Thyroiditis
Basics
Basics

Basics
Description
Description
Description
- Inflammatory dysfunction of the thyroid gland
- Painful thyroiditis:
- Subacute granulomatous thyroiditis—nonsuppurative thyroiditis, de Quervain thyroiditis, giant cell thyroiditis
- Infectious/suppurative thyroiditis is most commonly associated with Streptococcus and Staphylococcus spp. but can be due to fungal, mycobacterial, or parasitic thyroid infections. Radiation-induced thyroiditis: from radioactive iodine therapy (1%) or external irradiation
- Painless thyroiditis
- Hashimoto (autoimmune) thyroiditis: most common etiology of chronic hypothyroidism; 90% of patients with high-serum antithyroid peroxidase (TPO) antibodies
- Postpartum thyroiditis (PPT): thyrotoxicosis followed by hypothyroidism in the 1st year postpartum or after spontaneous/induced abortion
- Painless (silent) thyroiditis: mild hyperthyroidism
- Riedel (fibrous) thyroiditis: rare inflammatory process involving the thyroid and surrounding cervical tissues
- Drug-induced: interferon-α, interleukin-2, amiodarone, kinase inhibitors, or lithium
- Radiation-induced: from radioactive iodine therapy (1%) or external irradiation
Epidemiology
Epidemiology
Epidemiology
- Subacute granulomatous thyroiditis: most common cause of thyroid pain; peaks during summer; incidence: 3/100,000/year; female > male (4:1); peak age: 40 to 50 years
- Hashimoto thyroiditis (HT): peak onset 30 to 50 years of age; can occur in children; female > male (7:1)
- PPT: occurs within 12 months of pregnancy in 1–18% of pregnancies
- Painless (silent) thyroiditis: accounts for 1–5% of cases; female > male (4:1) with peak age 30 to 40 years; common in areas of iodine sufficiency
- Riedel thyroiditis: female > male (4:1); highest prevalence age 30 to 60 years; rare with estimated incidence of 1.06 cases per 100,000 patients
Etiology and Pathophysiology
Etiology and Pathophysiology
Etiology and Pathophysiology
- Subacute granulomatous thyroiditis: probably viral; can be associated with COVID-19 infection; the mechanism of thyroid injury can be due to direct destruction of thyroid tissue, as well as indirect immune-mediated responses, medicines used to treat COVID-19, and less frequently COVID-19 vaccinations (1).
- Hashimoto disease: Antithyroid antibodies may be produced in response to an environmental antigen and cross-react with thyroid proteins (molecular mimicry). Precipitating factors include infection, stress, sex steroids, pregnancy, iodine intake, and radiation exposure.
- PPT: autoimmunity-induced discharge of preformed hormone from the thyroid
- Painless (silent) thyroiditis: autoimmune
- Riedel (fibrous) thyroiditis: rare inflammatory process involving the thyroid and surrounding cervical tissues; associated with various forms of systemic fibrosis
Genetics
Genetics
Genetics
Autoimmune thyroiditis is associated with the CT60 polymorphism of cytotoxic T-cell lymphocyte–associated antigen 4; also associated with HLA-DR4, HLA-DR5, and HLA-DR6 in whites
Risk Factors
Risk Factors
Risk Factors
- Subacute granulomatous thyroiditis: recent viral respiratory infection, such as COVID-19 infection, or HLA-B35
- Hashimoto disease: family/personal history of thyroid/autoimmune disease, high iodine intake, cigarette smoking, selenium deficiency
General Prevention
General Prevention
General Prevention
Emerging evidence may support vitamin D or selenium supplementation, but more research is needed (2).
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