Subacute Thyroiditis Clinical Presentation

Patient presentation depends on the etiology of the thyrotoxicosis. Subacute granulomatous thyroiditis is associated with an acute virallike illness with fevers and myalgias with a painful thyroid. A recent birth signals postpartum thyroiditis. Often, the thyrotoxicosis of lymphocytic thyroiditis, postpartum thyroiditis, or surreptitious use of thyroid hormone is symptomatic because of persistent tachycardia, nervousness, and weight loss. Symptoms of thyrotoxicosis that persist for longer than 2 months are probably not caused by subacute thyroiditis.

• Subacute granulomatous thyroiditis - These patients have the classic presentation of a viral illness. The onset is sudden, with high fever, myalgia, and neck pain.
• Lymphocytic thyroiditis - This form is associated with a painless, firm enlargement of the thyroid gland and high thyroid hormone levels. Only suspicion by the clinician and use of radioactive iodine uptake measurement can distinguish Graves hyperthyroidism from lymphocytic thyroiditis.
• Subacute postpartum thyroiditis - This form is associated with a painless, firm enlargement of the thyroid gland and high thyroid hormone levels. The identifying feature is its occurrence 1-6 months after childbirth. Autoimmune hyperthyroidism from Graves disease can also occur for the first time postpartum and must be distinguished from postpartum thyroiditis. Both conditions are associated with high antithyroid antibody titers.

All conditions described are associated with thyrotoxicosis and the signs and symptoms of hypermetabolism. None of the forms of subacute thyroiditis is associated with the thyroid eye disease observed primarily with Graves hyperthyroidism. The presence of bilateral proptosis and chemosis with high thyroid hormone levels and goiter is highly suggestive of Graves disease.

• Subacute granulomatous thyroiditis - Patients often present with an acute virallike illness characterized by high spiking fever, malaise, myalgia, fatigue, and prostration. Neck pain from the thyroiditis can be extremely painful, preventing swallowing of saliva, liquids, and food. The pain starts in the lower neck and can radiate to the jaw or ear on that side. Thyroid hormone levels are often extremely elevated, resulting in marked signs and symptoms of thyrotoxicosis. Cases of lesser severity also exist, and the etiology may be confusing.
• Lymphocytic thyroiditis - Patients present with a nonpainful thyroid enlargement and elevated thyroid hormone levels. This condition must be distinguished from Graves thyrotoxicosis because antithyroid medication is not indicated in this temporary condition.
• Subacute postpartum thyroiditis - Patients present 1-6 months postpartum with painless thyroid enlargement and elevated thyroid hormone levels. Patients may report lack of sleep, nervousness, fatigue, and easy weight loss. Sometimes, distinguishing between the usual postpartum changes in physiology and additional thyroid pathology is difficult.

The causes of subacute thyroiditis, other than those of subacute granulomatous thyroiditis, are not entirely clear.

• Subacute granulomatous thyroiditis - The most accepted etiology is a viral illness.^[2] Viral particles have never been identified within the thyroid, but episodes often follow upper respiratory infections and are associated with falling postconvalescent viral titers of various viruses, including influenza, adenovirus, mumps, and coxsackievirus. This condition is not associated with autoimmune thyroiditis but is associated with HLA (human leukocyte antigen)-B35. A genetic predisposition clearly exists; patients with HLA-Bw35 have a significantly increased risk of developing this condition. Whether the destructive thyroiditis is caused by direct viral infection of the gland or by the host's response to the viral infection is unclear. Granulomatous thyroiditis is not an autoimmune disease of the thyroid.
• Lymphocytic thyroiditis - This condition most likely is autoimmune in nature. Patients develop an autoimmune goiter and permanent hypothyroidism more often than they do with the painful form of subacute thyroiditis.

  • An HLA association may be present, suggesting a genetic predisposition to painless thyroiditis.
  • Certain drug exposures relating to excess iodine and cytokines may cause this form of silent thyroiditis. These drugs include amiodarone (iodine-rich), interferon-alpha, interleukin 2, and lithium. Lymphocytic thyroiditis resulting from these different medications is typically treated similarly (see Medication).
    • Amiodarone has multiple established effects on thyroid function. One of the 2 types of amiodarone-induced thyrotoxicosis is a destructive lymphocytic thyroiditis. This form of thyroiditis is more common in men, likely due to the higher prevalence of amiodarone therapy in men. This form of silent thyroiditis typically occurs after more than 2 years of amiodarone therapy.
    • Up to 5% of patients taking interferon-alpha may experience lymphocytic thyroiditis. This condition is detected biochemically more often than clinically after 3 months of therapy. Lymphocytic thyroiditis in patients taking interferon-alpha is associated with an increased antithyroid antibody concentration.
    • Although case reports exist that interleukin 2 is associated with lymphocytic thyroiditis, its causative role is less established than is that of interferon-alpha.
    • Lithium is a well-known cause of either subclinical or clinical hypothyroidism, as well as of goiter. Because of lithium’s ability to inhibit the release of thyroid hormone, it has been used as a treatment for thyrotoxicosis. However, reports exist of lithium-associated thyrotoxicosis due to a lymphocytic thyroiditis, with the classic picture of hyperthyroidism, absent neck tenderness, and low radioactive iodine uptake (see Medication). The lymphocytic thyroiditis can occur during lithium administration, as well as up to 5 months following discontinuation of lithium therapy. Increased thyroid antibodies in lithium users and a direct toxic effect of lithium have been proposed as possible mechanisms.
• Subacute postpartum thyroiditis - This condition is likely autoimmune in nature.^[3] Patients develop an autoimmune goiter and permanent hypothyroidism more often than with the painful form of subacute thyroiditis. In iodine-sufficient countries, such as the United States, postpartum thyroiditis occurs in approximately 5-8% of pregnant women. In Japan, nearly 20% of pregnancies are associated with this condition. Patients with positive test results for thyroid autoantibodies either before their pregnancy or during the third trimester are at much higher risk of developing postpartum thyroiditis.
• Cigarette smoking is also associated with an increased incidence of postpartum thyroiditis. Once patients have an episode of subacute postpartum thyroiditis, they are likely to have additional episodes following each pregnancy.