Endocrine Abstracts

Introduction and objectives: The strategies for therapy of metastatic medullary thyroid carcinoma (MTC) are limited. Although Tyrosine kinase inhibitors (TKI) seem to be the first-line treatment, we want to explore other possibilities. Metaiodobenzylguanidine (MIBG) is a guanethidine derivative, structurally similar to norepinephrine. It was developed as an imaging agent with ¹²³I radiolabeling. MIBG localizes neuroendocrine tumors including MTC. We are investigating the use of high doses of ¹³¹I-MIBG as therapy for metastatic MTC. We present two case reports in which we used this therapeutic option.

Case reports: 1) A 40-year-old woman, diagnosed at 26 of MCT with lymph node metastasis. She was surgically treated up to three times (due to lymph node recurrence). In 2015, there was an increase of calcitonin and CEA levels (1859 pg/dl, 27.1 ng/ml), showing metastases at lung, bone and breast. A ¹²³I-MIBG scan was performed, revealing an uptake of the radiotracer by bone lesions. One therapeutic dose of 200mCi ¹³¹I-MIBG was administered, with uptake being appreciated by bone lesions but not by pulmonary lesions. After 6 months, the levels of calcitonin and CEA further raised (3353 pg/dl, 33.5 ng/ml). In the imaging study, an increase in the size of the pulmonary nodules was observed. TKI therapy was started.

2) A 39-year-old woman, diagnosed at 18 with endocrine neoplasia type 2B with CMT and bilateral pheochromocytoma, who underwent total thyroidectomy and bilateral adrenalectomy. In 2016, metastatic dissemination was observed with bone, liver and interaortocaval adenopathy lesions (calcitonin 10 279 pg/ml, CEA 64.7 ng/ml). It was treated with a high fractional dose of ¹³¹I-MIBG (300 mCi, 360 mCi), with radiological progression of the disease in the hepatic parenchyma after 1 year. However, biochemical markers remained stable (calcitonin 9253 pg/ml, 85.6 ng/ml).

Conclusion: In our experience, the benefits of ¹³¹I-MIBG therapy in metastatic medullary thyroid carcinoma are poor.