Introduction
	Thyrotoxicosis is the clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormones. In most instances, thyrotoxicosis is due to hyperthyroidism, a term reserved for disorders characterized by overproduction of thyroid hormones by the thyroid gland. Thyrotoxicosis may also result from a variety of conditions other than thyroid hyperfunction including those listed in Table 1. The present discussion will be focused on the treatment of the three most frequent causes of hyperthyroidism: toxic diffuse goiter (Graves' disease), toxic adenoma, and toxic multinodular goiter. Toxic diffuse goiter is an autoimmune disease characterized by hyperthyroidism, goiter, ophthalmopathy, and less frequently dermopathy (pretibial myxedema). In this condition, hyperthyroidism occurs from a disturbance of the immune system, resulting in the production of antibodies against the TSH receptor with thyroid stimulating activity F. The prevalence of Graves' disease in the general population is relatively high reaching 1-2 % or more in females, and the female/male ratio is 7/1. It may occur at any age, but the peak incidence is between the 3rd and 4th decade of life. In toxic multinodular goiter, hyperthyroidism is caused by the presence of autonomously functioning follicles within the thyroid gland. In contrast to the general effect of thyroid stimulating antibody on thyroid tissue in Graves' disease, a variable rate of replication and function in different parts of the gland results in the characteristic structure of this condition. Since hyperthyroidism usually arises from a long-standing multinodular goiter, the prevalence of this disorder largely depends on the iodine intake of a given population, being higher in iodine-deficient areas. In these regions toxic multinodular goiter is responsible of at least 10% of cases of hyperthyroidism among middle-aged and elderly patients. A third cause of hyperthyroidism is toxic adenoma, a lesion that presents as a solitary hot nodule suppressing the function of the rest of the thyroid. This condition may either result from areas of autonomously functioning thyroid follicles localized in one lobe, or arise as a true benign neoplasm that may be caused by a somatic mutation of the TSH-receptor. This mutation produces a continuous activation of adenylate cyclase irrespective to the TSH control.