 temporary inhibition of iodide organification by the thyrotoxic gland. In normal persons elevation of the inorganic 127-I level results, up to a point, in a progressive increase of accumulation of iodide in the gland. When the plasma concentration is above 20 µg/dl, organification is also inhibited in the normal gland . The sensitivity of the thyrotoxic gland, in comparison with that of the euthyroid gland, may be due to an increased ability to concentrate iodide in the thyroid, and its failure to “adapt” by decreasing the iodide concentrating mechanism.
When iodine is to be used therapeutically in Graves’ disease, one usually prescribes a saturated solution of potassium iodide (which contains about 50 mg iodide per drop) or Lugol’s solution (which contains about 8.3 mg iodide per drop). Thompson and co- workers  found that 6 mg of I- or KI produces a maximum response. This fact was reemphasized by Friend, who pointed out that the habit of prescribing the 5 drops of Lugol’s or SSKI three times daily is unnecessary . Two drops of Lugol’s solution or 1 drop of a saturated solution of potassium iodide two times daily is more than sufficient. The therapeutic response to iodide begins within two to seven days and is faster than can be obtained by any other methods of medical treatment. Only 3% of patients so treated fail to respond. Men, older persons, and those with nodular goiter are in the group less likely to have a response to iodide. Although almost all patients initially respond to iodide, about one-third respond partially and remain toxic, and another one-third initially respond but relapse after about six weeks . The use of iodide as definitive therapy for thyrotoxicosis has been discarded in favor of the modalities previously described. Iodides are sometimes given after 131-Itherapy to control hyperthyroidism, and are usually given as part of treatment before thyroidectomy.
Adjunctive Therapy for Graves’ Disease
Propranolol, metopranol, atenolol
Beta-adrenergic blocking agents have won a prominent position in the treatment of thyrotoxicosis. Although they alleviate many of the signs and symptoms, they have little effect on the fundamental disease process[ 166, 167]. Palpitations, excessive sweating, and nervousness improve, and tremor and tachycardia are controlled. Many patients feel much improved, but others are depressed by the drug and prefer not to take it. Improvement in myocardial efficiency and reduction in the exaggerated myocardial oxygen consumption have been demonstrated . Propranolol lowers oxygen consumption  and reverses the nitrogen wasting of thyrotoxicosis, although it does not inhibit excess urinary calcium and hydroxyproline loss . Propranolol is useful in symptomatic treatment while physician and patient are awaiting the improvement from antithyroid drug or 131-I therapy . Some patients appear to enter remission after using this drug alone for six months or so of therapy[ 169, 172]. It has been useful in neonatal thyrotoxicosis  and in thyroid storm . The drug must be used cautiously when there is evidence of severe thyrotoxicosis, or heart failure, but often control of tachycardia permits improved circulation. Beta blockade can induce cardiovascular collapse in patients with or without heart failure, and asystolic arrest (174a,b). Administration of beta blocker was shown by Ikram to reduce CO by 13% in patients with uncontrolled CHF, and apparently this reduction in CO can be near fatal in rare patients. Some surgical groups routinely prepare patients for thyroidectomy with propranolol for 20 – 40 days and add potassium iodide during the last week . The BMR and thyroid hormone level remain elevated at the time of operation, but the patient experiences no problems. We prefer conventional preoperativepreparation with thiocarbamides, with or without iodide, and would use propranolol as an adjunct, or if the patient is allergic to the usual drugs.
Propranolol is usually given orally as 20 – 40 mg every four to six hours, but up to 200 mg every six hours may be needed. In emergency management of th