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Hypothyroidism after radiation exposure: brief narrative review
Journal of Neural Transmission ( IF 3.3 ) Pub Date : 2020-10-09 , DOI: 10.1007/s00702-020-02260-5
Christoph Reiners 1 , Valentina Drozd 2 , Shunichi Yamashita 3, 4
Affiliation  

The thyroid gland is among the organs at the greatest risk of cancer from ionizing radiation. Epidemiological evidence from survivors of radiation therapy, atomic bombing, and the Chernobyl reactor accident, clearly shows that radiation exposure in childhood can cause thyroid cancer and benign thyroid nodules. Radiation exposure also may induce hypothyroidism and autoimmune reactions against the thyroid, but these effects are less well-documented. The literature includes only a few, methodologically weak animal studies regarding genetic/molecular mechanisms underlying hypothyroidism and thyroid autoimmunity after radiation exposure. Rather, evidence about radiation-induced hypothyroidism and thyroid autoimmunity derives mainly from follow-up studies in patients treated with external beam radiotherapy (EBRT) or iodine-131, and from epidemiological studies in the atomic bombing or nuclear accident survivors. Historically, hypothyroidism after external irradiation of the thyroid in adulthood was considered not to develop below a 10–20 Gy dose threshold. Newer data suggest a 10 Gy threshold after EBRT. By contrast, data from patients after iodine-131 “internal radiation therapy” of Graves´ disease indicate that hypothyroidism rarely occurs below thyroid doses of 50 Gy. Studies in children affected by the Chernobyl accident indicate that the dose threshold for hypothyroidism may be considerably lower, 3–5 Gy, aligning with observations in A-bomb survivors exposed as children. The reasons for these dose differences in radiosensitivity are not fully understood. Other important questions about the development of hypothyroidism after radiation exposure e.g., in utero, about the interaction between autoimmunity and hypofunction, and about the different effects of internal and external irradiation still must be answered.



中文翻译:

辐射暴露后甲状腺功能减退症:简要叙述回顾

甲状腺是电离辐射致癌风险最大的器官之一。来自放射治疗、原子弹爆炸和切尔诺贝利反应堆事故幸存者的流行病学证据清楚地表明,儿童时期的辐射暴露会导致甲状腺癌和良性甲状腺结节。辐射暴露也可能诱发甲状腺功能减退症和针对甲状腺的自身免疫反应,但这些影响的记录较少。文献仅包括少数关于辐射暴露后甲状腺功能减退和甲状腺自身免疫的遗传/分子机制的方法学上较弱的动物研究。相反,关于辐射引起的甲状腺功能减退和甲状腺自身免疫的证据主要来自对接受外照射放疗 (EBRT) 或碘 131 治疗的患者的随访研究,以及对原子弹爆炸或核事故幸存者的流行病学研究。从历史上看,成年期甲状腺外照射后甲状腺功能减退被认为不会低于 10-20 Gy 剂量阈值。较新的数据表明 EBRT 后的阈值为 10 Gy。相比之下,来自格雷夫斯病碘 131“内部放射治疗”后患者的数据表明,甲状腺功能减退症很少发生在低于 50 Gy 的甲状腺剂量。对受切尔诺贝利事故影响的儿童的研究表明,甲状腺功能减退症的剂量阈值可能要低得多,为 3-5 Gy,这与在儿童时期受到暴露的原子弹幸存者的观察结果一致。这些放射敏感性剂量差异的原因尚不完全清楚。关于辐射暴露后甲状腺功能减退发展的其他重要问题,例如,在子宫内,

更新日期:2020-10-11
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