Goiter is the most common anatomic disease, and the major cause of goiter worldwide is iodine deficiency. When simple goiter occurs in areas of adequate iodine intake, there appears to be a strong genetic component to the disease. In the United States, goiter is usually associated with CAT

Box 35-5 Anatomic Diseases of Thyroid

Goiter: Simple, toxic, iodine deficiency Nodule: Adenoma, incidental, toxic Cyst: Simple, complex Malignancy

Primary: Papillary/follicular, medullary, lymphoma Metastatic: Lymphoma, breast, pulmonary, other Familial: Multiple endocrine neoplasia type IIA (MEN-IIA) Familial medullary carcinoma of thyroid (FMCT)

(Hashimoto's thyroiditis) as the disease progresses to a hypothyroid state. Goiter is the result of both hypertrophy and hyperplasia of the thyroid gland. In the case of iodine deficiency, this is caused by excess thyrotropin production, leading to glandular growth and colloid production.

In Graves' disease, stimulation of the thyroid by TSH-RS Abs causes excess production of T4 and T3, in turn resulting in uncontrolled production of colloid to store the excess production of thyroid hormone. In fact, goiter is the most common clinical finding in Graves' disease after thyrotoxicosis, occurring in almost 100% of patients (Chiovato et al., 2001). Goiter is one of the five hallmarks of Graves' disease. Goiter, associated with hypothyroidism, will often improve once euthyroid doses of thyroxine have been achieved, although it may take 6 months to 1 year. If the goiter does not involute with thyroxine replacement, excision may be required. Besides goiter, the other four hallmarks of Graves' disease are thyrotoxicosis, ophthalmopathy, local myxedema, and acro-pachy (clubbing of fingers and toes).

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