分化型甲状腺癌术后放射性碘治疗与甲状旁腺激素水平相关性研究进展

Advances in the Study of the Correlation between Postoperative Radioiodine Therapy and Parathyroid Hormone Levels in Differentiated Thyroid Cancer

摘要: 目的：分化型甲状腺癌(differentiated thyroid cancers, DTC)术后常采用¹³¹I辅助清甲治疗，甲状旁腺与甲状腺解剖毗邻，放射性辐射或造成甲状旁腺损伤、甲状旁腺激素(parathyroid hormone, PTH)异常。本文系统梳理DTC术后¹³¹I治疗对甲状旁腺功能及PTH水平的影响、相关作用机制、危险因素与临床干预措施，为临床安全开展放射性碘治疗提供参考。方法：检索中英文数据库收录的分化型甲状腺癌、¹³¹I治疗、甲状旁腺功能相关回顾性队列、病例对照、基础机制研究文献，归纳¹³¹I治疗相关毒副作用、甲状旁腺损伤发生机制、功能评估手段、影响PTH波动的危险因素及防治策略，对比国内外现有研究争议与局限性。结果：现有研究对¹³¹I是否影响甲状旁腺功能尚未形成统一结论。术后甲状旁腺功能异常首先与手术相关因素密切相关，包括甲状旁腺误切、热损伤及供血血管受损；在此基础上，¹³¹I治疗可能产生额外的近距离辐射暴露及旁观者效应，从而使部分患者PTH短暂下降或功能恢复延迟。女性、大剂量¹³¹I及甲状旁腺原位保留数量不足可能与功能异常相关，但现有研究多为回顾性研究，且混杂因素控制有限，因此尚难将PTH变化完全归因于¹³¹I治疗。结论：术后甲状旁腺功能减退的主要原因仍是手术直接损伤，¹³¹I更适合作为可能的附加影响因素进行评价，而不宜将两者混为一谈。现阶段尚缺乏充分证据证明¹³¹I可独立导致甲状旁腺结构性损伤，因此暂不建议将甲状旁腺功能减退列为¹³¹I治疗禁忌。临床应在治疗前评估甲状旁腺基线功能，术中规范保留甲状旁腺及其血供，¹³¹I治疗后进行短期及长期PTH动态监测，并通过前瞻性研究进一步明确¹³¹I的独立效应。

Abstract: Objective: Postoperative radioiodine-131 (¹³¹I) ablation is a standard adjuvant therapy for differentiated thyroid carcinoma (DTC). The anatomical adjacency between parathyroid glands and thyroid tissue may lead to radiation injury of parathyroid glands and abnormal parathyroid hormone (PTH) secretion after ¹³¹I treatment. This review systematically summarizes the effects of postoperative ¹³¹I therapy on parathyroid function and PTH levels, related mechanisms, risk factors and clinical interventions, so as to provide evidence for safe clinical application of radioiodine therapy. Methods: Domestic and foreign literatures including retrospective cohorts, case-control studies and basic mechanism researches concerning DTC, ¹³¹I therapy and parathyroid function were retrieved. We sorted out radiation side effects of ¹³¹I, injury mechanism of parathyroid glands, functional evaluation methods, risk factors of PTH fluctuation and prevention strategies, and compared controversies and limitations of existing studies. Results: Consistent conclusions have not been reached regarding the effect of ¹³¹I therapy on parathyroid function. Postoperative parathyroid dysfunction is primarily related to surgery, including inadvertent resection, thermal injury, and disruption of the parathyroid blood supply. On this basis, ¹³¹I may exert an additional effect through local radiation exposure and radiation-induced bystander signaling, potentially causing transient PTH decline or delayed functional recovery in some patients. Female sex, higher ¹³¹I dose, and fewer parathyroid glands preserved in situ may be associated with abnormal PTH, but most available studies are retrospective and incompletely control for confounding factors; therefore, the observed PTH changes cannot yet be attributed independently to ¹³¹I therapy. Conclusion: The major cause of postoperative hypoparathyroidism remains direct surgical injury, whereas ¹³¹I should be considered a potential additional factor rather than being conflated with surgical injury. Current evidence is insufficient to establish that ¹³¹I independently causes structural parathyroid injury; therefore, hypoparathyroidism should not currently be regarded as a contraindication to ¹³¹I therapy. Baseline parathyroid function should be assessed before treatment, parathyroid glands and their blood supply should be carefully preserved during surgery, and PTH should be monitored dynamically after ¹³¹I therapy. Prospective studies are needed to determine the independent effect of ¹³¹I exposure.