Thyroid Factor

The Natural Thyroid Diet

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Figure 1-26. Suppurative thyroiditis is usually an acute disease that results from bacterial infections, but, on rare occasions, tuberculosis and fungi may infest the thyroid gland. A, Coccidioidomycosis thy-roiditis in a patient on long-term corticosteroids for systemic vasculitis. Linear cuts were made in the thyroid tissue to show evidence of central necrosis. Note the large pyramidal lobe that is also involved. B, Photomicrograph of the specimen in A showing a necrotic area of the thyroid gland formed by mature spherules of Coccidioides immitis filled with endospores (arrow) (hematoxylin and eosin; x100 original magnification). C, Photomicrograph of tuberculous thyroiditis reveals multiple giant cells and acid-fast bacilli (hematoxylin and eosin; x250 original magnification).

Acute Suppurative Thyroiditis

Although the thyroid gland is very resistant to infection, bacterial and very rarely fungal infections have been reported. Patients present with fever and erythema overlying a tender swollen gland. Isolation of the organism in FNA establishes the diagnosis and guides appropriate antimicrobial therapy. Organisms include staphylococcus, streptococcus, pneumococ-cus, salmonella, and bacteroides. Fungus and tuberculosis have been reported rarely (Figure 1-26).19,20 Some patients may need drainage of the abscess and, very rarely, thyroidectomy. FNA or occasionally open biopsy is also helpful to rule out an undifferentiated thyroid carcinoma with extensive necrosis. Some patients with thyroid neoplasms that rapidly infiltrate the thyroid can cause a pseudothyroiditis. This can also occur in patients with amyloidosis of the thyroid gland. In children with acute thyroiditis, the presence of a piriform fossa sinus must be excluded by a barium swallow of the pharynx.21 Recently, ultrasonog-raphy and esophagography have been used successfully in detecting this congenital anomaly.22 The sinus must be excised to avoid recurrence.

Subacute Granulomatous (de Quervain's) Thyroiditis

Subacute or de Quervain's thyroiditis frequently follows an upper respiratory viral infection and has been associated with human leukocyte antigen (HLA)-B35.

Figure 1-27. Photomicrograph of granulomatous thyroiditis showing foreign-body giant cells surrounding a colloid follicle. Note the fibrosis and squamous metaplasia that resulted from the chronicity of the illness (hematoxylin and eosin; x100 original magnification).

Although autoantibodies and lymphocytic infiltration of the thyroid gland have been detected in some patients, they are thought to represent a secondary phenomenon.23 The thyroid gland is enlarged, painful, edematous, and severely tender, although some patients may have no pain (painless thyroiditis).24 Microscopic features include foci of chronic inflammation and foreign-body giant cells that surround follicles and engulf colloid. An elevated sedimentation rate and a marked decrease in radioiodine uptake characterize this disorder, which is self-limited (Figure 1-27). However, some patients may need symptomatic therapy with aspirin and nonsteroidal anti-inflammatory medications during the initial hyperthyroid state and may occasionally need corticosteroids to suppress the inflammation and control the pain.25 Some experts recommend treating these patients with thyroid hormone once the thyrotoxicosis resolves, although most patients are euthyroid.

Hashimoto's Thyroiditis

Chronic lymphocytic thyroiditis was first recognized by Hashimoto in 1912 (Figure 1-28). Hashimoto's thyroiditis is an organ-specific autoimmune disease that affects about 15% of the women in the United

Figure 1-27. Photomicrograph of granulomatous thyroiditis showing foreign-body giant cells surrounding a colloid follicle. Note the fibrosis and squamous metaplasia that resulted from the chronicity of the illness (hematoxylin and eosin; x100 original magnification).

Figure 1-28. Hakaru Hashimoto. Reproduced with permission from Welbourn RB. The history of endocrine surgery. New York: Praeger; 1990.

States and Japan. It is about nine times more common in women than in men. Hashimoto's thyroiditis usually presents clinically between the third and fifth decade of life and can occur in combination with other autoimmune disorders such as Addison's disease and pernicious anemia (Schmidt's syndrome), as well as with diabetes mellitus. HLA association (DR3, 5, and B8), in addition to a preponderance of familial cases, has been reported. Hashimoto's thy-roiditis is differentiated from other autoimmune disorders of the thyroid gland by the intensity of lym-phocytic infiltration that destroys the thyroid follicles with the formation of lymphoid germinal centers. Autoantibodies are formed against the thyroglobulin and thyroid peroxidase. It is the most common cause of hypothyroidism in nonendemic goiter areas. There is no direct evidence of an increased risk of thyroid cancer in Hashimoto's thyroiditis patients, but the incidence of cancer in reported series ranged between 0.5 and 21%.26 Also, patients with Hashimoto's thyroiditis are at an increased risk of developing thyroid lymphoma. Patients with Hashimoto's thyroiditis and papillary thyroid cancer are reported to have fewer recurrences and improved survival, although our studies suggest that this may be because they have other good risk factors (young age, female gender, and a small primary tumor).

Hashimoto's thyroiditis is mostly an asymptomatic disease, although about 20% of patients may develop hypothyroidism, which may be the only clinical clue to the presence of Hashimoto's thy-roiditis. Typically, those patients present with lethargy, weight gain, cold intolerance, coarse skin, and menorrhagia. Most patients have a small firm goiter (Figure 1-29). About 5% of the patients may present with or develop hyperthyroidism (hashitoxi-cosis) (Figure 1-30). Occasionally, the thyroid gland may cause compressive symptoms.

Most patients have positive titers to thyroperoxi-dase, whereas nearly half have antithyroglobulin antibodies and about 15% have elevated TSI levels. Radionuclide scanning often reveals reduced, patchy uptake, although scanning with radioiodine is usually unnecessary. FNA should be performed on dominant nodules to rule out coexistent malignancy.

During the acute initial phase, patients may need symptomatic treatment with antithyroid medications or P-blockers. T4 replacement therapy is indicated in patients with large goiters and those patients with low normal T4 and/or elevated TSH levels. Surgery

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