Infectious: acute (suppurative), subacute (granulomatous, de Quervain’s)

 Autoimmune: chronic lymphocytic (Hashimoto’s disease), atrophic (primary myxedema), juvenile, postpartum

 Painless (non-postpartum)

 Drug-induced (certain medications, iodinated contrast material)

 Riedel’s struma

 Radiation-induced

 Traumatic

 Tumor embolization

This rare disease has an infectious etiology, most reported pathogens being Staphylococcus, Streptococcus, Pneumocystis carinii, and Mycobacterium species. Fungal, parasitic, or syphilitic infections have been reported, and immunocompromised patients may be at increased risk. Patients may demonstrate hypothyroid or hyperthyroid symptoms or may remain euthyroid. Rarely, metastatic disease to the thyroid gland can manifest as acute thyroiditis.

Treatment involves incision and drainage of the abscess or surgical excision and antimicrobials. Children often have a pyriform sinus fistula, which should be surgically repaired.

 Stage I: Patients have a painful (unilateral or bilateral) tender thyroid and may have systemic symptoms (fatigue, malaise, fever). Inflammatory destruction of thyroid follicles permits release of thyroxine (T₄) and triiodothyronine (T₃) into the blood, and thyrotoxicosis may ensue.

 Stage II: A transitory period (several weeks) of euthyroidism occurs after the T₄ is cleared from the body.

 Stage III: With severe disease, patients may become hypothyroid until the thyroid gland repairs itself.

 Stage IV: Euthyroid state returns.

Subacute thyroiditis is probably viral in origin. Histologically, the inflammation is granulomatous. Although patients almost always recover clinically, serum thyroglobulin (Tgb) levels remain elevated, and intrathyroidal iodine content is low for many months (Fig. 35-1). Such findings suggest persistent subclinical abnormalities after an episode of subacute thyroiditis. Nonsteroidal antiinflammatory agents are first-line treatment in mild to moderate cases, whereas steroids may be needed when the condition is more severe. Patients requiring steroids are more likely to become hypothyroid at a later time. Up to 4% of patients have a second episode many years later.

Autoimmune thyroid disease, which is recognized by the presence of thyroid peroxidase (TPO) antibody and, less frequently, thyroglobulin antibody in serum.

Chronic lymphocytic thyroiditis (Hashimoto’s disease) usually manifests as a euthyroid goiter that progresses to hypothyroidism in middle-aged and older persons, especially women. Atrophic thyroiditis is characterized by a very small thyroid gland in a hypothyroid patient. Some evidence suggests that thyroid growth–inhibitory antibodies may account for the lack of a goiter. Two thirds of adolescents with goiter have autoimmune (juvenile) thyroiditis.

Yes. Postpartum disease develops in women between the third and ninth months after delivery, sometimes even 1 year postpartum. It typically follows the stages seen in patients with subacute thyroiditis, although histologically, patients with postpartum disease have lymphocytic infiltration.

After delivery, 5% to 10% of women show biochemical evidence of thyroid dysfunction. Approximately one third of affected women have symptoms (either hyperthyroidism, hypothyroidism, or both) and benefit from 6 to 12 months of therapy with levothyroxine (LT₄) if they are hypothyroid. Up to 70% of patients experience recurrence with subsequent pregnancies. The frequency of each clinical presentation is depicted in Figure 35-2.

Postpartum thyroiditis is a destructive process; therefore an antithyroidal drug (methimazole) is not effective. If hyperthyroid symptoms are present, beta-blockers can be used. Hypothyroid patients with severe symptoms and those who desire conception should receive treatment with LT₄. In these cases, however, tapering off the medication should be tried 6 to 12 months after initiation, in the attempt to eventually discontinue therapy.

See Table 35-1.

Women in whom postpartum thyroiditis develops have underlying, usually asymptomatic, autoimmune thyroiditis. During pregnancy, the maternal immune system is partially suppressed, with a dramatic rebound rise in thyroid antibodies after delivery. Although TPO or thyroglobulin antibodies are not believed to be cytotoxic, they are currently the most reliable markers of susceptibility to postpartum disease.

Not always. Approximately 20% of women become permanently hypothyroid, and a similar number have persistent mild abnormalities. An annual thyroid-stimulating hormone (TSH) measurement is therefore recommended.

