Abstract
Graves' disease is an organ-specific autoimmune disorder. There is no universal agreement on the mechanism of Graves' disease, but the over-activity of the thyroid is due to an antibody capable of attaching to and activating the TSH receptor of follicular cells. There are other extrathyroidal features that are not caused either by this antibody or by hyperthyroidism. The clinical diagnosis is generally straightforward and can be confirmed by in vitro measurement of thyroid hormones and TSH. A measurement of radioiodine uptake is also valuable. Treatment is not specific for the immunologic defect, but its purpose is to lower the thyroid hormone levels to normal. This can be achieved with antithyroid medication, radioiodine iodine-131, or thyroidectomy. In most clinical situations, a strong argument can be made for iodine-131 therapy, which is safe and definitive, although posttreatment hypothyroidism and the need for lifelong thyroxine are to be expected.
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