engleski

THE ROLE OF 131I-MIBG THERAPY IN ADVANCED MEDULLARY THYROID CARCINOMA

Background: Medullary thyroid carcinoma (MTC), a type of thyroid carcinoma which originates from parafollicular C cells which produce calcitonin (hCt), makes up about 3% of all thyroid carcinoma cases, whereas treatment in advanced MTC has limited efficiency. Methods: Therapeutic doses of 100 mCi (3.7 GBq) 131I metaiodobenzylguanidine (131I-MIBG) were administered by slow i.v. infusion in our Center to 6 patients, 5 female and 1 male aged from 18 to 80 years, with proven disseminated medullary thyroid carcinoma. All patients underwent total thyreoidectomy and selective neck dissection prior to the treatment, but distant metastases were diagnosed. The total therapeutic doses the patients received ranged from 3.7 to 18.5 GBq of 131I-MIBG, for up to five total treatments at 3 months to 1.5 years intervals. Treatment was tolerated well in all patients. Tumor marker levels (hCt, carcinoembryonic antigen (CEA), neuron specific enolase (NSE), chromogranin A (CgA), pro- gastrin releasing peptide (pro-GRP)) were measured before and after therapy. Whole body scintigraphy performed after the therapy showed sites of metastatic disease. Results: In two patients we observed a decrease in hCt level, in one case the decrease lasted for 6 months, and in one patient no lung metastases were visible on whole body scan after second MIBG therapy. Other two cases showed a significant decrease in tumor marker levels only after neck dissection, but after that further dissemination was observed. In the last case we observer an increase in hCt level 10 months after therapy. Conclusions: Although there was individual impact on tumor marker levels, according to our experience objective response to 131I-MIBG therapy is limited.

medullary thyroid carcinoma ; MIBG therapy

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