Graves’ disease is an autoimmune thyroid disorder characterized by clinical hyperthyroidism and the presence of autoantibodies directed against the thyrotropin (TSH) receptor (1,2). The presentation of this disease varies with age. Younger patients manifest nervousness, weight loss, anxiety, heat intolerance, hyperdefecation, inability to concentrate, and tremulousness, while older patients may manifest few if any of these typical symptoms (3). Circulating TSH receptor-stimulating antibodies are present in at least 90% of patients and are responsible, in large part, for the thyroidal hyperactivity (4). An interesting aspect of Graves’ disease is its association with ophthalmopathy, which can cause tearing, burning, itching, proptosis, double vision, and/or (rarely) visual impairment (5,6). The
etiology of Graves’ hyperthyroidism and ophthalmopathy remains unclear. There are abnormalities in T-cell function that allow the TSH receptor antibodies to develop; these antibodies not only stimulate TSH receptor action in thyrocytes but may cross-react with orbital antigens (e.g., fibroblasts) as well (5,7-13). The term Graves’ disease commonly refers to patients who manifest clinical and biochemical hyperthyroidism (1), but in certain circumstances this term may require further delineation. For example, patients with Graves’ disease and hyperthyroidism may become spontaneously euthyroid or hypothyroid because, over time, the stimulatory TSH receptor antibodies have become blocking antibodies (7,10) or because the chronic inflammatory process has resulted in thyroid failure.