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Radioactive iodine (RAI) is often the first-line treatment for patients with Graves' disease (GD) in North America. It is preferred over antithyroid drugs and surgical therapy due to:

• High relapse rate following antithyroid drug therapy (over 50%)
• Concern over complications following surgery

RAI treatment may also be indicated under various circumstances including:

• If there is a recurrence of hyperthyroidism after a surgical subtotal thyroidectomy
• If the patient has either not responded to or has relapsed after antithyroid medication
• For older patients since the effects of relapse following antithyroid drugs can be more severe and less tolerated by this population

Radioactive iodine treatment decreases the activity of the overactive thyroid gland by destroying thyroid cells. The RAI is administered orally as a capsule or in water. The radioactive iodine becomes concentrated in the thyroid gland where it emits radiation causing inflammation and necrosis of the cells in the gland. The objective of this treatment is to permanently destroy just enough of the gland to achieve euthyroidism. The full effect of RAI treatment may not be felt for several months, though individual symptoms may begin to show improvement before that time.

The ideal dose of RAI continues to be debated. If the dose is too high, it can cause hypothyroidism. In an effort to prevent subsequent hypothyroidism, some doctors lower the initial dose of radioiodine. Some studies, however, have found that this may result in persistent subclinical hyperthyroidism (where levels of T4 and T3 hormones are normal but TSH is very low or undetectable) or complete treatment failure. Controversy continues regarding the benefit of a fixed dose of RAI versus an individually-optimized dose.

As RAI takes effect and causes necrosis to thyroid cells, the risk exists of large amounts of thyroid hormones being released into the blood stream in a surge. To prevent this, antithyroid drugs and beta-blockers may given before and after treatment to help the patient become euthyroid. Patients with mild or moderate hyperthyroidism may not require pre- or post-treatment with antithyroid drugs and their symptoms can usually be managed with beta-blockers until the RAI takes effect. Elderly patients and those with heart disease must be monitored carefully since the excess thyroid hormone levels can exacerbate cardiac symptoms. Although the practice of giving antithyroid drugs pre and/or post treatment with RAI is common, debate continues as to whether the drugs may reduce the efficacy of the RAI treatment.

In some patients, the remaining cells in the thyroid gland may be overactive for several years but overproduction is compensated for by the fact that there are fewer cells producing hormone. Consequently, these patients may experience euthyroidism for many years and then begin to exhibit signs of hypothyroidism. At that point, the deficiency of thyroid hormone requires supplementation with synthetic thyroid hormone for the remainder of the person's life.

If an inadequate amount of the thyroid gland has been destroyed after RAI treatment and signs and symptoms of hyperthyroidism persist, the patient may be eligible for a second treatment of radioiodine. Approximately 10% of patients undergoing this procedure will require a second dose. Those patients whose hyperthyroidism persists may be treated subsequently by surgery.