Therapeutic Options in Hyperthyroidism
	The ideal treatment of hyperthyroidism would be the elimination of its cause. This is however not possible in the more common diseases producing thyroid hypersecretion. At present, treatment of hyperthyroidism is directed to reduce overproduction of thyroid hormones by inhibiting their synthesis or release, or by ablating thyroid tissue with surgery or radioiodine [2-4]. Amelioration of the impact of thyroid hormones on peripheral tissues is an additional objective of treatment. There are several means of accomplishing these goals, and their efficacy depends, to some extent, on the cause of thyroid hormone hypersecretion. Because of this, the etiopathogenesis of hyperthyroidism should be determined by means of history, physical examination and selected laboratory tests before making a decision on the plan of therapy. The patient should participate in the choice of treatment, and must be informed of the therapeutic alternatives. The several forms of treatment of hyperthyroidism and their actions are summarized in Table 2. Table 1: Etiology of thyrotoxicosis 1) Conditions associated with overproduction of thyroid hormones by the thyroid gland.  Toxic diffuse goiter (Grave's disease) Toxic adenoma Toxic multinodular goiter TSH-secreting pituitary adenoma Hydatidiform Mole Iodine induced thyrotoxicosis Partial pituitary resistance to thyroid hormones Congenital non-autoimmune hyperthyroidism caused by mutated TSH receptor 2) Conditions associated with extrathyroidal overproduction of thyroid hormones  Struma ovarii Functioning metastatic thyroid cancer 3) Conditions associated with destruction of thyroid tissues  Sub-acute thyroiditis Painless thyroiditis Amiodarone-induced thyroid cancer 4) Conditions associated with an excess of exogenous thyroid hormone  Thyrotoxicosis factitia Iatrogenic thyrotoxicosis "Hamburger" thyrotoxicosis Table 2: Available forms of treatment of hyperthyroidism Therapeutic Agent  Action  1) Drugs inhibiting thyroid hormone synthesis, release or peripheral conversion of T4 to T3. Thionamides  Inhibition of iodide orgnification (methimazole,  Inhibition of coupling of iodotyrosines  propylthiouracil,  Inhibition of T4 to T3 conversion (PTU) carbimazole)  Iodide  Inhibition of iodide oxidation and (Lugol's solution, SSKI) organification Inhibition of thyroid hormone release Decreased thyroid vascularity Iodinated constrast  Inhibition of T4 to T3 conversion agents(iopanoic acid,  Release of inorganic iodide and consequent sodium ipodate) inhibition of thyroid hormone synthesis and secretion Potassium perchlorate  Competitive inhibition of iodide pump (inhibition of iodide uptake and consequent release of iodide from the thyroid) Glucocorticoids Inhibition of thyroid hormone secretion (efficiency unknown) Inhibition of peripheral conversion of T4 to T3 2) Drugs inhibiting the effects of thyroid hormones on peripheral tissues Beta-adrenergic  Inhibition of adrenergic effects of thyroid antagonists (propranolol, hormones metoprolol, nadolol) Inhibition of peripheral conversion of T4 (atenolol, bisoprolol) to T3 (propranolol) Calcium antagonists Anti-arrhythmic effect and reduction of heart (diltiazem, verapamil) rate 3) Ablative forms of treatment. Radioactive iodide Destruction of thyroid follicular cells by beta radiation Surgery Removal of tissue responsible for excessive secretion of thyroid hormones