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Delayed presentation of aggravation of thyrotoxicosis after radioactive iodine therapy at Graves disease

그레이브스병에서 방사성요오드 치료 후 발생한 갑상샘항진증 악화의 지연된 발현

  • Lee, Ji-Hyun (Department of Internal Medicine, Myongji Hospital) ;
  • Na, Hyun-Jin (Department of Internal Medicine, Myongji Hospital) ;
  • Park, Jin-Woo (Department of Internal Medicine, Myongji Hospital) ;
  • Lee, Cheol-Ho (Department of Internal Medicine, Myongji Hospital) ;
  • Han, Hyun-Jeong (Department of Internal Medicine, Myongji Hospital) ;
  • Kim, Tae-Ho (Department of Internal Medicine, Catholic Kwandong University College of Medicine) ;
  • Kim, Se-Hwa (Department of Internal Medicine, Catholic Kwandong University College of Medicine)
  • Received : 2013.09.11
  • Accepted : 2014.01.08
  • Published : 2014.12.31

Abstract

Radioactive iodine (RAI) therapy is widely used for the treatment of Graves disease. After RAI therapy, 44% become hypothyroid and up to 28% remain hyperthyroid. The development of thyrotoxicosis after RAI therapy is believed to be mediated by 2 different mechanisms: a transient increased release of thyroid hormone due to radiation thyroiditis and the rare development of Graves disease due to the formation of antibodies to the thyroid-associated antigens released from the damaged follicular cells. A 55-year-old woman was hospitalized with severe headache, weight loss, and palpitation. She received a dose of 7 mCi of RAI (I-131) about 6 weeks earlier. Thyroid function test showed 7.98 ng/dL free T4, >8 ng/mL T3, < $0.08{\mu}IU/L$ thyroid stimulating hormone, and high titer thyroid stimulating immunoglobulin (TSI) (85.8 IU/L). She improved with propylthiouracil, propranolol, and steroid treatment. The TSI, however, was persistently elevated for 11 months.

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