid antibody titers can be elevated temporarily in all causes of subacute thyroiditis. The highest elevation in subacute thyroiditis is associated with postpartum subacute thyroiditis.
    • The antithyroid titers are usually elevated significantly in the most common type of hyperthyroidism, Graves thyrotoxicosis.
  • Subacute granulomatous thyroiditis (see image below and Image 3)
Example of laboratory values during subacute gran...

Example of laboratory values during subacute granulomatous thyroiditis. The entire episode may evolve through all 3 phases over a period of as long as 6 months.

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Example of laboratory values during subacute gran...

Example of laboratory values during subacute granulomatous thyroiditis. The entire episode may evolve through all 3 phases over a period of as long as 6 months.


    • The thyroid hormone levels are very elevated. The 6- to 8-week destructive phase of thyroiditis causes the release of preformed hormone stores from the thyroid. This form of thyroid hormone is highly iodinated, such that the release of hormone has a lower ratio of total T3 to total T4 than does Graves disease. A ratio of T3 to T4 of less than 15 usually increases suspicion of subacute thyroiditis.
    • Episodes are associated with high fever, severe myalgia, thyroid pain that often radiates to the ear, and very high levels of thyroid hormone.
    • The hallmarks of subacute granulomatous thyroiditis are a very high erythrocyte sedimentation rate (ESR), often as high as 60-100, and a radioiodine uptake of less than 1% at 24 hours (see image below and Image 2).


Absence of iodine-123 (<SUP><FONT size=-1>123</FO...

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.

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Absence of iodine-123 (<SUP><FONT size=-1>123</FO...

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.


    • After the thyroid is depleted of thyroid hormone, patients' serum levels of T4 and T3 decrease into the hypothyroid range. The hypothyroidism is usually mild but persists for 2-4 months. Supplementation with thyroid hormone is necessary only if the patients become symptomatic from the hypothyroidism. Ninety to 95% of patients spontaneously return to normal thyroid function.
  • Lymphocytic thyroiditis
    • The time course is identical to subacute granulomatous thyroiditis (see Image 3). Thyroid hormone levels are very elevated. The destructive phase of thyroiditis causes the release of preformed hormone stores in the thyroid. This form of thyroid hormone is highly iodinated, such that the release of hormone has a lower ratio of total T3 to total T4 than does Graves disease. A ratio of T3 to T4 of less than 15 usually increases suspicion of subacute thyroiditis.
    • The hallmark of lymphocytic thyroiditis is a radioiodine uptake of less than 1% at 24 hours. The ESR is within the reference range and the thyroid is not painful, which distinguishes this condition from subacute granulomatous thyroiditis.
    • After the thyroid is depleted of thyroid hormone, patients' serum levels of T4 and T3 decrease into the hypothyroid range. The hypothyroidism is usually mild but persists for 2-4 months. Supplementation with thyroid hormone is necessary only if the patient becomes symptomatic.
  • Postpartum subacute thyroiditis
    • The time course of thyroid dysfunction is the same as that for subacute granulomatous thyroiditis (see Image 3). The ESR is within the reference range, and the thyroid is not painful, which distinguishes this condition from subacute granulomatous thyroiditis.
    • Thyroid hormone levels can be moderately or extremely elevated, with a radioiodine uptake of less than 1% at 24 hours.
    • After the thyroid is depleted of thyroid hormone, patients' serum levels of T4 and T3 decrease into the hypothyroid range. The hypothyroidism is usually mild but persists for 2-4 months. Supplementation with thyroid hormone is necessary only if patients become symptomatic.
    • Antithyroid antibody levels can transiently become very elevated.

Imaging Studies

  • Nuclear scintigraphy
    • Subacute thyroiditis results in a very low radioactive iodine uptake (123 I or131 I) or technetium-99m (99m Tc) trapping. No iodine uptake occurs, because the release of preformed thyroid hormone from the thyroid gland suppresses TSH levels, which are needed to express the sodium-iodine (Na-I) symporter responsible for iodine uptake into the gland.
    • Subacute thyroiditis causes focal thyroid destruction and release of preformed thyroid hormone. The unaffected parts of the gland do not take up iodine, because the high thyroid hormone levels suppress the TSH level.
  • Doppler ultrasonography
    • Thyroid ultrasonography alone is not helpful in distinguishing between abnormalities resulting from subacute thyroiditis and other causes of high thyroid hormone levels, including Graves thyroiditis.4
    • The use of Doppler ultrasonography to detect increased blood flow has been shown to allow reliable differentiation between Graves disease and subacute thyroiditis in most patients. Subacute thyroiditis is not associated with increase in blood flow or Doppler signals, while the hyperthyroidism of Graves thyrotoxicosis is associated with a markedly increased blood flow and high Doppler signals. Thus, Doppler results may help to distinguish between these 2 types of thyrotoxicosis.

Procedures

  • Fine-needle aspiration (FNA) biopsy - Occasionally, patients with subacute thyroiditis may present with a solitary, hard nodule. An FNA in subacute thyroiditis contains a mononuclear infiltrate composed of mostly lymphocytes and multinucleated giant cells (see image below and Image 1).
Three multinuclear, giant cell granulomas observe...

Three multinuclear, giant cell granulomas observed in a fine-needle aspiration biopsy of the thyroid; from a patient with thyrotoxicosis from lymphocytic or subacute granulomatous thyroiditis.

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Three multinuclear, giant cell granulomas observe...

Three multinuclear, giant cell granulomas observed in a fine-needle aspiration biopsy of the thyroid; from a patient with thyrotoxicosis from lymphocytic or subacute granulomatous thyroiditis.


