Thyroiditis, inflammation of the thyroid gland, can be acute,subacute, or chronic. Each type of thyroiditis is characterized by inflammation, fibrosis, or lymphocytic infiltration of the thyroid gland.
Acute thyroiditis is a rare disorder caused by infection of the thy-roid gland by bacteria, fungi, mycobacteria, or parasites. Staphylo-coccus aureus and other staphylococci are the most common causes. Infection typically causes anterior neck pain and swelling, fever, dysphagia, and dysphonia. Pharyngitis or pharyngeal pain is often present. Examination may reveal warmth, erythema (redness), and tenderness of the thyroid gland. Treatment of acute thyroiditis includes antimicrobial agents and fluid replacement. Surgical inci-sion and drainage may be needed if an abscess is present.
Subacute thyroiditis may be subacute granulomatous thyroiditis (deQuervain’s thyroiditis) or painless thyroiditis (silent thyroid-itis or subacute lymphocytic thyroiditis). Subacute granuloma-tous thyroiditis is an inflammatory disorder of the thyroid gland that predominantly affects women between 40 and 50 years old (Smallridge, 2000). The condition presents as a painful swelling in the anterior neck that lasts 1 to 2 months and then disappears spontaneously without residual effect. It often follows a respiratory infection. The thyroid enlarges symmetrically and may be painful. The overlying skin is often reddened and warm. Swallowing may be difficult and uncomfortable. Irritability, nervousness, insom-nia, and weight loss—manifestations of hyperthyroidism—are common, and many patients experience chills and fever as well.
Treatment aims to control the inflammation. In general, non-steroidal anti-inflammatory drugs (NSAIDs) are used to relieve neck pain. Acetylsalicylic acid (aspirin) is avoided if symptoms of hyperthyroidism occur because aspirin displaces thyroid hor-mone from its binding sites and increases the amount of circu-lating hormone. Beta-blocking agents (eg, propranolol [Inderal]) may be used to control symptoms of hyperthyroidism. Antithy-roid agents, which block the synthesis of T3 and T4, are not ef-fective in thyroiditis because the associated thyrotoxicosis results from the release of stored thyroid hormones rather than from their increased synthesis. In more severe cases, oral corticosteroids may be prescribed to reduce swelling and relieve pain; however, they do not usually affect the underlying cause. In some cases, temporary hypothyroidism may develop and may necessitate thy-roid hormone therapy. Follow-up monitoring is necessary to doc-ument the patient’s return to a euthyroid state.
Painless thyroiditis (subacute lymphocytic thyroiditis) often occurs in the postpartum period and is thought to be an auto-immune process. Symptoms of hyperthyroidism or hypothy-roidism are possible. Treatment is directed at symptoms, and yearly follow-up is recommended to determine the patient’s need for treatment of subsequent hypothyroidism.
Chronic thyroiditis, which occurs most frequently in women be-tween 30 and 50 years old, has been termed Hashimoto’s disease, or chronic lymphocytic thyroiditis; its diagnosis is based on the his-tologic appearance of the inflamed gland. In contrast to acute thy-roiditis, the chronic forms are usually not accompanied by pain, pressure symptoms, or fever, and thyroid activity is usually normal or low rather than increased. Cell-mediated immunity may play a significant role in the pathogenesis of chronic thyroiditis, and there may be a genetic predisposition to it. If untreated, the disease runs a slow, progressive course, leading eventually to hypothyroidism.
The objective of treatment is to reduce the size of the thyroid gland and prevent hypothyroidism. Thyroid hormone therapy is prescribed to reduce thyroid activity and the production of thy-roglobulin. If hypothyroid symptoms are present, thyroid hor-mone therapy is prescribed. Surgery may be required if pressure symptoms persist.
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