yroid storm (see also Chapter 12) or tachycardia, it may be given intravenously (1 – 3 mg, rarely up to 6 mg) over 3 – 10 minutes and repeated every four to six hours under electrocardiographic control. Atropine (0.5 – 1.0 mg) is the appropriate antidote if severe brachycardia is seen.
Reserpine and Guanethidine Drugs such as reserpine  and guanethidine  that deplete tissue catecholamines were used extensively in the past as adjuncts in the therapy for thyrotoxicosis, but fell into disuse as the value of beta -sympathetic blockade with propranolol became recognized. Glucocorticoids,
Ipodate, and Other Treatments As described elsewhere, potassium iodide acts promptly to inhibit thyroid hormone secretion from the Graves’ disease thyroid gland. PTU, propranolol, glucocorticoids , amiodarone, and sodium ipodate (Oragrafin Sodium) inhibit peripheral T4 to T3 conversion, and glucocorticoids may have a more prolonged suppressive effect on thyrotoxicosis . Orally administered resins bind T 4in the intestine and prevent recirculation . All of these agents have been used for control of thyrotoxicosis [ 184, 185]. Combined dexamethasone, potassium iodide, and PTU can lower the serum T3 level to normal in 24 hours, which is useful in severe thyrotoxicosis. Prednisone has been reported to induce remission of Graves’ disease, but at the expense of causing Cushing’s syndrome . Ipodate (0.5 – 1 g orally per day) acts to inhibit hormone release because of its iodine content, in addition to its action to inhibit T4 to T3 conversion. This dose of ipodate given to patients with Graves’ disease reduced the serum T3 level by 58% and the T 4level by 20% within 24 hours, and the effect persisted for three weeks[ 188, 189]. This dose of ipodate was more effective than 600 mg of PTU, which decreased the T3 level by only 23% during the first 24 hours, whereas the T4 level did not drop.Ipodate may prove to be a useful adjunct in the early therapy of hyperthyroidism, but will increase total body and thyroidal iodine. However, when the drug is stopped, the RAIU in Graves’ patients usually returns to pre- treatment levels within a week . Because it is the most effective agent available in preventing conversion of T4 to T3, it has a useful role in managing thyroid storm. Immunosuppressive Therapy- Development of new targeted and relatively safe immune suppressive treatments has allowed their extension to Graves’ disease. Rituximab, an anti CD20 B cell lymphocyte depleting monoclonal antibody, was initially found to induce remission in Graves’ ophthalmopathy. It also mediates decreases in anti thyroid antibodies, and is currently employed in a Phase II trial for therapy of mild, relapsing Graves’ disease (175.1, 175.2). Significant adverse events during therapy with rituximab (“serum sickness”, mild colitis, iridocyclitis, polyarthritis) have been reported, andwill probably limit its usefulness (175.21) Use of agents of this type, that work by increasing function of regulatory T cells, will probably become common in the next few years. Another approach has been pioneered by Gershengorn and colleagues, who devised a small molecule that is an “allosteric inverse agonist” of TSHR, and inhibits stimulation of TSH receptor activation by TSAbs (175.3 )
Subtotal thyroidectomy is an established and effective form of therapy for Graves’ disease, providing the patient has been suitably prepared for surgery. In competent hands, the risk of hypoparathyroidism or recurrent nerve damage is under 1%, and the discomfort and transient disability attendant upon surgery may be a reasonable price to pay for the rapid relief from this unpleasant disease. In some clinics it is the therapy of choice for most young male adults, especially if a trial of antithyroid drugs has failed. Total thyroidectomy may be preferred in patients with serious eye disease or high TRAb levels, in order to help the eye disease and to keep down the incidence of recurrence . iAs with other effective methods available, it is necessary for the physician and the patient to decide on the form of therap