Department of Nuclear Medicine, University Hospital Frankfurt, Frankfurt am Main, Germany.
Semin Nucl Med. 2010 Mar;40(2):153-63. doi: 10.1053/j.semnuclmed.2009.11.004.
Treatment with (131)I-metaiodobenzylguanidine (MIBG) has been introduced to the management of neuroendocrine tumors (NET) nearly 30 years ago. It provides efficient internal radiotherapy of chromaffin tumors (neuroblastoma, pheochromocytoma, and paraganglioma), but also of carcinoid and other less frequent tumors. Although for various NET types the role of this treatment form decreased by the emergence of peptide receptor radionuclide therapy, (131)I-MIBG still remains the primary radiopharmaceutical for targeting chromaffin tumors with outstanding efficiency. Results in neuroblastoma with overall response rates around 30% in refractory or recurrent diseases have been improved by combinations with chemotherapy, radiosensitizers, and autologous stem cell support. For adult chromaffin tumors, that is, pheochromocytoma and/or paraganglioma, (131)I-MIBG therapy is currently the most efficient nonsurgical therapeutic modality and applies for inoperable, disseminated disease. The antisecretory effect with powerful palliation of symptomatic disease (response rate: 75%-90%) should also be considered when judging treatment benefit. The results in carcinoid tumors are less pronounced, primarily achieving arrest of tumor growth, and most importantly effective functional control. With the presence of peptide receptor radionuclide therapy, (131)I-MIBG remains the alternative radionuclide in this tumor entity, for example, for patients with renal impairment. Another worthwhile mentioning indication-although less prevalent-are metastatic medullary thyroid carcinomas, especially if functioning. These patients are good candidates for this treatment form in the absence of reasonable surgical options and presence of diagnostic MIBG uptake. This article outlines the current status, results, and methodological improvements of (131)I-MIBG therapy.
治疗用（131）I-间碘苄胍（MIBG）引入神经内分泌肿瘤（NET）的治疗已有近 30 年的历史。它为嗜铬细胞瘤（神经母细胞瘤、嗜铬细胞瘤和副神经节瘤）提供了有效的内部放射治疗，也为类癌和其他较少见的肿瘤提供了治疗。尽管由于肽受体放射性核素治疗的出现，各种 NET 类型的这种治疗形式的作用有所下降，但（131）I-MIBG 仍然是靶向嗜铬细胞瘤的主要放射性药物，具有出色的疗效。在难治性或复发性疾病中，总体反应率约为 30%的神经母细胞瘤的联合化疗、放射增敏剂和自体干细胞支持，改善了这种治疗方法的结果。对于成人嗜铬细胞瘤，即嗜铬细胞瘤和/或副神经节瘤，（131）I-MIBG 治疗目前是最有效的非手术治疗方法，适用于无法手术的、播散性疾病。在判断治疗获益时，还应考虑其抗分泌作用，对有症状疾病有强有力的缓解作用（缓解率：75%-90%）。类癌肿瘤的疗效不那么显著，主要是肿瘤生长停止，最重要的是功能控制有效。随着肽受体放射性核素治疗的出现，（131）I-MIBG 仍然是这种肿瘤实体的替代放射性药物，例如，对于肾功能损害的患者。另一个值得一提的适应症——尽管不太常见——是转移性甲状腺髓样癌，尤其是功能性的。对于没有合理手术选择且存在诊断性 MIBG 摄取的这些患者，这种治疗形式是很好的选择。本文概述了（131）I-MIBG 治疗的现状、结果和方法学改进。
