Abstract
The manifestation of Graves' disease (GD) in patients treated with radioactive iodine (RAI) for hyperfunctioning thyroid nodules (RAI-induced GD or post-RAI GD) remains a long-standing challenge in radionuclide therapy. Known risk factors for post-RAI GD include preexisting subclinical hyperthyroidism, positive thyroid peroxidase autoantibodies (TPOAb), positive TSH receptor autoantibodies (TRAb) or otherwise undiagnosed GD. However, these risk factors are not present in all patients with post-RAI GD, and therefore it cannot always be predicted in a reliable manner if a given patient has a high risk for RAI-induced GD or not. We describe the case of a 64 year-old woman known for hyperthyroidism due to toxic nodular goiter; she was treated initially with carbimazole, and then, due to recurrence, underwent RAI treatment. Three months later, symptomatic hyperthyroidism persisted. Diagnosis of new-onset GD was made based on typical ultrasound findings and newly-positive TRAb. Our patient had only positive thyroglobulin antibodies (TgAb) before RAI treatment, whereas TPOAb were negative. In the literature, TgAb have never been reported as a possible risk factor for RAI-induced GD. The present case suggests that the assessment for pre-existing autoimmunity in patients considering RAI for hyperfunctioning thyroid nodules should probably also include TgAb.
Highlights
New-onset Graves’ disease (GD) after radioiodine (RAI) treatment for toxic nodular goiter (RAI-induced GD or post-RAI GD) is a rare phenomenon that is reported in the literature yet not broadly known among clinicians
We report here a patient with RAI-induced GD who had neither thyroid-stimulating hormone (TSH) receptor autoantibodies (TRAb) nor thyroid peroxidase autoantibodies (TPOAb), but only thyroglobulin antibodies (TgAb)
The Marine-Lenhart syndrome, in which toxic nodules coexist with GD; an unusual case of Marine-Lenhart syndrome has been reported, in which an autonomous thyroid nodule developed after RAI treatment for GD [2]
Summary
The manifestation of Graves’ disease (GD) in patients treated with radioactive iodine (RAI) for hyperfunctioning thyroid nodules (RAI-induced GD or post-RAI GD) remains a long-standing challenge in radionuclide therapy. Known risk factors for post-RAI GD include preexisting subclinical hyperthyroidism, positive thyroid peroxidase autoantibodies (TPOAb), positive TSH receptor autoantibodies (TRAb) or otherwise undiagnosed GD. These risk factors are not present in all patients with post-RAI GD, and it cannot always be predicted in a reliable manner if a given patient has a high risk for RAI-induced GD or not. Case Presentation: We describe the case of a 64 year-old woman known for hyperthyroidism due to toxic nodular goiter; she was treated initially with carbimazole, and due to recurrence, underwent RAI treatment. Our patient had only positive thyroglobulin antibodies (TgAb) before RAI treatment, whereas TPOAb were negative
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