High‐dose 131I‐metaiodobenzylguanidine therapy for 12 patients with malignant pheochromocytoma
Open Access
- 2 July 2003
- Vol. 98 (2), 239-248
- https://doi.org/10.1002/cncr.11518
Abstract
BACKGROUND 131I‐Metaiodobenzylguanidine (131I‐MIBG) can be used systemically to treat malignant pheochromocytoma. To improve outcome, the authors used higher levels of activity of 131I‐MIBG than previously reported. The authors reported the response rates and toxicity levels in patients with malignant pheochromocytoma or paraganglioma who were treated with high‐dose 131I‐MIBG. METHODS Following debulking surgery and stem cell harvest, 12 patients with malignant pheochromocytoma or paraganglioma were treated with 131I‐MIBG. Five had received previous external beam radiation and/or chemotherapy. The median single treatment dose was 800 mCi (37 gigabecquerels; range, 386–866 mCi) or 11.5 mCi/kg (range, 5.6–18.3 mCi/kg). The median cumulative dose was 1015 mCi (range, 386–1690 mCi). RESULTS Three patients had a complete response, two of whom had soft tissue and skeletal metastases. Their median follow‐up was 45 months (range, 23–101 months). Seven patients had a partial response (PR), with a median follow‐up 43 months (range, 6–47 months). Two patients without a response died with progressive disease (PD) and 2 patients with an initial PR died of PD at 13 and 11 months, respectively. Grade 3 thrombocytopenia occurred after 79% (15 of 19) of treatments had been administered. Grade 3 and 4 neutropenia followed 53% (10 of 19) and 19% (4 of 19) of treatments, respectively. One patient required stem cell infusion, and one developed primary ovarian failure. CONCLUSIONS The single and cumulative doses of 131I‐MIBG were approximately 2–3.5 times higher than those used at other centers. Unlike previous reports, two patients with both skeletal and soft tissue metastases had a complete response. Hematologic toxicity was significant but tolerable. High‐dose 131I‐MIBG may lead to long‐term survival in patients with malignant pheochromocytoma. Cancer 2003;98:239–48. © 2003 American Cancer Society. DOI 10.1002/cncr.11518Keywords
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