ESSENTIALS OF DIAGNOSIS
Autoimmune thyroiditis (Hashimoto)
Painful subacute thyroiditis
Hallmark is tender thyroid gland with painful dysphagia.
Elevated erythrocyte sedimentation rate (ESR).
Low antithyroid antibodies distinguish it from autoimmune thyroiditis.
Autoimmune thyroiditis, also known as “Hashimoto thyroiditis,” is the most common thyroid disorder in the United States. It predisposes to hypothyroidism and less frequently to hyperthyroidism. 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, is present in most but not all affected patients. Elevated serum levels of antithyroid antibodies (TPO Ab or Tg Ab, or both) 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 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).
Autoimmune thyroiditis often progresses to hypothyroidism, which may be linked to thyrotropin receptor–blocking antibodies, detected in 10% of patients with autoimmune thyroiditis. Hypothyroidism is more likely to develop in smokers than in nonsmokers, possibly due to the thiocyanates in cigarette smoke. High serum levels of TPO Ab also predict progression from subclinical to symptomatic hypothyroidism. Although the hypothyroidism is usually permanent, up to 11% of patients experience a remission after several years. There are two possible causes for such remissions: (1) the autoimmune thyroiditis may improve spontaneously; and (2) thyroid-stimulating immunoglobulin (TSI) is produced in sufficient quantities to overwhelm the destructive effects of concurrent autoimmune thyroiditis, causing the thyroid to produce more thyroid hormone. Hyperthyroidism can be caused by the destructive release ...