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Subacute thyroiditis

Last updated: January 25, 2021

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Subacute thyroiditis refers to a transient patchy inflammation of the thyroid gland that is associated either with granuloma formation (subacute granulomatous thyroiditis) or lymphocytic infiltration (subacute lymphocytic thyroiditis). While subacute granulomatous thyroiditis usually occurs after a viral upper respiratory tract infection, subacute lymphocytic thyroiditis occurs either during the postpartum period, in association with other autoimmune diseases, or as a side effect of certain drugs. Both forms of subacute thyroiditis are more common among women and are characterized by a triphasic clinical course that classically transitions from hyperthyroidism to hypothyroidism, before returning to a euthyroid phase. During the thyrotoxic phase, patients usually complain of fever, malaise, and goiter, which is tender in subacute granulomatous thyroiditis and painless in subacute lymphocytic thyroiditis. Diagnosis is confirmed by a combination of raised ESR and decreased iodine uptake in a radioiodine uptake study. During the thyrotoxic phase, beta blockers may be used to control the symptoms of thyrotoxicosis, and NSAIDs may be used to control pain among patients with subacute granulomatous thyroiditis. Small doses of levothyroxine may be considered during the hypothyroid phase. As spontaneous remission is seen in about 80% of cases, symptomatic treatment is sufficient in most cases.


References:[1][2]

Epidemiological data refers to the US, unless otherwise specified.

Subacute thyroiditis is characterized by transient patchy inflammation of the thyroid gland (transient thyroiditis). Depending on the underlying cause, one of two types of histological changes is seen:

Subacute granulomatous thyroiditis (De Quervain thyroiditis)

Subacute granulomatous thyroiditis is characterized by damage to follicular cells, the appearance of large multinucleated giant cells, and the formation of granuloma and fibrosis.

Subacute lymphocytic thyroiditis

Subacute lymphocytic thyroiditis is characterized by damage to follicular cells with lymphocytic infiltration resembling Hashimoto thyroiditis, rather than granuloma formation.

References:[3][4][5][6]

Inflammation of the thyroid gland manifests with a triphasic response. The duration of each phase may vary:

  1. Thyrotoxic phase
    • Lasts 2–8 weeks
    • Caused by damage to follicular cells and the release of pre-formed colloid (stored thyroid hormones)
  2. Hypothyroid phase
  3. Euthyroid phase: Thyroid function recovers and pathological changes are no longer visible in the thyroid gland.

The disease is self-limiting in most cases but a few patients may experience relapses, and permanent hypothyroidism occurs in ∼ 15% of cases!
References:[6]

Subacute granulomatous thyroiditis (De Quervain thyroiditis)

To recall the main clinical features of subacute granulomatous thyroiditis, remember that De Quervain causes pain.

Subacute lymphocytic thyroiditis


References:[2]

References:[3][6][7]

Antithyroid drugs should not be administered in the thyrotoxic phase of subacute thyroiditis!References:[3][6]

  1. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. McGraw-Hill Education ; 2015
  2. Walker BR, Colledge NR, Raston SR, Penman ID. Davidson's Principles and Practice of Medicine. Elsevier ; 2013
  3. Lee SL. Subacute Thyroiditis. In: Khardori R, Subacute Thyroiditis. New York, NY: WebMD. http://emedicine.medscape.com/article/125648. Updated: January 4, 2017. Accessed: February 9, 2017.
  4. Kumar V, Abbas AK, Aster JC. Robbins & Cotran Pathologic Basis of Disease. Elsevier Saunders ; 2015
  5. Burman KD. Overview of thyroiditis. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/overview-of-thyroiditis.Last updated: July 8, 2015. Accessed: April 17, 2017.
  6. Burman KD. Subacute thyroiditis. In: Post TW, ed. UpToDate. Waltham, MA: UpToDate. https://www.uptodate.com/contents/subacute-thyroiditis.Last updated: February 2, 2016. Accessed: April 17, 2017.
  7. Goljan EF. Rapid Review Pathology. Elsevier Saunders ; 2013
  8. Herold G. Internal Medicine. Herold G ; 2014