131I treatment is an effective alternative to surgery in patients with a large, (non-)toxic, compressive
goiter. Late development of
hyperthyroidism after 131I
therapy for nontoxic
nodular goiter is considered rare. We have seen this complication in 3 of approximately 80 patients treated with radioiodine for volume reduction of a large, multinodular
goiter. Three women, aged 60 to 71 years, had large, multinodular
goiters causing tracheal compression. They were clinically euthyroid before 131I
therapy and had normal free
thyroxine (FT4) levels. Serum
thyroid-stimulating hormone (TSH) levels were normal in 2 patients and undetectable in 1 patient. Patients 1 and 2 received a single dose of 86 and 48 mCi 131I, respectively. Patient 3 received 20 mCi 131I twice (interval 1 month). Clinical and biochemical
thyrotoxicosis with high thyroid radioactive
iodide uptake (RAIU) developed 10, 6, and 3 months after 131I
therapy, respectively, although at control visits 1 to 3 months earlier, serum TSH and FT4 levels were normal.
Thyrotoxicosis responded well to
methimazole in all three patients. The late occurrence of
thyrotoxicosis, high RAIU, and good response to
methimazole argue against
thyroiditis as the cause of
thyrotoxicosis. Serum levels of
TSH receptor antibodies, which were undetectable before
therapy (patients 1 and 2), were clearly elevated in all three patients during
thyrotoxicosis. This is in favor of autoimmune
hyperthyroidism as the cause of
thyrotoxicosis. These cases illustrate that severe autoimmune
hyperthyroidism may occur several months after radioiodine treatment for nontoxic, multinodular
goiter. Information about symptoms of
hyperthyroidism and regular control visits in the first year after
therapy are important in these patients.