Graves' disease and hyperthyroidism

Graves' disease, an autoimmune condition in which antibodies stimulate the TSH receptor, is the most common cause of hyperthyroidism, accounting for 60-80% of cases. Oral radioactive iodine-131 has been used to treat it since the 1940s: because the thyroid concentrates iodine, an orally administered dose is taken up almost exclusively by thyroid tissue, which is then irradiated from within by the beta particles, over weeks progressively destroying overactive follicular cells.

Work-up before therapy establishes that the gland is actually iodine-avid: thyroid function tests, and a radioiodine uptake measurement (with I-123 or I-131) or Tc-99m pertechnetate scan, distinguish Graves' disease and toxic nodules (high uptake) from destructive thyroiditis or factitious thyrotoxicosis (low uptake), which will not respond to I-131. Dosing is either a fixed empiric activity or calculated from gland size and the 24-hour uptake to target roughly 2.96-7.4 MBq per gram of thyroid tissue; a serum TSH above about 30 mIU/mL maximises uptake. Antithyroid drugs (methimazole or propylthiouracil) are often used first, or stopped a few days before treatment, to reduce the risk of a transient post-therapy surge in circulating hormone.

The intended endpoint is a non-hyperthyroid state, and permanent hypothyroidism requiring lifelong levothyroxine is the expected outcome in most patients rather than a complication - it is easier to manage than recurrent thyrotoxicosis. Alternatives are long-term antithyroid drugs or thyroidectomy; the choice among the three is guided by goitre size, ophthalmopathy, pregnancy plans and patient preference rather than by radiopharmaceutical availability. Graves' orbitopathy can worsen after I-131 and this needs to be discussed and sometimes covered with steroids beforehand.