Graves disease is the most common cause of thyrotoxicosis. It is an autoimmune disorder characterized by a constellation of clinical features including hyperthyroidism, diffuse goitre, ophthalmopathy, and dermopathy. Conventional principal management of thyrotoxicosis includes antithyroid drugs, radioactive iodine, and surgery. Adjunctive treatment in the form of beta-blockers, corticosteroids, inorganic iodide, and iopanoic acid may also be used for more prompt control of symptoms. However, a few cases may require additional treatment despite these conventional modalities to achieve euthyroid state.
A 22-year-old woman with severe Graves’ disease was referred from a local clinic because of her refractory hyperthyroidism. She presented with exophthalmos, nodule goiter, and tachycardia. She was treated with a maximal dose of methimazole and switching to propylthiouracil (PTU), and administering maximum doses of beta blocker and steroid. However, her thyroid function test (TFT) did not improve. TFT showed T3 level > 600 ng/dL (normal : 58 - 156), free T4 level > 24 µg/dL (normal 4.87 - 11.72), thyroid stimulating hormone (TSH) level < 0.0083 mIU/L (normal : 0.36 - 4.94) and Thyrotropin (TSH) Receptor Antibodies (TRAb) > 40 IU/L (normal : <1.75). She was then administered for radioactive iodine (RAI) and effective to achieve treatment goals after the second RAI.
Hyperthyroidism resistant to antithyroid drug therapy is rare but potentially life-threatening. Radioactive iodine is one of the definitive approaches used in the treatment of thyrotoxicosis, especially in patients resistant to medical treatment.
However, it is necessary to consider why the patient was resistant to the antithyroid drugs. Possible reasons may include drug malabsorption, rapid drug metabolism, antidrug antibodies, impairment of intrathyroidal drug accumulation or action, and predominant elevation of T3 rather than T4 levels.