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高剂量辐射暴露与甲状腺功能减退症:病因、预防及替代治疗

High-dose radiation exposure and hypothyroidism: aetiology, prevention and replacement therapy.

作者信息

Reiners Christoph, Hänscheid Heribert, Schneider Rita

机构信息

Department of Nuclear Medicine and WHO REMPAN Collaboration Center, University Hospital, Würzburg, Germany.

出版信息

J Radiol Prot. 2021 Dec 6;41(4). doi: 10.1088/1361-6498/ac28ee.

Abstract

Without any doubt, high dose radiation exposure can induce hypothyroidism. However, there are open questions related to the mechanisms of its induction, corresponding dose thresholds and possible countermeasures. Therefore, this review addresses the aetiology, prevention and therapy of radiation induced hypothyroidism. External beam radiotherapy with several 10 Gy to the head and neck region and radioiodine therapy with several 100 Gy thyroid absorbed dose can destroy the thyroid gland and can induce autoantibodies against thyroid tissue. According to recent literature, clinical hypothyroidism is observed at threshold doses of ∼10 Gy after external beam radiotherapy and of ∼50 Gy after radioiodine therapy, children being more sensitive than adults. In children and adolescents exposed by the Chernobyl accident with mean thyroid absorbed doses of 500-800 mGy, subclinical hypothyroidism has been detected in 3%-6% of the cases with significant correlation to thyroid absorbed doses above 2.5 Gy. In case of nuclear emergencies, iodine thyroid blocking (ITB) is the method of choice to keep thyroid absorbed doses low. Large doses of stable iodine affect two different steps of internalization of radioiodine (transport and organification); perchlorate affecting the transport only may be an alternative to iodine. Administered before radioiodine incorporation, the effect of 100 mg iodide or more is still about 90% after 1 days, 80% after 2 days, and 50% or less after 3 days. If administered (too) late after exposure to radioiodine, the theoretically expected protective effect of ITB is about 50% after 6 h, 25% after 12 h, and about 6% after 24 h. In case of repeated or continuous exposure, repeated administration of 50 mg of iodide daily is indicated. If radiation-induced hypothyroidism cannot be avoided, thyroid hormone replacement therapy with individualized dosing and regular monitoring in order to maintain thyroid-stimulating hormone levels within the normal range ensures normal life expectancy.

摘要

毫无疑问,高剂量辐射暴露可诱发甲状腺功能减退。然而,关于其诱发机制、相应剂量阈值及可能的应对措施仍存在一些悬而未决的问题。因此,本综述探讨辐射诱发甲状腺功能减退的病因、预防及治疗。对头颈部区域进行数次10 Gy的外照射放疗以及对甲状腺吸收剂量进行数次100 Gy的放射性碘治疗可破坏甲状腺,并可诱发针对甲状腺组织的自身抗体。根据最近的文献,外照射放疗后阈值剂量约为10 Gy、放射性碘治疗后阈值剂量约为50 Gy时可观察到临床甲状腺功能减退,儿童比成人更敏感。在切尔诺贝利事故中受照的儿童和青少年,甲状腺平均吸收剂量为500 - 800 mGy,3% - 6%的病例检测到亚临床甲状腺功能减退,且与甲状腺吸收剂量高于2.5 Gy显著相关。在核紧急情况下,碘甲状腺阻断(ITB)是使甲状腺吸收剂量保持在低水平的首选方法。大剂量稳定碘影响放射性碘内化的两个不同步骤(转运和有机化);仅影响转运的高氯酸盐可能是碘的替代物。在摄入放射性碘之前给药,100 mg或更多碘化物的效果在1天后仍约为90%,2天后为80%,3天后为50%或更低。如果在接触放射性碘后(过)晚给药,ITB的理论预期保护效果在6小时后约为50%,12小时后为25%,24小时后约为6%。在重复或持续暴露的情况下,建议每日重复给予50 mg碘化物。如果无法避免辐射诱发的甲状腺功能减退,采用个体化给药并定期监测以维持促甲状腺激素水平在正常范围内的甲状腺激素替代疗法可确保正常寿命。

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