destroyed. The increased sensitivity of fetal structures to radiation damage has already been described. Physicians treating women of childbearing age with 131-I should be certain that the patients are not pregnant when given the isotope. Therapy during or immediately after a normal menstrual period or performance of a pregnancy test are appropriate precautions if pregnancy is possible. Women should be advised to avoid pregnancy for at least six months, since it usually takes this long to be certain that retreatment will not be needed.
TREATMENT OF THYROTOXICOSIS WITH DRUGS
Drug therapy for thyrotoxicosis was introduced by Plummer when he observed that the administration of iodide ameliorated the symptoms of this disease . (Fig 11-6). Administration of iodide has since been used occasionally as the complete therapeutic program for thyrotoxicosis, and widely as an adjunct in preparing patients for subtotal thyroidectomy. In 1941 the pioneering observations of MacKenzie and MacKenzie  and Astwood  led to the development of the thiocarbamide drugs, which reliably block the formation of thyroid hormones. It soon became apparent that, in a certain proportion of patients with Graves’ disease, use of these drugs could induce a prolonged or permanent remission of the disease even after the medication was discontinued. It is not yet understood why a temporary reduction in the formation of thyroid hormone should result in permanent amelioration of the disease.
The antithyroid drug initially introduced for treatment of Graves’ disease was thiourea, but this drug proved to have a large number of undesirable toxic effects. Subsequently a number of derivatives and related compounds were introduced that have potent antithyroid activity without the same degree of toxicity. Among these substances are propyl- and methylthiouracil, methimazole, and carbimazole. In addition to this class of compounds, potassium perchlorate has been used in the treatment of thyrotoxicosis, but is infrequently employed for this purpose because of occasional bone marrow depression. This drug prevents the concentration of iodide by the thyroid. Beta adrenergic blockers such as propranolol have a place in the treatment of thyrotoxicosis. These drugs alleviate some of the signs and symptoms of the disease but have little or no direct effect on the metabolic abnormality itself. They do not uniformly induce a remission of the disease and can be regarded as adjuncts, not as a substitute for more definitive therapy.
Mechanism of Action– Antithyroid drugs inhibit thyroid peroxidase, and PTU (not methimazole) has the further beneficial action of inhibiting T4 to T3 conversion in peripheral tissues. Antithyroid therapy is associated with a reduction in circulating antithyroid antibody titers , and anti-receptor antibodies [77, 78, 102]. Studies by MacGregor and colleagues  indicate that antibody reduction also occurs during antithyroid therapy in patients with thyroiditis maintained in a euthyroid state, thus indicating that the effect is not due only to lowering of the FTI in Graves’ disease. These authors also found a direct inhibitory effect of PTU and carbimazole on antithyroid antibody synthesis in vitro and postulate that this is the mechanism for diminished antibody levels . Other data argue against this hypothesis [105, 105.1]. Antithyroid drug therapy is also associated with a prompt reduction in the abnormally high levels of activated T lymphocytes in the circulation ., although Totterman and co-workers found that this therapy caused a prompt and transient elevation of activated T suppressor lymphocytes in blood . During antithyroid drug treatment the reduced numbers of T suppressor cells present in most thyrotoxic patients return to normal[106, 108]. Antithyroid drugs do not directly inhibit T cell function . All of these data argue that antithyroid drugs exert a powerful beneficial immunosuppressive effect on patients with Graves’ disease. While much has been learned about this process, the exact mechanism remains uncertain. Evidence that antithyroid drugs e