Women with a higher TPO antibody titer are more likely to have thyroiditis. Thyroiditis develops after delivery in approximately 25% of women with type 1 diabetes mellitus. For high-risk patients, screening for thyroid antibodies and careful monitoring of thyroid function at 3 to 6 months postpartum are indicated.

Both men and non-postpartum women may present with transient thyrotoxic symptoms. Like patients with subacute thyroiditis, they often experience subsequent hypothyroidism. Unlike subacute disease, this disorder is painless. It has been given a variety of names, including hyperthyroiditis, silent thyroiditis, transient painless thyroiditis with hyperthyroidism, and lymphocytic thyroiditis with spontaneously resolving hyperthyroidism. This disease was first described in the 1970s and reached its peak incidence in the early 1980s. It seems to occur less often now.

Some investigators believe that it is a variant of subacute thyroiditis because a small percentage of patients with biopsy-proven subacute disease have had no pain (they may have fever and weight loss and may be mistaken for having systemic disease or malignancy). Others believe that it is a variant of Hashimoto’s disease because of similar histologic features. Hashimoto’s thyroiditis can occasionally manifest as thyroid pain; rarely, surgery is necessary to relieve symptoms.

Destruction-induced thyroiditis refers to disorders (subacute, postpartum, drug-induced, and painless thyroiditis) in which an inflammatory infiltrate destroys thyroid follicles and excessive amounts of T₄ and T₃ are released into the circulation.

A 24-hour radioactive iodine uptake (RAIU) test should be performed. When the thyroid is overactive (as in Graves’ disease or toxic nodular disease), the RAIU value is elevated. In destruction-induced thyroiditis, the RAIU value is low, as a result of both suppression of TSH by the acutely increased level of serum T₄ and the diminished ability of damaged thyroid follicles to trap and organify iodine.

In the thyrotoxic stage, beta-blockers relieve adrenergic symptoms. All forms of antithyroid therapy (drugs, radioactive iodine ablation, and surgery) are absolutely contraindicated. Analgesics (salicylates or prednisone) provide prompt relief of thyroid pain. Thyroid hormone relieves hypothyroid symptoms and should be continued for 6 to 12 months, depending on the severity of disease. Some patients require no therapy.

Amiodarone, an iodine-containing antiarrhythmic drug, may cause thyroid damage and thyrotoxicosis. Lithium therapy has been associated with granulomatous thyroiditis as well as with destructive thyroiditis without lymphocytic infiltration. Interferon-alpha (less commonly, interferon-beta) and interleukin-2 (e.g., denileukin diftitox, an antineoplastic agent that combines interleukin-2 with diphtheria toxin) can cause thyroiditis, and both hyperthyroidism and hypothyroidism have occurred during therapy with these agents. Tyrosine kinase inhibitors (e.g., sunitinib, sorafenib) have been noted to cause hypothyroidism, potentially by causing destructive thyroiditis. Nonionic contrast materials (e.g., HEXABRIX) have been reported to cause destructive thyroiditis.

No. Because of the large amount of iodine in this drug, it can cause either iodine-induced hypothyroidism or hyperthyroidism. Distinguishing hyperthyroidism due to iodine excess (type 1 disease) from amiodarone-induced destructive thyroiditis (type 2 disease) can be difficult. Some differentiating features are listed in Table 35-2. Absence of blood flow on Doppler flow ultrasonography is particularly helpful in confirming type 2 disease.

Riedel’s struma is a rare disorder in which the thyroid becomes densely fibrotic and hard. Local fibrosis of adjacent tissues may produce obstructive symptoms that require surgery. In some cases, fibrosis of other tissues (fibrosing retroperitonitis, orbital fibrosis, or sclerosing cholangitis) may occur.

Surgical removal of the thyroid isthmus may relieve constrictive symptoms. Glucocorticoids have been helpful, as has tamoxifen (by stimulating transforming growth factor-beta, which inhibits fibroblast growth). Use of a combination of mycophenolate mofetil and prednisone has been reported.

Yes. External beam radiotherapy can cause painless thyrotoxic thyroiditis. Various forms of neck trauma (neck surgery, cyst aspiration, seat-belt injury) and tumor emboli have also been reported.