Yeungnam Univ J Med.  2014 Dec;31(2):148-151. 10.12701/yujm.2014.31.2.148.

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

Affiliations
  • 1Department of Internal Medicine, Myongji Hospital, Goyang, Korea.
  • 2Department of Internal Medicine, Catholic Kwandong University College of Medicine, Gangneung, Korea. bonesh@naver.com

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 microIU/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.

Keyword

Thyrotoxicosis; Graves disease; Radioactive iodine therapy

MeSH Terms

Antibodies
Female
Graves Disease*
Headache
Humans
Immunoglobulins, Thyroid-Stimulating
Iodine*
Middle Aged
Propranolol
Propylthiouracil
Thyroid Function Tests
Thyroid Gland
Thyroiditis
Thyrotoxicosis*
Thyrotropin
Weight Loss
Antibodies
Immunoglobulins, Thyroid-Stimulating
Iodine
Propranolol
Propylthiouracil
Thyrotropin
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