Cseke Béla, Balázs Csaba
Kenézy Gyula Kórház és Rendelóintézet, III. Belgyógyászati osztály, Debrecen.
Orv Hetil. 2003 Nov 23;144(47):2327-9.
It has been observed in the past few years, that radioiodine therapy triggers autoimmune thyrotoxicosis. The possible mechanism of this phenomenon is that protein fragments enter the circulation after thyroid cell damage induced by radiation. TSH-receptor autoantibodies are produced in genetically susceptible patients after radiotherapy. In treating nodular goiter--a non-immune thyroid disease--with 131I, an immunogenic disorder--Basedow-Graves' disease--may develop. The authors present this phenomenon in a case of a 67 year-old woman with a history of operation for euthyroid nodular goiter in 1977. In November 2001, she was admitted to the hospital with local signs and symptoms of relapse of euthyroid nodular goiter (TSH-receptor antibodies were not detected). She was treated with oral doses of 320 MBq of radioiodine to reduce the thyroid volume. Four months after radioiodine therapy the patient had developed signs of thyrotoxicosis. At that time TSH-receptor antibodies were found to be positive. Thyreostatic therapy was administered and still being in use till today. The authors draw the attention to the fact that, when a hyperthyrosis develops after radioiodine therapy of a non-immune thyroid disease, the possibility of Graves-Basedow disease should be raised, especially in a patient with a positive family history.
在过去几年中观察到，放射性碘治疗会引发自身免疫性甲状腺毒症。这种现象的可能机制是，在辐射诱导甲状腺细胞损伤后，蛋白质片段进入循环系统。放疗后，基因易感性患者会产生促甲状腺激素受体自身抗体。在用131I治疗结节性甲状腺肿（一种非免疫性甲状腺疾病）时，可能会发展出一种免疫原性疾病——格雷夫斯病。作者在一位67岁女性患者的病例中呈现了这一现象，该患者在1977年有过甲状腺功能正常的结节性甲状腺肿手术史。2001年11月，她因甲状腺功能正常的结节性甲状腺肿复发的局部体征和症状入院（未检测到促甲状腺激素受体抗体）。她接受了口服320兆贝可放射性碘的治疗以缩小甲状腺体积。放射性碘治疗四个月后，患者出现了甲状腺毒症的体征。当时发现促甲状腺激素受体抗体呈阳性。给予了抗甲状腺药物治疗，至今仍在使用。作者提请注意这样一个事实，即在对非免疫性甲状腺疾病进行放射性碘治疗后出现甲状腺功能亢进时，应考虑格雷夫斯病的可能性，尤其是在有阳性家族史的患者中。
