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Autoimmune thyroiditis

  • Chronic lymphocytic (Hashimoto) thyroiditis is the most common thyroiditis and often progresses to hypothyroidism.

  • Postpartum thyroiditis and subacute lymphocytic thyroiditis (silent thyroiditis) can cause transient hyperthyroidism due to passive release of stored thyroid hormone.

  • Thyroid peroxidase antibodies (TPO Ab) or thyroglobulin antibodies (Tg Ab) are usually high.

Painful subacute thyroiditis (de Quervain thyroiditis)

  • Hallmark is tender thyroid gland with painful dysphagia.

  • Elevated erythrocyte sedimentation rate (ESR).

  • Viral etiology. Antithyroid antibodies are absent or low, distinguishing it from autoimmune thyroiditis.

Infectious (suppurative) thyroiditis

  • Severe, painful thyroid gland.

  • Febrile with leukocytosis and elevated ESR.

IgG4-related thyroiditis (Riedel thyroiditis)

  • Most often in middle age or older women.

  • Usually part of a systemic fibrosing syndrome.


Chronic lymphocytic thyroiditis, also known as “Hashimoto thyroiditis,” is the most common thyroid disorder in the United States. It predisposes to hypothyroidism. Cell-mediated autoimmunity is present with T-lymphocytes invading the thyroid gland, giving the microscopic appearance of “lymphocytic thyroiditis.” Humoral autoimmunity, with detectable serum antithyroid antibodies (TPO Ab or Tg Ab, or both), is present in most but not all affected patients. Elevated serum levels of antithyroid antibodies are detectable in the general population in 3% of men and 13% of women. Women over the age of 60 years have a 25% incidence of elevated serum levels of antithyroid antibodies, yet thyroid dysfunction develops in only a small subset of such individuals. However, 1% of the population has serum antithyroid antibody titers greater than 1:640, and they are at particular risk for thyroid dysfunction. The humoral autoimmunity of autoimmune thyroiditis differs from that of Graves disease, where thyroid-stimulating immunoglobulins (TSI) bind to the TSH receptor in thyroid cell membranes and stimulate the gland to hyperfunction. The incidence of autoimmune thyroiditis varies by kindred, race, and sex. It is commonly familial. In the United States, elevated levels of antithyroid antibodies are found in 14.3% of Whites, 10.9% of Mexican Americans, and 5.3% of Blacks.

Childhood or occupational exposure to head-neck external beam radiation increases the lifetime risk of autoimmune thyroiditis. Women with gonadal dysgenesis (Turner syndrome) have a 15% incidence of thyroiditis by age 40 years. Thyroiditis is also commonly seen in patients with hepatitis C. Subclinical thyroiditis is extremely common; autopsy series have found focal thyroiditis in about 40% of women and 20% of men.

Dietary iodine supplementation (especially when excessive) increases the risk of autoimmune thyroiditis. Certain drugs can trigger autoimmune thyroiditis, including tyrosine kinase inhibitors, alemtuzumab, interferon-alpha, interleukin-2, thalidomide, lenalidomide, lithium, amiodarone, and immune checkpoint inhibitors (pembrolizumab, ipilimumab, nivolumab, avelumab, tremelimumab, atezolizumab, durvalumab).

Chronic hepatitis C is associated with an increased risk of autoimmune thyroiditis, with 21% of affected patients having antithyroid antibodies and 13% having hypothyroidism. The risk of thyroid dysfunction is even higher when patients are treated with interferon. Interferon-alpha and interferon-beta treatment can induce thyroid dysfunction (usually hypothyroidism, sometimes hyperthyroidism) in 6% of patients. Spontaneous ...

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