Delayed presentation of aggravation of thyrotoxicosis after radioactive iodine therapy at Graves disease.
10.12701/yujm.2014.31.2.148
- Author:
Ji Hyun LEE
1
;
Hyun Jin NA
;
Jin Woo PARK
;
Cheol Ho LEE
;
Hyun Jeong HAN
;
Tae Ho KIM
;
Se Hwa KIM
Author Information
1. Department of Internal Medicine, Myongji Hospital, Goyang, Korea.
- Publication Type:Case Report
- Keywords:
Thyrotoxicosis;
Graves disease;
Radioactive iodine therapy
- MeSH:
Antibodies;
Female;
Graves Disease*;
Headache;
Humans;
Immunoglobulins, Thyroid-Stimulating;
Iodine*;
Middle Aged;
Propranolol;
Propylthiouracil;
Thyroid Function Tests;
Thyroid Gland;
Thyroiditis;
Thyrotoxicosis*;
Thyrotropin;
Weight Loss
- From:Yeungnam University Journal of Medicine
2014;31(2):148-151
- CountryRepublic of Korea
- Language:Korean
-
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.
