What is Thyroiditis?
Several disorders that involve inflammation of the thyroid gland are categorized as thyroiditis.
Autoimmune thyroiditis (long-term inflammatory disease) or Hashimoto's thyroiditis (lymphadenoid goiter) is a common chronic inflammatory disease of the thyroid gland in which autoimmune factors play a prominent role. It occurs most often in middle-aged women and is the most common cause of sporadic goiter in children.
Postpartum thyroiditis (silent thyroiditis) is another form of autoimmune thyroiditis that occurs in women within 1 year of the delivery.
Subacute thyroiditis (granulomatous, giant cell, silent, or de Quervain's thyroiditis) is a transient inflammation of the thyroid gland.
Miscellaneous thyroiditis may be classified as acute suppuratory chronic infective and chronic infective. Thyroiditis is more common in women than in men.
Riedel's thyroiditis causes intense fibrosis of the thyroid and surrounding structures, leading to an induration of the tissues in the neck, and may be associated with mediastinal and retroperitoneal fibrosis. This rare disorder needs to be differentiated from thyroid neoplasm.
Causes of Thyroiditis
Each type of thyroiditis has a different etiology. Hashimoto's thyroiditis is thought to result from lymphocytic infiltration of the thyroid gland and formation of antibodies to thyroid antigens in the blood. Glandular atrophy and Graves' disease are linked to this type of thyroiditis.
Subacute thyroiditis is viral and may follow mumps, influenza, coxsackievirus, or adenovirus infections.
Miscellaneous thyroiditis results from bacterial invasion of the gland due to acute suppurative thyroiditis; to tuberculosis, syphilis, actinomycosis, or other infectious agents in chronic infection; and to sarcoidosis and amyloidosis in chronic reinfective thyroiditis.
Riedel's thyroiditis is a rare condition with unknown etiology.
Signs & Symptoms of Thyroiditis
The following symptoms are listed from the most common to the least common:
Precise diagnosis depends on the type of thyroiditis.
In Hashimoto's thyroiditis, thyroid failure is evidenced by an increase in thyroid-stimulating hormone (TSH), decreasing titers of triiodothyronine and thyroxine, and high titers of antimicrosomal and antithyroglobulin antibodies. Histologic confirmation by fine-needle biopsy is usually performed. Autoimmune processes show high titers of thyroglobulin and microsomal antibodies in the serum.
In subacute thyroiditis, thyroid hormone levels may be elevated, suppressed, or normal, depending on the phase of the disorder. Protein-bound iodine levels are elevated. During the thyrotoxic phase, TSH levels are low and fail to respond to thyrotropin-releasing hormone. TSH levels then increase in the hypothyroid phase. Radioactive iodine (¹³¹I) uptake is suppressed, and erythrocyte sedimentation rate, white blood cell (WBC) count, and hepatic enzyme levels also increase. Thyroid antibodies may appear transiently low in the serum. A thyroid scan may show isolated areas of function or total failure to visualize the gland.
An elevated WBC count accompanying physical symptoms suggests chronic infective or noninfective thyroiditis. A biopsy of the thyroid tissue for Gram stain, culture, microscopy, and histologic examination may be performed. Radioisotope scanning and ultrasonography may be used to isolate the infected area. ¹³¹I uptake and serum hormone levels are usually within normal limits.
In Riedel's thyroiditis, ¹³¹I uptake is normal or decreased. Some patients may have elevated titers of antimicrosomal antibodies but not as high as in Hashimoto's thyroiditis.
Appropriate treatment varies with the type of thyroiditis. Drug therapy includes levothyroxine for accompanying hypothyroidism, analgesics and antiinflammatory drugs for mild subacute granulomatous thyroiditis, propranolol for transient hyperthyroidism, and steroids for severe episodes of acute illness. Suppurative thyroiditis requires antibiotic therapy. A partial thyroidectomy may be necessary to relieve tracheal or esophageal compression in Riedel's thyroiditis.
There is no known way to prevent this disorder. Awareness of risk factors may allow earlier diagnosis and treatment.
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