Subacute Thyroiditis Follow-up

  • Author: Stephanie L Lee, MD, PhD; Chief Editor: George T Griffing, MD   more...
 
Updated: Oct 17, 2011
 

Further Outpatient Care

  • All forms of subacute thyroiditis - Patients should be seen every 4 weeks for reassurance and for measurement of thyroid hormone levels. Occasionally, patients have relapses of the thyrotoxic phase and have persistent symptoms. Monitor for the subsequent hypothyroid phase and treat with L-thyroxine if patients are symptomatic from the hypothyroidism.
  • Subacute granulomatous thyroiditis - Patients usually recover completely from painful subacute thyroiditis. The episodes rarely reoccur. Generally, patients are not prone to other thyroid disease and do not need long-term follow-up.
  • Lymphocytic and subacute postpartum thyroiditis - These conditions are sometimes associated with chronic thyroiditis. Postpartum thyroiditis usually recurs after each pregnancy. Occasionally, subacute painless thyroiditis is recurrent. Patients should be observed routinely every 6-12 months for the development of goiter or hypothyroidism from chronic thyroiditis.
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Deterrence/Prevention

  • No medical intervention is known to prevent any form of subacute thyroiditis.
  • Recurrent episodes in patients with recurrent subacute thyroiditis with severe symptoms can be prevented with thyroidectomy.
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Complications

  • Subacute granulomatous thyroiditis - This condition generally resolves completely in more than 90-95% of patients. No special follow-up of the thyroid is needed.
  • Lymphocytic thyroiditis - Occasionally, patients have recurrent episodes of painless thyrotoxicosis.[6] No treatment exists to prevent the recurrences except subtotal thyroidectomy. This condition generally resolves completely in more than 90-95% of patients. Patients with goiters or permanent thyroid dysfunction should be monitored with a thyroid examination and thyroid function tests every 6 months.
  • Subacute postpartum thyroiditis - Usually, repeat episodes occur after each pregnancy, and no known treatment exists to prevent these. Patients may have a residual goiter and thyroid hypofunction after postpartum thyroiditis, because this condition is associated with chronic autoimmune thyroiditis. Patients should be observed routinely for goiter enlargement and thyroid hypofunction every 6-12 months.
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Prognosis

  • The prognosis is excellent in 90-95% of patients who experience subacute thyroiditis. Approximately 5-10% of patients have permanent thyroid dysfunction, usually hypothyroidism, after an episode of subacute thyroiditis. Permanent goiter and thyroid dysfunction occur most frequently after postpartum thyroiditis.
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Patient Education

  • Patients with subacute postpartum thyroiditis should be counseled that repeat episodes are likely to occur following every pregnancy.
  • For excellent patient education resources, visit eMedicine's Endocrine System Center. Also, see eMedicine's patient education article Thyroid Problems.
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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, Associate Chief, 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, and Endocrine Society

Disclosure: Nothing to disclose.

Coauthor(s)

Sonia Ananthakrishnan, MD  Assistant Professor of Medicine, Section of Endocrinology, Diabetes and Nutrition, Boston University School of Medicine, Boston Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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

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.

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.

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. Masuoka H, Miyauchi A, Tomoda C, et al. Imaging studies in sixty patients with acute suppurative thyroiditis. Thyroid. Oct 2011;21(10):1075-80. [Medline].

  5. 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].

  6. 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].

  7. 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].

  8. 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].

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

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

  11. 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.

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

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

  14. 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].

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

  16. 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].

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