Histologic Findings

As with all types of thyroid inflammation, the thyroid histology contains inflammatory cells, primarily lymphocytes. The destructive nature of this condition is reflected in the disruption and disarray of the normal follicular unit, composed of a monolayered sheet of thyroid follicular cells surrounding the storage form of thyroid hormone, colloid. Specific to subacute granulomatous thyroiditis, a plethora of multinucleated giant cells is present in the inflammatory cell mix (see Image 1).

More on Subacute Thyroiditis

Overview: Subacute Thyroiditis
Differential Diagnoses & Workup: Subacute Thyroiditis
Treatment & Medication: Subacute Thyroiditis
Follow-up: Subacute Thyroiditis
Multimedia: Subacute Thyroiditis
References
Further Reading
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References

  1. Nishihara E, Ohye H, Amino N, et al. Clinical characteristics of 852 patients with subacute thyroiditis before treatment. Intern Med. 2008;47(8):725-9. [Medline]. [Full Text].

  2. Desailloud R, Hober D. Viruses and thyroiditis: an update. Virol J. Jan 12 2009;6:5. [Medline]. [Full Text].

  3. Filippi U, Brizzolara R, Venuti D, et al. Prevalence of post-partum thyroiditis in Liguria (Italy): an observational study. J Endocrinol Invest. Dec 2008;31(12):1063-8. [Medline].

  4. Omori N, Omori K, Takano K. Association of the ultrasonographic findings of subacute thyroiditis with thyroid pain and laboratory findings. Endocr J. Jul 2008;55(3):583-8. [Medline]. [Full Text].

  5. Nishimaki M, Isozaki O, Yoshihara A, Okubo Y, Takano K. Clinical characteristics of frequently recurring painless thyroiditis: contributions of higher thyroid hormone levels, younger onset, male gender, presence of thyroid autoantibody and absence of goiter to repeated recurrence. Endocr J. Feb 18 2009;[Medline]. [Full Text].

  6. Bartalena L, Brogioni S, Grasso L, Bogazzi F, Burelli A, Martino E. Treatment of amiodarone-induced thyrotoxicosis, a difficult challenge: results of a prospective study. J Clin Endocrinol Metab. Aug 1996;81(8):2930-3. [Medline]. [Full Text].

  7. Bartalena L, Grasso L, Brogioni S, et al. Serum interleukin-6 in amiodarone-induced thyrotoxicosis. J Clin Endocrinol Metab. Feb 1994;78(2):423-7. [Medline]. [Full Text].

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

  9. Dang AH, Hershman JM. Lithium-associated thyroiditis. Endocr Pract. May-Jun 2002;8(3):232-6. [Medline].

  10. Emerson CE, Farwell AP. Sporadic silent thyroiditis, postpartum thyroiditis, and subacute thyroiditis. In: Braverman LE, Utiger RD, eds. Werner and Ingbar's The Thyroid. 8th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2000:579-89.

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

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

  13. Lambert M, Unger J, De Nayer P, et al. Amiodarone-induced thyrotoxicosis suggestive of thyroid damage. J Endocrinol Invest. Jun 1990;13(6):527-30. [Medline].

  14. Miller KK, Daniels GH. Association between lithium use and thyrotoxicosis caused by silent thyroiditis. Clin Endocrinol (Oxf). Oct 2001;55(4):501-8. [Medline].

  15. Nikolai TF, Brosseau J, Kettrick MA, et al. Lymphocytic thyroiditis with spontaneously resolving hyperthyroidism (silent thyroiditis). Arch Intern Med. Apr 1980;140(4):478-82. [Medline].

  16. Roti E, Minelli R, Giuberti T, et al. Multiple changes in thyroid function in patients with chronic active HCV hepatitis treated with recombinant interferon-alpha. Am J Med. Nov 1996;101(5):482-7. [Medline].

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Keywords

subacute thyroiditis, thyroid, hypothyroidism, thyroid disease, hyperthyroidism, hypothyroid, thyroid symptoms, thyroiditis, hyperthyroid, thyroid hormone, symptoms of thyroid, symptoms of thyroid problems, thyroid disorder, thyroxine, thyroid disorders, thyroid tests, thyroid hormones, T3 thyroid, T4 thyroid, thyrotoxicosis, postpartum thyroiditis, triiodothyronine, lymphocytic thyroiditis, de Quervain's, silent thyroiditis, de Quervain thyroiditis, subacute painless thyroiditis, subacute lymphocytic thyroiditis, subacute postpartum thyroiditis, subacute granulomatous thyroiditis, subacute painful thyroiditis, de Quervain's thyroiditis

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Contributor Information and Disclosures

Author

Stephanie L Lee, MD, PhD, Fellow, Association of Clinical Endocrinology; Director of Thyroid Nodule and Cancer Center, Associate Chief, Section of Endocrinology, Diabetes and Nutrition, Boston Medical Center; Associate Professor, Department of Medicine, Boston University School of Medicine
Stephanie L Lee, MD, PhD is a member of the following medical societies: American College of Endocrinology, American Thyroid Association, and Endocrine Society
Disclosure: Nothing to disclose.

Coauthor(s)

Sonia Ananthakrishnan, MD, Attending Physician, Department of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine/Boston Medical Center
Disclosure: Nothing to disclose.

Medical Editor

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 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.

Pharmacy Editor

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

Managing Editor

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 Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Medical Informatics Association, American Society for Bone and Mineral Research, American Society of Law Medicine and Ethics, 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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