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辐射暴露后甲状腺功能减退症:简要叙述性综述。

Hypothyroidism after radiation exposure: brief narrative review.

机构信息

Department of Nuclear Medicine, University Hospital, Oberduerbacherstr.6, 97080, Wuerzburg, Germany.

International Foundation Arnica, Minsk, Belarus.

出版信息

J Neural Transm (Vienna). 2020 Nov;127(11):1455-1466. doi: 10.1007/s00702-020-02260-5. Epub 2020 Oct 9.

Abstract

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.

摘要

甲状腺是受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。辐射暴露还可能导致甲状腺功能减退和针对甲状腺的自身免疫反应,但这些影响的记录较少。文献中只有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/分子机制的方法学较弱的动物研究。相反,关于辐射诱导的甲状腺功能减退症和甲状腺自身免疫的证据主要来自接受外部束放射治疗(EBRT)或碘-131 治疗的患者的随访研究,以及原子爆炸或核事故幸存者的流行病学研究。从历史上看,成年人甲状腺外照射后发生甲状腺功能减退症被认为在 10-20Gy 剂量阈值以下不会发展。新数据表明 EBRT 后阈值为 10Gy。相比之下,来自碘-131“内部放射治疗”格雷夫斯病患者的数据表明,甲状腺剂量低于 50Gy 很少发生甲状腺功能减退症。切尔诺贝利事故受影响儿童的研究表明,甲状腺功能减退症的剂量阈值可能低得多,为 3-5Gy,与儿童时期暴露的原子弹幸存者的观察结果一致。对于这种辐射敏感性的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症的发展的其他重要问题,例如宫内、自身免疫与功能减退之间的相互作用,以及内部和外部照射的不同影响,仍然需要回答。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1bbb/7578155/f90d6d319f47/702_2020_2260_Fig1_HTML.jpg

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